From 6153a1deec25581a9cb1d1553478192787d89bf3 Mon Sep 17 00:00:00 2001 From: mfl15 <144844529+mfl15@users.noreply.github.com> Date: Wed, 22 Jan 2025 19:13:11 +0000 Subject: [PATCH 1/2] refactoring_rag --- .env.example | 5 - .gitignore | 184 - LICENSE.txt | 2 +- README.md | 277 +- config.py | 1 - data/filtered_triple_data.csv | 88 - data/human_labeled_neo4j.csv | 1001 --- data/human_labeled_semmed.csv | 101 - data/predicate-remap.yaml | 5034 ---------------- data/semmed_sentence_data.csv | 329 - data/semmed_triple_data.csv | 200 - data/test_df_gpt_3_5_turbo_icl.csv | 31 - data/test_df_gpt_4_0_icl.csv | 31 - data/test_df_llama_icl.csv | 31 - data/true_false_chembl_labeled.csv | 99 - data/true_false_chembl_labeled_sentense.csv | 98 - data/true_false_chembl_labeled_triple.csv | 98 - data/updated_neo4j_sentence_data.csv | 103 - data/updated_neo4j_triple_data.csv | 1000 --- docker-compose.yml | 17 + env/LLMFactCheck.yml | 4 + json/local_items_single_3.json | 6022 +++++++++++++++++++ main.py | 43 - process.py | 161 - src/data_processing.py | 108 - src/extract_filtered_data.py | 217 + src/fact_check_processor.py | 169 + src/get_result.py | 76 - src/kg_data_extractor.py | 175 + src/kg_data_processor.py | 172 + src/langfuse_config.py | 13 + src/langfuse_main.py | 778 +++ src/load_documents_chromadb.py | 197 + src/load_model.py | 92 +- src/logger_config.py | 13 + src/process_result.py | 34 - src/processdb.py | 121 + src/processing.py | 77 - src/progress.py | 60 - src/progress_path.py | 36 - src/result_writing.py | 50 - src/retrieval_rag.py | 140 + src/triple_processing.py | 41 - test/__init__.py | 0 test/test_data_processing.py | 58 - test/test_process_result.py | 46 - test/test_progress.py | 45 - test/test_result_writing.py | 39 - test/test_triple_processing.py | 22 - util/chembl/chembl_triple.py | 55 - util/chembl/convert.py | 89 - util/chembl/create_dataset.py | 89 - util/chembl/semmed_triple_mapping.py | 52 - util/model_accuracy/accuracy.py | 127 - 54 files changed, 8197 insertions(+), 9954 deletions(-) delete mode 100644 .env.example delete mode 100644 .gitignore delete mode 100644 config.py delete mode 100644 data/filtered_triple_data.csv delete mode 100644 data/human_labeled_neo4j.csv delete mode 100644 data/human_labeled_semmed.csv delete mode 100644 data/predicate-remap.yaml delete mode 100644 data/semmed_sentence_data.csv delete mode 100644 data/semmed_triple_data.csv delete mode 100644 data/test_df_gpt_3_5_turbo_icl.csv delete mode 100644 data/test_df_gpt_4_0_icl.csv delete mode 100644 data/test_df_llama_icl.csv delete mode 100644 data/true_false_chembl_labeled.csv delete mode 100644 data/true_false_chembl_labeled_sentense.csv delete mode 100644 data/true_false_chembl_labeled_triple.csv delete mode 100644 data/updated_neo4j_sentence_data.csv delete mode 100644 data/updated_neo4j_triple_data.csv create mode 100644 docker-compose.yml create mode 100644 json/local_items_single_3.json delete mode 100644 main.py delete mode 100644 process.py delete mode 100644 src/data_processing.py create mode 100644 src/extract_filtered_data.py create mode 100644 src/fact_check_processor.py delete mode 100644 src/get_result.py create mode 100644 src/kg_data_extractor.py create mode 100644 src/kg_data_processor.py create mode 100644 src/langfuse_config.py create mode 100644 src/langfuse_main.py create mode 100644 src/load_documents_chromadb.py create mode 100644 src/logger_config.py delete mode 100644 src/process_result.py create mode 100644 src/processdb.py delete mode 100644 src/processing.py delete mode 100644 src/progress.py delete mode 100644 src/progress_path.py delete mode 100644 src/result_writing.py create mode 100644 src/retrieval_rag.py delete mode 100644 src/triple_processing.py delete mode 100644 test/__init__.py delete mode 100644 test/test_data_processing.py delete mode 100644 test/test_process_result.py delete mode 100644 test/test_progress.py delete mode 100644 test/test_result_writing.py delete mode 100644 test/test_triple_processing.py delete mode 100644 util/chembl/chembl_triple.py delete mode 100644 util/chembl/convert.py delete mode 100644 util/chembl/create_dataset.py delete mode 100644 util/chembl/semmed_triple_mapping.py delete mode 100644 util/model_accuracy/accuracy.py diff --git a/.env.example b/.env.example deleted file mode 100644 index 3e938cb..0000000 --- a/.env.example +++ /dev/null @@ -1,5 +0,0 @@ -DB_USER= -DB_PASSWORD= -DB_HOST= -DB_PORT= -STARTING_ID= diff --git a/.gitignore b/.gitignore deleted file mode 100644 index 1e4e679..0000000 --- a/.gitignore +++ /dev/null @@ -1,184 +0,0 @@ -# Conda -myLLMFactCheck.yml - -# Python -*.pyc -*.pyo -*.pyd -*.pyc.pytest_cache - -# IDE -.idea/ -.vscode/ - -# Temporary files -temp/ -*.sqlite - -# Large data folder (if applicable) -large_data_folder/ - -# Byte-compiled / optimized / DLL files -__pycache__/ -*.py[cod] -*$py.class - -# C extensions -*.so - -# Distribution / packaging -.Python -build/ -develop-eggs/ -dist/ -downloads/ -eggs/ -.eggs/ -lib/ -lib64/ -parts/ -sdist/ -var/ -wheels/ -share/python-wheels/ -*.egg-info/ -.installed.cfg -*.egg -MANIFEST - -# PyInstaller -# Usually these files are written by a python script from a template -# before PyInstaller builds the exe, so as to inject date/other infos into it. -*.manifest -*.spec - -# Installer logs -pip-log.txt -pip-delete-this-directory.txt - -# Unit test / coverage reports -htmlcov/ -.tox/ -.nox/ -.coverage -.coverage.* -.cache -nosetests.xml -coverage.xml -*.cover -*.py,cover -.hypothesis/ -.pytest_cache/ -cover/ - -# Translations -*.mo -*.pot - -# Django stuff: -*.log -local_settings.py -db.sqlite3 -db.sqlite3-journal - -# Flask stuff: -instance/ -.webassets-cache - -# Scrapy stuff: -.scrapy - -# Sphinx documentation -docs/_build/ - -# PyBuilder -.pybuilder/ -target/ - -# Jupyter Notebook -.ipynb_checkpoints - -# IPython -profile_default/ -ipython_config.py - -# pyenv -# For a library or package, you might want to ignore these files since the code is -# intended to run in multiple environments; otherwise, check them in: -# .python-version - -# pipenv -# According to pypa/pipenv#598, it is recommended to include Pipfile.lock in version control. -# However, in case of collaboration, if having platform-specific dependencies or dependencies -# having no cross-platform support, pipenv may install dependencies that don't work, or not -# install all needed dependencies. -#Pipfile.lock - -# poetry -# Similar to Pipfile.lock, it is generally recommended to include poetry.lock in version control. -# This is especially recommended for binary packages to ensure reproducibility, and is more -# commonly ignored for libraries. -# https://python-poetry.org/docs/basic-usage/#commit-your-poetrylock-file-to-version-control -#poetry.lock - -# pdm -# Similar to Pipfile.lock, it is generally recommended to include pdm.lock in version control. -#pdm.lock -# pdm stores project-wide configurations in .pdm.toml, but it is recommended to not include it -# in version control. -# https://pdm.fming.dev/#use-with-ide -.pdm.toml - -# PEP 582; used by e.g. github.com/David-OConnor/pyflow and github.com/pdm-project/pdm -__pypackages__/ - -# Celery stuff -celerybeat-schedule -celerybeat.pid - -# SageMath parsed files -*.sage.py - -# Environments -.env -.venv -venv/ -env.bak/ -venv.bak/ - -# Spyder project settings -.spyderproject -.spyproject - -# Rope project settings -.ropeproject - -# mkdocs documentation -/site - -# mypy -.mypy_cache/ -.dmypy.json -dmypy.json - -# Pyre type checker -.pyre/ - -# pytype static type analyzer -.pytype/ - -# Cython debug symbols -cython_debug/ - -# PyCharm -# JetBrains specific template is maintained in a separate JetBrains.gitignore that can -# be found at https://github.com/github/gitignore/blob/main/Global/JetBrains.gitignore -# and can be added to the global gitignore or merged into this file. For a more nuclear -# option (not recommended) you can uncomment the following to ignore the entire idea folder. -#.idea/ - -# Test results -test/test_result/ - -# Secret_key -config/ diff --git a/LICENSE.txt b/LICENSE.txt index 82f8c2d..68bc105 100644 --- a/LICENSE.txt +++ b/LICENSE.txt @@ -1,6 +1,6 @@ MIT License -Copyright (c) 2023 KoslickiLab +Copyright (c) 2025 KoslickiLab Permission is hereby granted, free of charge, to any person obtaining a copy of this software and associated documentation files (the "Software"), to deal diff --git a/README.md b/README.md index c0d7870..40f9013 100644 --- a/README.md +++ b/README.md @@ -38,6 +38,10 @@ To ensure a seamless experience, it's crucial to have GCC installed on your MacO ## Installation +## Command +docker-compose up -d +docker-compose ps + ### Conda Environment To run the LLMFactCheck tool, follow these steps to set up the necessary Conda environment. Follow these steps: 🛠️ @@ -66,145 +70,116 @@ To run the LLMFactCheck tool, follow these steps to set up the necessary Conda e conda activate myLLMFactCheck -6. Create a `config` folder in the root of the project, create the file `key.py` with the following contents: -OPENAI_API_KEY = 'your-openai-api-key' +6. Create a `.env` file in the root directory: +```plaintext +OPENAI_API_KEY='your-openai-api-key' +LANGFUSE_PUBLIC_KEY='langfuse_public_key' +LANGFUSE_SECRET_KEY='langfuse_secret_key' +LANGFUSE_HOST='langfuse_host' + + +DB_USERNAME='db_username' +DB_PASSWORD='db_password' +DB_NAME='db_name' +DB_HOST='db_host' +DB_PORT='db_port' + +``` # Usage (Run LLMFactCheck) 💡 After completing the installation, you can run the LLMFactCheck tool using the following command: -For LLAMA2 model: - - ```bash - python main.py --model llama --triple_file semmed_triple_data.csv --sentence_file semmed_sentence_data.csv - ``` - -For LLAMA model with ic: - - ```bash - python main.py --model llama --icl --triple_file semmed_triple_data.csv --sentence_file semmed_sentence_data.csv - ``` - -For GPT-3.5-turbo model: - - ```bash - python main.py --model gpt_3_5_turbo --triple_file semmed_triple_data.csv --sentence_file semmed_sentence_data.csv - ``` - -For GPT-3.5-turbo model with icl: - - ```bash - python main.py --model gpt_3_5_turbo --icl --triple_file semmed_triple_data.csv --sentence_file semmed_sentence_data.csv - ``` - -For GPT-4_0 model: - +**ChromaDB Document Creation** + Run the following command to initialize and process documents for ChromaDB:: ```bash - python main.py --model gpt_4_0 --triple_file semmed_triple_data.csv --sentence_file semmed_sentence_data.csv + python src/load_documents_chromadb.py ``` -For GPT-4_0 model with icl: - + +**Dataset Management & Experiment Runner** + The pipeline now automatically checks for an existing dataset and uploads data when necessary: ```bash - python main.py --model gpt_4_0 --icl --triple_file semmed_triple_data.csv --sentence_file semmed_sentence_data.csv + python src/langfuse_main.py ``` - + +## Additional Scripts + +### processdb.py +- Manages the database connection and cursor, loads nodes, processes edges, and provides a main entry point. +- Usage: + ```bash + python src/processdb.py + ``` + +### kg_data_processor.py +- Defines a KGDataExtractor class for loading nodes and edges, extracting sentences, and saving processed data. +- Usage: + ```bash + python src/kg_data_processor.py + ``` + +### kg_data_extractor.py +- Similar functionality with a KGDataExtractor class, but includes mapping of equivalent curies, sentence extraction, and saving multiple CSV outputs. +- Usage: + ```bash + python src/kg_data_extractor.py + ``` + +### fact_check_processor.py +- Implements a DBFactChecker class connecting to a database, pulling records in batches, running a language model check, and updating the DB. +- Usage: + ```bash + python src/fact_check_processor.py + ``` + +### extract_filtered_data.py +- Loads and filters knowledge graph data from JSONL files into CSV outputs. Also extracts relevant sentences and modifies the data accordingly. +- Usage: + ```bash + python src/extract_filtered_data.py + ``` + ## Project Structure This part of the project follows a well-organized structure for easy navigation and management. Here's a quick overview: - -- **main.py:** Main file that invokes the core logic of all models. - -- **data:** Your data for validation. - - `human_labeled_semmed.csv` - human-marked triples with sentences for correctness - - `semmed_triple_data.csv` - all the columns you need for a triple from SemMedDB - - `semmed_sentence_data.csv` - sentences from SemMedDB - - `filtered_triple_data.csv` - only those triples from SemMedDB that match the predicates from the yaml file - - `predicate-remap.yml` - all predicates have been re-mapped (including mapping SemMedDB predicates to Biolink) - - `test_df_3_5_turbo_icl` - test part human_data_semmed to determine the accuracy of the model GPT 3.5-turbo (with in-context learning) - - `test_df_4_0_icl` - test part human_data_semmed to determine the accuracy of the model GPT 4.0 (with in-context learning) - - `test_df_llama_icl` - test part human_data_semmed to determine the accuracy of the LLAMA2 model (with in-context learning) - -- **result:** Results of Semmed predicate validation will be stored here. - - **progress:** - Progress of a models - - `llama_semmed_result.csv`: results of the LLAMA2 model - - `llama_icl_semmed_result.csv`: results of the LLAMA2 model (with in-context learning) - - `gpt_3_5_turbo_semmed_result.csv`: results of the GPT-3.5-turbo model - - `gpt_3_5_turbo_icl_semmed_result.csv`: results of the GPT-3.5-turbo model (with in-context learning) - - `gpt_4_0_semmed_result.csv`: results of GPT-4.0 model - - `gpt_4_0_icl_semmed_result.csv`: results of GPT-4.0 model - -- **src:** Contains the main code for working with model and the Semmed database . - - `data_processing.py`: File for data processing. - - `triple_processing.py`: File for triple processing. - - `load_model.py`: This file contains functions related to loading and initializing the language model you're using in your project. It might include setting up the Llama model or OpenAI models with appropriate configurations and API keys. - - `get_result.py`: In this file, you can find functions related to obtaining results from the language model. This includes sending prompts to the model, receiving responses, and processing the model's output to extract meaningful information or answers. - - `result_writing.py`: File for writing results. - - `progress.py` - File to track the progress of predicate validation. - - `progress_path.py`: This file related to managing file paths for storing progress information. - - `progressing.py`: The purpose of this file is to manage the progression of tasks and processes within the project. + +## 📂 Project Structure +### **data/** +- `kg2c-2.8.4-nodes.jsonl` and `kg2c-2.8.4-edges.jsonl`: Source files containing nodes and edges data for ChromaDB. -- **util:** The util directory contains the following subdirectories and files: - - - model_accuracy directory - - This directory is used to calculate the model's accuracy. It uses human-annotated SemMedDB data to verify the model's ptriple accuracy. - - To see the model's accuracy, follow these steps: - Make sure you are at the root of the project and then: - - For LLAMA2 model: - - ```bash - cd util - cd model_accuracy - python accuracy.py --model llama --test_df_file test_df --result_file semmed_result - ``` - - For LLAMA2 model with ICL: - - ```bash - cd util - cd model_accuracy - python accuracy.py --model llama --icl --test_df_file test_df --result_file semmed_result - ``` - - For GPT-3.5.-turbo model: - - ```bash - cd util - cd model_accuracy - python accuracy.py --model gpt_3_5_turbo --test_df_file test_df --result_file semmed_result - ``` - - For GPT-3.5.-turbo model with ICL: - - ```bash - cd util - cd model_accuracy - python accuracy.py --model gpt_3_5_turbo --icl --test_df_file test_df --result_file semmed_result - ``` - - For GPT-4.0 model: - - ```bash - cd util - cd model_accuracy - python accuracy.py --model gpt_4_0 --test_df_file test_df --result_file semmed_result - ``` - - For GPT-4.0 model with ICL: - - ```bash - cd util - cd model_accuracy - python accuracy.py --model gpt_4_0 --icl --test_df_file test_df --result_file semmed_result - ``` - - You will see a visual representation of the model's accuracy in the form of a pie chart - - - - chembl directory + +### **env/** +- `LLMFactCheck.yml`: Conda environment configuration file. + +### **json/** +- `local_items_single_3.json`: Local dataset JSON file used for uploading to Langfuse. + + +### **src/** +1. **`__init__.py`** + - Initializes the `src` module. + +2. **`langfuse_config.py`** + - Initializes the Langfuse client for dataset operations. + +3. **`langfuse_main.py`** + - Defines the `DatasetManager` class for managing datasets: creating, retrieving, and uploading items to Langfuse. + +4. **`load_documents_chromadb.py`** + - Defines the `FileReader` class for reading and processing nodes and edges to create ChromaDB documents. + +5. **`load_model.py`** + - Initializes the ChromaDB collection for indexing and querying. + +6. **`logger_config.py`** + - Configures logging for the entire project to monitor execution steps and errors. + +7. **`retrieval_rag.py`** + - Defines the `ChromaDBQuery` class for querying ChromaDB to retrieve relevant documents for triples. + + +- chembl directory This directory contains files for testing the model's performance on the ChEMBL database. It includes the `chembl_triple.py` file, which generates triples. @@ -225,7 +200,7 @@ Here's a quick overview: ``` You don't have to do this (unless you think it's necessary), because we've already done this work and the result is already in the filtered_triple_data.py file - + - **test:** This directory contains tests for the project. Tests help verify if the code functions correctly and identify any errors or issues. Running Tests: @@ -239,28 +214,54 @@ Here's a quick overview: These tests utilize Python's built-in unittest.mock library to mock the file operations and csv.writer methods. This helps isolate the functions from the actual file system and ensure that the tests are repeatable and reliable. By patching the built-in open and csv.writer methods with unittest.mock.patch, we are able to simulate different scenarios and test how our functions react to them. Each test utilizes fixtures and mocks to simulate real data and code behavior. This helps ensure that the tests are reliable and repeatable. +--- + + +## 🛡️ How It Works + +1. **ChromaDB Initialization**: + - Use `load_documents_chromadb.py` to process and index nodes and edges into ChromaDB. + +2. **Langfuse Pipeline**: + - Upload datasets using `langfuse_main.py` and validate triples with the pipeline. -## How It Works +3. **Run the Tool**: Execute the main script, and watch as the tool works its magic. -1. **Run the Tool**: Execute the main script, and watch as the tool works its magic. +4. **View Results**: The results of the triple validation process will be stored in the "result". You can review them to identify any issues with the references. -2. **View Results**: The results of the triple validation process will be stored in the "result". You can review them to identify any issues with the references. +5. **Celebrate**: You've successfully checked triples with LLMFactCheck! 🎉 -3. **Celebrate**: You've successfully checked triples with LLMFactCheck! 🎉 +6. **Database Interaction (processdb.py)**: + - Manages DB connections, executes batch inserts, and prepares loaded edges and nodes. -Feel free to explore the source code in the "src" folder for customization or to understand the inner workings of the tool. +7. **KG Data Processing (kg_data_processor.py, kg_data_extractor.py)**: + - Extracts, filters, and converts edge/node data into CSVs (with sentence mapping and CURIE resolution). -### New Features +8. **Fact Checking (fact_check_processor.py)**: + - Connects to a DB, retrieves triples/sentences, runs them through a language model, then updates the DB with results. -- **Support for Multiple Sources**: LLMFactCheck now supports validating triples in various sources, not limited to Semmed. You can easily extend its functionality for different datasets. +9. **Filtered Extraction (extract_filtered_data.py)**: + - Loads and filters nodes/edges from JSONL, matches them with sentences, and exports multiple CSV outputs. +--- -- **Console Application**: We've introduced a new console application that allows you to validate triples in different sources using the command line. This provides more flexibility and ease of use, especially in environments where a database connection may not be available. -Enjoy using LLMFactCheck for all your triple validation needs! +## 🎉 New Features +1. **ChromaDB Integration**: Streamlined processes to load, query, and manage ChromaDB documents. +2. **Langfuse Dataset Management**: Automatic creation and uploading of datasets. +3. **Modular Design**: Classes and scripts are refactored for clarity and reusability. +4. **Flexible Pipeline Execution**: Multiple components to process and validate data. +5. **Support for Multiple Sources**: LLMFactCheck now supports validating triples in various sources, not limited to Semmed. You can easily extend its functionality for different datasets. +6. **Console Application**: We've introduced a new console application that allows you to validate triples in different sources using the command line. This provides more flexibility and ease of use, especially in environments where a database connection may not be available. +--- -## Conclusion +### Example Command Recap: +```bash +# Generate ChromaDB documents +python src/load_documents_chromadb.py -LLMFactCheck simplifies the process of checking triples in various sources. Whether you're a researcher or a data enthusiast, our tool will help you ensure the accuracy and quality of your data. Happy validating! +# Manage Langfuse datasets and run experiments +python src/langfuse_main.py +``` -Please do not hesitate to contact us if you have any questions or see that the code needs to be improved. +Happy Fact-Checking! 🎉 diff --git a/config.py b/config.py deleted file mode 100644 index fbce9b8..0000000 --- a/config.py +++ /dev/null @@ -1 +0,0 @@ -OPENAI_API_KEY="" diff --git a/data/filtered_triple_data.csv b/data/filtered_triple_data.csv deleted file mode 100644 index 3e28abf..0000000 --- a/data/filtered_triple_data.csv +++ /dev/null @@ -1,88 +0,0 @@ -Predicate ID,Triple,Sentence ID -10592832,Disease process of Human,18 -10592873,Virus causes Disease,18 -10593057,Lepus capensis location of Antibodies,23 -10593208,Binding Protein part of FHL1,26 -10593243,COMPLEMENT FACTOR H|CFH part of Borrelia burgdorferi,26 -10593287,Binding Protein part of Borrelia burgdorferi,26 -10593621,XS part of Borrelia burgdorferi,34 -10593815,XS produces homocysteine,39 -10593856,Bacteria interacts with Methionine,39 -10593932,Pheromone affects Gene Expression,40 -10594285,B.S.S. treats Adult,50 -10594435,host part of Vertebrates,53 -10594472,B.S.S. affects host,53 -10594689,Disease process of Farm Animals,57 -10594898,Therapeutic procedure uses Microbicides,62 -10595006,Therapeutic procedure uses Microbicides,64 -10595193,enrofloxacin coexists with Pharmaceutical Preparations,67 -10595361,Covers treats Tick-Borne Encephalitis,70 -10595474,Behavior process of Human,72 -10595632,Infection process of Adult,75 -10595725,Fever process of Patients,76 -10595759,Fever process of Females,76 -10595794,Fever process of Males,76 -10595906,Recombinant DNA part of 16s,78 -10595985,Tick-Borne Infections process of Individual,79 -10596143,"Glossitis, Benign Migratory process of Patients",81 -10596199,"Glossitis, Benign Migratory process of Patients",81 -10596244,Symptoms process of Patients,81 -10596294,Lyme Disease process of Patients,81 -10596383,Diagnosis treats Patients,82 -10596492,Immunofluorescence diagnoses Infection,83 -10596565,Lyme Disease process of Patients,84 -10596660,Lyme Disease process of Individual,85 -10596772,Disease process of Adult,87 -10596805,Disorder characterized by fever process of Adult,87 -10597199,"4,5-dibromo-2-pyrrolic acid compared with 1-oleoyl-2-stearoylphosphatidylcholine",97 -10597287,"4,5-dibromo-2-pyrrolic acid inhibits DNA",98 -10597421,"4,5-dibromo-2-pyrrolic acid interacts with Specific antigen",100 -10597542,Neuropeptides affects Inflammation,102 -10597633,Crosstalk causes Autoimmunity,103 -10597756,neuropeptide Y|NPY interacts with T-Lymphocyte,105 -10597803,neuropeptide Y|NPY stimulates Antigen-Presenting Cells,105 -10597925,Mammals location of Toll-like receptors,107 -10598015,Endosomes location of Compartments,108 -10598051,Cell surface location of receptor,108 -10598148,"RNA, Small Interfering interacts with Ribose",110 -10598263,E2F1 gene|E2F1|UBE2L3 causes Apoptosis,112 -10598476,E2F1 gene|E2F1|UBE2L3 interacts with Pharmaceutical Preparations,116 -10598517,E2F1 gene|E2F1|UBE2L3 causes Apoptosis,116 -10599076,Gene Expression process of Scorpaenidae,123 -10599190,Vitellogenins part of Scorpaenidae,124 -10599329,Vitellogenins part of Scorpaenidae,125 -10599368,Vitellogenins part of Scorpaenidae,125 -10599395,Vitellogenins affects No past history,125 -10599484,Vitellogenins part of Scorpaenidae,126 -10599560,Vitellogenins part of Scorpaenidae,127 -10599602,Vitellogenins part of Scorpaenidae,127 -10599653,Injection procedure treats Female,127 -10599747,Vitellogenins part of Scorpaenidae,128 -10599840,Vitellogenins part of Scorpaenidae,129 -10600338,Homologous Gene part of Hemicentrotus pulcherrimus,141 -10600422,cDNA Library part of Gastrula,142 -10600456,Homologous Gene part of Hemicentrotus pulcherrimus,142 -10600542,Blastocyst structure part of Mesenchyma,144 -10600645,In Situ Hybridization uses Mounts,146 -10600813,Embryo location of PPY,151 -10600845,Inferior Colliculus part of Males,151 -10600962,PPY part of Mothers,153 -10600997,Cells part of Nurses,153 -10601037,Cytoplasm location of PPY,153 -10601150,Cytoplasm part of Spermatocytes,155 -10601184,Inferior Colliculus location of PPY,155 -10601265,Cell Nucleus part of Cells,156 -10601441,Column location of Diastasis,160 -10601592,Drug Kinetics process of Rattus norvegicus,163 -10601803,Extracellular Matrix location of Proteoglycan,166 -10601941,GAG Gene converts to Glycosaminoglycans,168 -10601994,GAG Gene converts to Oligosaccharides,168 -10602026,Electrophoresis uses Structural analysis,168 -10602109,Enzymes interacts with Glycosaminoglycans,169 -10602147,Chemicals interacts with Glycosaminoglycans,169 -10602185,Glycosaminoglycans converts to Disaccharides,169 -10602215,Glycosaminoglycans converts to Oligosaccharides,169 -10602419,Diabetes process of Patients,173 -10602491,Detection uses Sorbate,174 -10603013,"PTH protein, human|PTH associated with osteosarcoma",187 -10603069,"PTH protein, human|PTH associated with Malignant Neoplasms",187 diff --git a/data/human_labeled_neo4j.csv b/data/human_labeled_neo4j.csv deleted file mode 100644 index 8d8a750..0000000 --- a/data/human_labeled_neo4j.csv +++ /dev/null @@ -1,1001 +0,0 @@ -Predicate ID,Triple,Sentence ID,Sentence,Question,Label,Reference -26452786,Fenbendazole causes helminthiasis,546,"Veterinary anthelmintic. Fenbendazole is a fda approved for use in cattle, pigs and goats Fenbendazole (Hoechst brand names Panacur and Safe-Guard, Intervet Panacur and Panacur Rabbit) is a broad spectrum benzimidazole anthelmintic used against gastrointestinal parasites including roundworms, hookworms, whipworms, the taenia species of tapeworms, pinworms, aelurostrongylus, paragonimiasis, strongyles and strongyloides and can be administered to sheep, cattle, horses, fish, dogs, cats, rabbits and seals. Drug interactions may occur if using bromsalan flukicides (Dibromsalan, Tribromsalan). Abortions in cattle and death in sheep have been reported after using these medications together. (Plumb's Veterinary Drug Handbook, Fifth Edition. 2005","Is the triple Fenbendazole causes helminthiasis supported by the sentence Veterinary anthelmintic. Fenbendazole is a fda approved for use in cattle, pigs and goats Fenbendazole (Hoechst brand names Panacur and Safe-Guard, Intervet Panacur and Panacur Rabbit) is a broad spectrum benzimidazole anthelmintic used against gastrointestinal parasites including roundworms, hookworms, whipworms, the taenia species of tapeworms, pinworms, aelurostrongylus, paragonimiasis, strongyles and strongyloides and can be administered to sheep, cattle, horses, fish, dogs, cats, rabbits and seals. Drug interactions may occur if using bromsalan flukicides (Dibromsalan, Tribromsalan). Abortions in cattle and death in sheep have been reported after using these medications together. (Plumb's Veterinary Drug Handbook, Fifth Edition. 2005",True,http://en.wikipedia.org/wiki/helminth -24413653,Fenbendazole treats helminthiasis,546,"Veterinary anthelmintic. Fenbendazole is a fda approved for use in cattle, pigs and goats Fenbendazole (Hoechst brand names Panacur and Safe-Guard, Intervet Panacur and Panacur Rabbit) is a broad spectrum benzimidazole anthelmintic used against gastrointestinal parasites including roundworms, hookworms, whipworms, the taenia species of tapeworms, pinworms, aelurostrongylus, paragonimiasis, strongyles and strongyloides and can be administered to sheep, cattle, horses, fish, dogs, cats, rabbits and seals. Drug interactions may occur if using bromsalan flukicides (Dibromsalan, Tribromsalan). Abortions in cattle and death in sheep have been reported after using these medications together. (Plumb's Veterinary Drug Handbook, Fifth Edition. 2005","Is the triple Fenbendazole treats helminthiasis supported by the sentence Veterinary anthelmintic. Fenbendazole is a fda approved for use in cattle, pigs and goats Fenbendazole (Hoechst brand names Panacur and Safe-Guard, Intervet Panacur and Panacur Rabbit) is a broad spectrum benzimidazole anthelmintic used against gastrointestinal parasites including roundworms, hookworms, whipworms, the taenia species of tapeworms, pinworms, aelurostrongylus, paragonimiasis, strongyles and strongyloides and can be administered to sheep, cattle, horses, fish, dogs, cats, rabbits and seals. Drug interactions may occur if using bromsalan flukicides (Dibromsalan, Tribromsalan). Abortions in cattle and death in sheep have been reported after using these medications together. (Plumb's Veterinary Drug Handbook, Fifth Edition. 2005",True,http://en.wikipedia.org/wiki/helminth -22762728,Fenbendazole prevents helminthiasis,546,"Veterinary anthelmintic. Fenbendazole is a fda approved for use in cattle, pigs and goats Fenbendazole (Hoechst brand names Panacur and Safe-Guard, Intervet Panacur and Panacur Rabbit) is a broad spectrum benzimidazole anthelmintic used against gastrointestinal parasites including roundworms, hookworms, whipworms, the taenia species of tapeworms, pinworms, aelurostrongylus, paragonimiasis, strongyles and strongyloides and can be administered to sheep, cattle, horses, fish, dogs, cats, rabbits and seals. Drug interactions may occur if using bromsalan flukicides (Dibromsalan, Tribromsalan). Abortions in cattle and death in sheep have been reported after using these medications together. (Plumb's Veterinary Drug Handbook, Fifth Edition. 2005","Is the triple Fenbendazole prevents helminthiasis supported by the sentence Veterinary anthelmintic. Fenbendazole is a fda approved for use in cattle, pigs and goats Fenbendazole (Hoechst brand names Panacur and Safe-Guard, Intervet Panacur and Panacur Rabbit) is a broad spectrum benzimidazole anthelmintic used against gastrointestinal parasites including roundworms, hookworms, whipworms, the taenia species of tapeworms, pinworms, aelurostrongylus, paragonimiasis, strongyles and strongyloides and can be administered to sheep, cattle, horses, fish, dogs, cats, rabbits and seals. Drug interactions may occur if using bromsalan flukicides (Dibromsalan, Tribromsalan). Abortions in cattle and death in sheep have been reported after using these medications together. (Plumb's Veterinary Drug Handbook, Fifth Edition. 2005",True,http://en.wikipedia.org/wiki/helminth -45041532,Ibuprofen treats Pain,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Pain supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",False,https://orcid.org/0000-0001-5208-3432 -16658505,Albendazole affects malaria,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole affects malaria supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=malaria -16658503,Albendazole disrupts malaria,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole disrupts malaria supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=malaria -30646571,Ibuprofen treats Pain,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Pain supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",False,https://orcid.org/0000-0001-5208-3432 -30650567,Ibuprofen treats patent ductus arteriosus,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats patent ductus arteriosus supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",False,https://orcid.org/0000-0002-0736-9199 -30383540,Ibuprofen treats Alzheimer disease,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Alzheimer disease supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",False,http://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-fact-sheet -25735916,Albendazole affects trichuriasis,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole affects trichuriasis supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/trichuriasis -9588560,Albendazole treats trichuriasis,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole treats trichuriasis supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/trichuriasis -21848143,Albendazole causes helminthiasis,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole causes helminthiasis supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/helminth -13946207,Albendazole affects helminthiasis,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole affects helminthiasis supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/helminth -8712067,Albendazole treats helminthiasis,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole treats helminthiasis supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/helminth -24729219,Albendazole disrupts helminthiasis,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole disrupts helminthiasis supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/helminth -13732336,Albendazole prevents helminthiasis,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole prevents helminthiasis supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/helminth -18452252,Albendazole affects toxocariasis,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole affects toxocariasis supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www.dpd.cdc.gov/dpdx/html/toxocariasis.htm -10114050,Albendazole treats toxocariasis,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole treats toxocariasis supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www.dpd.cdc.gov/dpdx/html/toxocariasis.htm -7789677,Albendazole treats strongyloidiasis,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole treats strongyloidiasis supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www.dpd.cdc.gov/dpdx/html/strongyloidiasis.htm -10750815,Albendazole treats onchocerciasis,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole treats onchocerciasis supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www.dpd.cdc.gov/dpdx/html/filariasis.htm -30648628,Ivabradine treats congestive heart failure,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine treats congestive heart failure supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",False,http://en.wikipedia.org/wiki/heart_disease -13637338,Albendazole disrupts Hookworm Infections,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole disrupts Hookworm Infections supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -24685635,Albendazole affects filarial elephantiasis,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole affects filarial elephantiasis supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://www.who.int/news-room/fact-sheets/detail/lymphatic-filariasis -30645138,Cefixime treats bacterial urinary tract infection,558,"A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefixime treats bacterial urinary tract infection supported by the sentence A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-6601-2165 -7226097,Albendazole treats cysticercosis,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole treats cysticercosis supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/cysticercosis -22678969,Albendazole treats Infection,551,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Albendazole treats Infection supported by the sentence A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -25678577,Latamoxef treats bacterial infectious disease,553,"A semisynthetic oxa-beta-lactam antibiotic, with antibacterial activity used mainly against gram-negative aerobic bacteria. Replacing the beta-lactam sulfur atom for an oxygen atom and the presence of the methyltetrazolethio moiety and the para-hydroxyphenylmalonyl group, increases the antibacterial activity of moxalactam. The 7-alpha-methoxy group and the para-hydroxyphenylmalonyl group increases the stability of this agent against beta-lactamases. The use of this agent has been associated with fatal bleeding events.; A parenteral oxacephem antibiotic with an oxygen molecule substituted for the sulfur atom in the beta-lactam nucleus. Moxalactam is a thrid-generation cephalosporin that has broad-spectrum antibiotic activity and high resistance to beta-lactameses. This agent is active against gram-negative enteric bacilli, including multiple drug-resistant strains.; Broad- spectrum beta-lactam antibiotic similar in structure to the CEPHALOSPORINS except for the substitution of an oxaazabicyclo moiety for the thiaazabicyclo moiety of certain CEPHALOSPORINS. It has been proposed especially for the meningitides because it passes the blood-brain barrier and for anaerobic infections.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Latamoxef treats bacterial infectious disease supported by the sentence A semisynthetic oxa-beta-lactam antibiotic, with antibacterial activity used mainly against gram-negative aerobic bacteria. Replacing the beta-lactam sulfur atom for an oxygen atom and the presence of the methyltetrazolethio moiety and the para-hydroxyphenylmalonyl group, increases the antibacterial activity of moxalactam. The 7-alpha-methoxy group and the para-hydroxyphenylmalonyl group increases the stability of this agent against beta-lactamases. The use of this agent has been associated with fatal bleeding events.; A parenteral oxacephem antibiotic with an oxygen molecule substituted for the sulfur atom in the beta-lactam nucleus. Moxalactam is a thrid-generation cephalosporin that has broad-spectrum antibiotic activity and high resistance to beta-lactameses. This agent is active against gram-negative enteric bacilli, including multiple drug-resistant strains.; Broad- spectrum beta-lactam antibiotic similar in structure to the CEPHALOSPORINS except for the substitution of an oxaazabicyclo moiety for the thiaazabicyclo moiety of certain CEPHALOSPORINS. It has been proposed especially for the meningitides because it passes the blood-brain barrier and for anaerobic infections.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/pathogenic_bacteria -45049643,Prednisolone treats Shock,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats Shock supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",False,http://www.merriam-webster.com/medlineplus/shock -45049629,Prednisolone treats hepatitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats hepatitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",False,https://orcid.org/0000-0002-0736-9199 -14332005,Ibuprofen predisposes bronchopulmonary dysplasia,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen predisposes bronchopulmonary dysplasia supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://www.nhlbi.nih.gov/health/bronchopulmonary-dysplasia -24384432,Ibuprofen affects migraine disorder,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen affects migraine disorder supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.mayoclinic.com/health/migraine-headache/ds00120 -8452594,Ibuprofen treats migraine disorder,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats migraine disorder supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.mayoclinic.com/health/migraine-headache/ds00120 -9106384,Ibuprofen related to osteoarthritis,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen related to osteoarthritis supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.mayoclinic.com/health/osteoarthritis/ds00019 -13826486,Ibuprofen affects osteoarthritis,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen affects osteoarthritis supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.mayoclinic.com/health/osteoarthritis/ds00019 -45049572,Prednisolone treats exfoliative dermatitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats exfoliative dermatitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",False,https://orcid.org/0000-0002-0736-9199 -45049556,Prednisolone treats contact dermatitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats contact dermatitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",False, -19399624,Ibuprofen prevents osteoarthritis,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen prevents osteoarthritis supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.mayoclinic.com/health/osteoarthritis/ds00019 -13653982,Ibuprofen causes Alzheimer disease,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen causes Alzheimer disease supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-fact-sheet -9436288,Ibuprofen treats Alzheimer disease,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Alzheimer disease supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-fact-sheet -8331095,Ibuprofen disrupts Alzheimer disease,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen disrupts Alzheimer disease supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-fact-sheet -7843138,Ibuprofen prevents Alzheimer disease,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen prevents Alzheimer disease supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-fact-sheet -14294004,Ibuprofen predisposes Alzheimer disease,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen predisposes Alzheimer disease supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-fact-sheet -9800201,Ibuprofen causes arthritic joint disease,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen causes arthritic joint disease supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.arthritis.org/ -7686895,Ibuprofen treats arthritic joint disease,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats arthritic joint disease supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.arthritis.org/ -18599970,Ibuprofen disrupts arthritic joint disease,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen disrupts arthritic joint disease supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.arthritis.org/ -21268743,Ibuprofen treats glioma,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats glioma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0736-9199 -26701175,Ibuprofen affects rheumatoid arthritis,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen affects rheumatoid arthritis supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0736-9199 -8397426,Ibuprofen treats rheumatoid arthritis,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats rheumatoid arthritis supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0736-9199 -17292168,Ibuprofen treats Chronic pain,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Chronic pain supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0736-9199 -13710734,Ibuprofen prevents Chronic pain,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen prevents Chronic pain supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0736-9199 -8698382,Ibuprofen treats Tension-type headache,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Tension-type headache supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0736-9199 -9536612,Ibuprofen treats Low back pain,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Low back pain supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True, -12482174,Ibuprofen causes pancreatitis,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen causes pancreatitis supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://medlineplus.gov/pancreatitis.htm -21354514,Ibuprofen prevents pancreatitis,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen prevents pancreatitis supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://medlineplus.gov/pancreatitis.htm -12079834,Ibuprofen causes adult acute respiratory distress syndrome,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen causes adult acute respiratory distress syndrome supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://www.ncbi.nlm.nih.gov/pmc/articles/pmc5392788/ -23500890,Ibuprofen affects adult acute respiratory distress syndrome,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen affects adult acute respiratory distress syndrome supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://www.ncbi.nlm.nih.gov/pmc/articles/pmc5392788/ -11440746,Ibuprofen related to Toothache,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen related to Toothache supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://www.merriam-webster.com/dictionary/toothache -12438812,Ibuprofen causes Toothache,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen causes Toothache supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://www.merriam-webster.com/dictionary/toothache -30340568,Prednisolone treats nephrotic syndrome,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats nephrotic syndrome supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",False,https://www.niddk.nih.gov/health-information/kidney-disease/nephrotic-syndrome-adults -10195210,Ibuprofen treats influenza,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats influenza supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.merck.com/mmhe/sec17/ch198/ch198d.htm -9550056,Ibuprofen treats Acute Pain,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Acute Pain supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.nationalpainfoundation.org/mytreatment/articles/cancer_paindefinitions.asp -27630106,Ibuprofen disrupts Acute Pain,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen disrupts Acute Pain supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.nationalpainfoundation.org/mytreatment/articles/cancer_paindefinitions.asp -8748381,Ibuprofen treats Dysmenorrhea,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Dysmenorrhea supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0001-5208-3432 -15961024,Ibuprofen prevents Dysmenorrhea,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen prevents Dysmenorrhea supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0001-5208-3432 -13722152,Ibuprofen treats Neck pain,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Neck pain supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0003-6754 -45041115,Hydrocortisone treats contact dermatitis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats contact dermatitis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",False, -13726345,Ibuprofen causes patent ductus arteriosus,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen causes patent ductus arteriosus supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0736-9199 -45041106,Hydrocortisone treats atopic eczema,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats atopic eczema supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",False,http://en.wikipedia.org/wiki/atopic_dermatitis -7851777,Ibuprofen treats patent ductus arteriosus,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats patent ductus arteriosus supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0736-9199 -8584177,Ibuprofen prevents patent ductus arteriosus,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen prevents patent ductus arteriosus supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0736-9199 -25518118,Ibuprofen treats Fractured ankle,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Fractured ankle supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://www.hss.edu/condition-list_ankle-fractures.asp -26824955,Ibuprofen treats spondylosis,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats spondylosis supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www.nlm.nih.gov/medlineplus/ency/article/000436.htm -8106985,Ibuprofen related to burn,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen related to burn supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True, -22125431,Ibuprofen treats preeclampsia,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats preeclampsia supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,PMID:24400024 -8163776,Ibuprofen causes injury,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen causes injury supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True, -15746938,Ibuprofen affects injury,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen affects injury supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True, -9104501,Ibuprofen treats injury,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats injury supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True, -9104502,Ibuprofen prevents injury,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen prevents injury supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True, -15342704,Ibuprofen exacerbates injury,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen exacerbates injury supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True, -30382081,Hydrocortisone treats congenital adrenal hyperplasia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats congenital adrenal hyperplasia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",False,http://www.genome.jp/dbget-bin/www_bget?ds:h00216 -20886939,Ibuprofen affects Cognitive impairment,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen affects Cognitive impairment supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0009-0006-4530-3154 -13584223,Ibuprofen affects Cognitive impairment,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen affects Cognitive impairment supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0009-0006-4530-3154 -17621968,Ibuprofen treats Cognitive impairment,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Cognitive impairment supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0009-0006-4530-3154 -30368705,Hydrocortisone treats Hypoxemia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats Hypoxemia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",False,https://orcid.org/0000-0001-5208-3432 -7852264,Ibuprofen treats Headache,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Headache supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=headache -10201705,Ibuprofen prevents Headache,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen prevents Headache supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=headache -20691057,Ibuprofen prevents altitude sickness,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen prevents altitude sickness supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True, -25670779,Ibuprofen treats sunburn,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats sunburn supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True, -17687542,Ibuprofen prevents canker sore,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen prevents canker sore supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,PMID:25346356 -11381904,Ibuprofen treats Premature birth,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Premature birth supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0736-9199 -20007370,Ibuprofen predisposes cerebral palsy,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen predisposes cerebral palsy supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://en.wikipedia.org/wiki/cerebral_palsy -30352089,Hydrocortisone treats atopic eczema,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats atopic eczema supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",False,http://en.wikipedia.org/wiki/atopic_dermatitis -13826476,"Ibuprofen treats osteoarthritis, spine",554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats osteoarthritis, spine supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True, -10429873,Ibuprofen causes Hemorrhage,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen causes Hemorrhage supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://www.ncbi.nlm.nih.gov/books/nbk542273/ -30352078,Hydrocortisone treats Insulin resistance,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats Insulin resistance supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",False,https://orcid.org/0000-0002-0736-9199 -9889792,Ibuprofen affects Hemorrhage,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen affects Hemorrhage supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://www.ncbi.nlm.nih.gov/books/nbk542273/ -8420965,Ibuprofen treats Hemorrhage,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Hemorrhage supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://www.ncbi.nlm.nih.gov/books/nbk542273/ -22159382,Ibuprofen prevents Hemorrhage,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen prevents Hemorrhage supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://www.ncbi.nlm.nih.gov/books/nbk542273/ -9950431,Ibuprofen treats rheumatic disorder,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats rheumatic disorder supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://en.wikipedia.org/wiki/connective_tissue_disease -20821983,Ibuprofen treats common cold,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats common cold supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=common%20cold -13133316,Ibuprofen causes peptic ulcer disease,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen causes peptic ulcer disease supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,PMID:28242110 -11207850,Ibuprofen affects peptic ulcer disease,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen affects peptic ulcer disease supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,PMID:28242110 -11790277,Ibuprofen treats hypertensive disorder,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats hypertensive disorder supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,PMID:24352797 -25657729,Ibuprofen prevents hypertensive disorder,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen prevents hypertensive disorder supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,PMID:24352797 -30650036,Methylprednisolone treats lupus nephritis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats lupus nephritis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",False,https://medlineplus.gov/ency/article/000481.htm -12673407,Ibuprofen predisposes bone fracture,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen predisposes bone fracture supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True, -16265626,Ibuprofen related to Arthralgia,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen related to Arthralgia supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0736-9199 -9444914,Ibuprofen treats Arthralgia,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Arthralgia supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0736-9199 -11536369,Ibuprofen treats seasonal allergic rhinitis,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats seasonal allergic rhinitis supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,PMID:11449200 -30361930,Methylprednisolone treats Edema,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats Edema supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",False,https://orcid.org/0000-0002-0736-9199 -11157616,Ibuprofen causes Pain,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen causes Pain supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0001-5208-3432 -30361925,Methylprednisolone treats Pain,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats Pain supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",False,https://orcid.org/0000-0001-5208-3432 -14486259,Ibuprofen disrupts Pain,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen disrupts Pain supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0001-5208-3432 -9022792,Ibuprofen prevents Pain,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen prevents Pain supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0001-5208-3432 -10026104,Ibuprofen affects Myalgia,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen affects Myalgia supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0736-9199 -9913360,Ibuprofen treats Myalgia,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Myalgia supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0736-9199 -30353075,Methylprednisolone treats lupus nephritis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats lupus nephritis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",False,https://medlineplus.gov/ency/article/000481.htm -10026105,Ibuprofen prevents Myalgia,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen prevents Myalgia supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,https://orcid.org/0000-0002-0736-9199 -12641386,Ibuprofen causes Fever,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen causes Fever supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,PMID:9759682 -12659717,Ibuprofen affects Fever,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen affects Fever supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,PMID:9759682 -45033468,Ciprofloxacin treats Recurrent lower respiratory tract infections,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats Recurrent lower respiratory tract infections supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-0736-9199 -7258310,Ibuprofen treats Fever,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen treats Fever supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,PMID:9759682 -15072611,Ibuprofen disrupts Fever,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen disrupts Fever supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,PMID:9759682 -22123299,Ibuprofen prevents Fever,554,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]","Is the triple Ibuprofen prevents Fever supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",True,PMID:9759682 -30644543,Ciprofloxacin treats osteomyelitis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats osteomyelitis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-0736-9199 -30376352,Ciprofloxacin treats prostatitis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats prostatitis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-6601-2165 -25984950,Cefmenoxime treats bacterial infectious disease,556,"A third-generation, semi-synthetic, beta-lactam cephalosporin antibiotic with antibacterial activity. Cefmenoxime binds to penicillin-binding proteins (PBPs), transpeptidases that are responsible for crosslinking of peptidoglycan. By preventing crosslinking of peptidoglycan, cell wall integrity is lost and cell wall synthesis is halted.; A cephalosporin antibiotic that is administered intravenously or intramuscularly. It is active against most common gram-positive and gram-negative microorganisms, is a potent inhibitor of Enterobacteriaceae, and is highly resistant to hydrolysis by beta-lactamases. The drug has a high rate of efficacy in many types of infection and to date no severe side effects have been noted.","Is the triple Cefmenoxime treats bacterial infectious disease supported by the sentence A third-generation, semi-synthetic, beta-lactam cephalosporin antibiotic with antibacterial activity. Cefmenoxime binds to penicillin-binding proteins (PBPs), transpeptidases that are responsible for crosslinking of peptidoglycan. By preventing crosslinking of peptidoglycan, cell wall integrity is lost and cell wall synthesis is halted.; A cephalosporin antibiotic that is administered intravenously or intramuscularly. It is active against most common gram-positive and gram-negative microorganisms, is a potent inhibitor of Enterobacteriaceae, and is highly resistant to hydrolysis by beta-lactamases. The drug has a high rate of efficacy in many types of infection and to date no severe side effects have been noted.",True,http://en.wikipedia.org/wiki/pathogenic_bacteria -21500374,Ivabradine treats hypotensive disorder,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine treats hypotensive disorder supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True,https://orcid.org/0000-0002-0736-9199 -15323306,Ivabradine affects coronary artery disorder,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine affects coronary artery disorder supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True,PMID:31420554 -12424888,Ivabradine treats coronary artery disorder,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine treats coronary artery disorder supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True,PMID:31420554 -30354207,Ciprofloxacin treats osteomyelitis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats osteomyelitis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-0736-9199 -30347289,Ciprofloxacin treats infectious disease,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats infectious disease supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://www.merriam-webster.com/medical/communicable%20disease -10817471,Ivabradine prevents Tachycardia,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine prevents Tachycardia supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True,https://orcid.org/0000-0002-0736-9199 -18841652,Ivabradine treats toxic shock syndrome,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine treats toxic shock syndrome supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True,http://en.wikipedia.org/wiki/toxic_shock_syndrome -19228519,Ivabradine causes atrial fibrillation,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine causes atrial fibrillation supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -20784958,Ivabradine affects atrial fibrillation,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine affects atrial fibrillation supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -17604342,Ivabradine treats atrial fibrillation,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine treats atrial fibrillation supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -19514713,Ivabradine disrupts atrial fibrillation,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine disrupts atrial fibrillation supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -17822394,Ivabradine prevents atrial fibrillation,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine prevents atrial fibrillation supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -19153602,Ivabradine predisposes atrial fibrillation,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine predisposes atrial fibrillation supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -15681673,Ivabradine treats multiple organ dysfunction syndrome,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine treats multiple organ dysfunction syndrome supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True,https://www.ncbi.nlm.nih.gov/books/nbk6868/ -15641743,Ivabradine treats systolic heart failure,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine treats systolic heart failure supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True, -20520107,Ivabradine affects mitral valve stenosis,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine affects mitral valve stenosis supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True,http://en.wikipedia.org/wiki/mitral_valve_stenosis -18126606,Ivabradine treats mitral valve stenosis,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine treats mitral valve stenosis supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True,http://en.wikipedia.org/wiki/mitral_valve_stenosis -12164130,Ivabradine treats Stable angina,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine treats Stable angina supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True, -17604344,Ivabradine related to diastolic heart failure,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine related to diastolic heart failure supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True, -20004006,Ivabradine affects diastolic heart failure,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine affects diastolic heart failure supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True, -17604340,Ivabradine treats diastolic heart failure,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine treats diastolic heart failure supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True, -15323309,Ivabradine affects cardiovascular disorder,557,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.","Is the triple Ivabradine affects cardiovascular disorder supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",True,http://en.wikipedia.org/wiki/circulatory_system -30376059,Nicergoline treats depressive disorder,647,UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; An ergot derivative that has been used as a cerebral vasodilator and in peripheral vascular disease. It has been suggested to ameliorate cognitive deficits in cerebrovascular disease.,Is the triple Nicergoline treats depressive disorder supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; An ergot derivative that has been used as a cerebral vasodilator and in peripheral vascular disease. It has been suggested to ameliorate cognitive deficits in cerebrovascular disease.,False,PMID:23902698 -30350761,Thioctic acid treats hypertensive disorder,682,"A naturally occurring micronutrient, synthesized in small amounts by plants and animals (including humans), with antioxidant and potential chemopreventive activities. Alpha-lipoic acid acts as a free radical scavenger and assists in repairing oxidative damage and regenerates endogenous antioxidants, including vitamins C and E and glutathione. This agent also promotes glutathione synthesis. In addition, alpha-lipoic acid exerts metal chelating capacities and functions as a cofactor in various mitochondrial enzyme complexes involved in the decarboxylation of alpha-keto acids. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C61595"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C61595"" NCI Thesaurus); A naturally occurring micronutrient, synthesized in small amounts by plants and animals (including humans), with antioxidant and potential chemopreventive activities. Alpha-lipoic acid acts as a free radical scavenger and assists in repairing oxidative damage and regenerates endogenous antioxidants, including vitamins C and E and glutathione. This agent also promotes glutathione synthesis. In addition, alpha-lipoic acid exerts metal chelating capacities and functions as a cofactor in various mitochondrial enzyme complexes involved in the decarboxylation of alpha-keto acids.; An octanoic acid bridged with two sulfurs so that it is sometimes also called a pentanoic acid in some naming schemes. It is biosynthesized by cleavage of LINOLEIC ACID and is a coenzyme of oxoglutarate dehydrogenase (KETOGLUTARATE DEHYDROGENASE COMPLEX). It is used in DIETARY SUPPLEMENTS.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T127; UMLS Semantic Type: STY:T109","Is the triple Thioctic acid treats hypertensive disorder supported by the sentence A naturally occurring micronutrient, synthesized in small amounts by plants and animals (including humans), with antioxidant and potential chemopreventive activities. Alpha-lipoic acid acts as a free radical scavenger and assists in repairing oxidative damage and regenerates endogenous antioxidants, including vitamins C and E and glutathione. This agent also promotes glutathione synthesis. In addition, alpha-lipoic acid exerts metal chelating capacities and functions as a cofactor in various mitochondrial enzyme complexes involved in the decarboxylation of alpha-keto acids. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C61595"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C61595"" NCI Thesaurus); A naturally occurring micronutrient, synthesized in small amounts by plants and animals (including humans), with antioxidant and potential chemopreventive activities. Alpha-lipoic acid acts as a free radical scavenger and assists in repairing oxidative damage and regenerates endogenous antioxidants, including vitamins C and E and glutathione. This agent also promotes glutathione synthesis. In addition, alpha-lipoic acid exerts metal chelating capacities and functions as a cofactor in various mitochondrial enzyme complexes involved in the decarboxylation of alpha-keto acids.; An octanoic acid bridged with two sulfurs so that it is sometimes also called a pentanoic acid in some naming schemes. It is biosynthesized by cleavage of LINOLEIC ACID and is a coenzyme of oxoglutarate dehydrogenase (KETOGLUTARATE DEHYDROGENASE COMPLEX). It is used in DIETARY SUPPLEMENTS.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T127; UMLS Semantic Type: STY:T109",False,PMID:24352797 -15252860,Cefixime affects gonorrhea,558,"A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefixime affects gonorrhea supported by the sentence A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,http://www.cdc.gov/std/gonorrhea/stdfact-gonorrhea.htm -8827692,Cefixime treats gonorrhea,558,"A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefixime treats gonorrhea supported by the sentence A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,http://www.cdc.gov/std/gonorrhea/stdfact-gonorrhea.htm -45029234,Ampicillin treats bacterial urinary tract infection,686,Ampicillin is found in common pea. It is also a potential contaminant of cow's milk arising from its veterinary use. Ampicillin is a semi-synthetic derivative of penicillin that functions as an orally active broad-spectrum antibiotic. It has been used extensively to treat bacterial infections since 1961. It is considered part of the aminopenicillin family and is roughly equivalent to amoxicillin in terms of spectrum and level of activity,Is the triple Ampicillin treats bacterial urinary tract infection supported by the sentence Ampicillin is found in common pea. It is also a potential contaminant of cow's milk arising from its veterinary use. Ampicillin is a semi-synthetic derivative of penicillin that functions as an orally active broad-spectrum antibiotic. It has been used extensively to treat bacterial infections since 1961. It is considered part of the aminopenicillin family and is roughly equivalent to amoxicillin in terms of spectrum and level of activity,False,https://orcid.org/0000-0002-6601-2165 -45029207,Ampicillin treats bacterial infectious disease with sepsis,686,Ampicillin is found in common pea. It is also a potential contaminant of cow's milk arising from its veterinary use. Ampicillin is a semi-synthetic derivative of penicillin that functions as an orally active broad-spectrum antibiotic. It has been used extensively to treat bacterial infections since 1961. It is considered part of the aminopenicillin family and is roughly equivalent to amoxicillin in terms of spectrum and level of activity,Is the triple Ampicillin treats bacterial infectious disease with sepsis supported by the sentence Ampicillin is found in common pea. It is also a potential contaminant of cow's milk arising from its veterinary use. Ampicillin is a semi-synthetic derivative of penicillin that functions as an orally active broad-spectrum antibiotic. It has been used extensively to treat bacterial infections since 1961. It is considered part of the aminopenicillin family and is roughly equivalent to amoxicillin in terms of spectrum and level of activity,False,PMID:20421654 -7594422,Cefixime treats bacterial infectious disease,558,"A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefixime treats bacterial infectious disease supported by the sentence A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/pathogenic_bacteria -26843374,Cefixime treats tonsillitis,558,"A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefixime treats tonsillitis supported by the sentence A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,PMID:15897415 -22138225,Cefixime treats syphilis,558,"A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefixime treats syphilis supported by the sentence A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/syphilis -23970374,Cefixime treats Infection,558,"A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefixime treats Infection supported by the sentence A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True, -12941415,Cefixime treats otitis media,558,"A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefixime treats otitis media supported by the sentence A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/otitis_media -18811968,Cefixime prevents otitis media,558,"A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefixime prevents otitis media supported by the sentence A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/otitis_media -26078551,Ceftizoxime treats bacterial infectious disease,559,"A semisynthetic, broad-spectrum, beta-lactamase-resistant, third-generation cephalosporin with antibacterial activity. Ceftizoxime binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Ceftizoxime treats bacterial infectious disease supported by the sentence A semisynthetic, broad-spectrum, beta-lactamase-resistant, third-generation cephalosporin with antibacterial activity. Ceftizoxime binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/pathogenic_bacteria -25661332,Ceftizoxime treats osteomyelitis,559,"A semisynthetic, broad-spectrum, beta-lactamase-resistant, third-generation cephalosporin with antibacterial activity. Ceftizoxime binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Ceftizoxime treats osteomyelitis supported by the sentence A semisynthetic, broad-spectrum, beta-lactamase-resistant, third-generation cephalosporin with antibacterial activity. Ceftizoxime binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -17748395,Trimetazidine related to diabetic kidney disease,560,"An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C76590"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C76590"" NCI Thesaurus); An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function.; A vasodilator used in angina of effort or ischemic heart disease.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Trimetazidine related to diabetic kidney disease supported by the sentence An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C76590"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C76590"" NCI Thesaurus); An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function.; A vasodilator used in angina of effort or ischemic heart disease.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -30645129,Pirenzepine treats peptic ulcer disease,710,"An antimuscarinic agent that inhibits gastric secretion at lower doses than are required to affect gastrointestinal motility, salivary, central nervous system, cardiovascular, ocular, and urinary function. It promotes the healing of duodenal ulcers and due to its cytoprotective action is beneficial in the prevention of duodenal ulcer recurrence. It also potentiates the effect of other antiulcer agents such as CIMETIDINE and RANITIDINE. It is generally well tolerated by patients.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Pirenzepine treats peptic ulcer disease supported by the sentence An antimuscarinic agent that inhibits gastric secretion at lower doses than are required to affect gastrointestinal motility, salivary, central nervous system, cardiovascular, ocular, and urinary function. It promotes the healing of duodenal ulcers and due to its cytoprotective action is beneficial in the prevention of duodenal ulcer recurrence. It also potentiates the effect of other antiulcer agents such as CIMETIDINE and RANITIDINE. It is generally well tolerated by patients.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,PMID:28242110 -23911647,Trimetazidine treats diabetic kidney disease,560,"An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C76590"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C76590"" NCI Thesaurus); An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function.; A vasodilator used in angina of effort or ischemic heart disease.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Trimetazidine treats diabetic kidney disease supported by the sentence An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C76590"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C76590"" NCI Thesaurus); An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function.; A vasodilator used in angina of effort or ischemic heart disease.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -30383163,Urea treats type 2 diabetes mellitus,721,"Urea is a highly soluble organic compound formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids. Urea is formed in a cyclic pathway known simply as the urea cycle. In this cycle, amino groups donated by ammonia and L-aspartate are converted to urea. Urea is essentially a waste product; it has no physiological function. It is dissolved in blood (in humans in a concentration of 2.5 - 7.5 mmol/liter) and excreted by the kidney in the urine. In addition, a small amount of urea is excreted (along with sodium chloride and water) in human sweat. Urea is found to be associated with primary hypomagnesemia, which is an inborn error of metabolism.","Is the triple Urea treats type 2 diabetes mellitus supported by the sentence Urea is a highly soluble organic compound formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids. Urea is formed in a cyclic pathway known simply as the urea cycle. In this cycle, amino groups donated by ammonia and L-aspartate are converted to urea. Urea is essentially a waste product; it has no physiological function. It is dissolved in blood (in humans in a concentration of 2.5 - 7.5 mmol/liter) and excreted by the kidney in the urine. In addition, a small amount of urea is excreted (along with sodium chloride and water) in human sweat. Urea is found to be associated with primary hypomagnesemia, which is an inborn error of metabolism.",False,http://en.wikipedia.org/wiki/diabetes_mellitus_type_2 -17755056,Trimetazidine treats Cardiotoxicity,560,"An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C76590"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C76590"" NCI Thesaurus); An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function.; A vasodilator used in angina of effort or ischemic heart disease.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Trimetazidine treats Cardiotoxicity supported by the sentence An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C76590"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C76590"" NCI Thesaurus); An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function.; A vasodilator used in angina of effort or ischemic heart disease.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -18547788,Trimetazidine prevents Cardiotoxicity,560,"An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C76590"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C76590"" NCI Thesaurus); An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function.; A vasodilator used in angina of effort or ischemic heart disease.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Trimetazidine prevents Cardiotoxicity supported by the sentence An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C76590"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C76590"" NCI Thesaurus); An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function.; A vasodilator used in angina of effort or ischemic heart disease.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -45036517,Mannitol treats Edema,724,"Mannitol is a diuretic and renal diagnostic aid related to sorbitol. It has little significant energy value as it is largely eliminated from the body before any metabolism can take place. It can be used to treat oliguria associated with kidney failure or other manifestations of inadequate renal function and has been used for determination of glomerular filtration rate. Mannitol is also commonly used as a research tool in cell biological studies, usually to control osmolarity. Chemically, mannitol is an alcohol and a sugar, or a polyol; it is similar to xylitol or sorbitol. However, mannitol has a tendency to lose a hydrogen ion in aqueous solutions, which causes the solution to become acidic. For this, it is not uncommon to add a substance to adjust its pH, such as sodium bicarbonate. Mannitol is a non-permeating molecule i.e. it cannot cross biological membranes. Mannitol or hexan-1,2,3,4,5,6-hexol (C6H8(OH)6) is an osmotic diuretic agent and a weak renal vasodilator. It is a sorbitol isomer.","Is the triple Mannitol treats Edema supported by the sentence Mannitol is a diuretic and renal diagnostic aid related to sorbitol. It has little significant energy value as it is largely eliminated from the body before any metabolism can take place. It can be used to treat oliguria associated with kidney failure or other manifestations of inadequate renal function and has been used for determination of glomerular filtration rate. Mannitol is also commonly used as a research tool in cell biological studies, usually to control osmolarity. Chemically, mannitol is an alcohol and a sugar, or a polyol; it is similar to xylitol or sorbitol. However, mannitol has a tendency to lose a hydrogen ion in aqueous solutions, which causes the solution to become acidic. For this, it is not uncommon to add a substance to adjust its pH, such as sodium bicarbonate. Mannitol is a non-permeating molecule i.e. it cannot cross biological membranes. Mannitol or hexan-1,2,3,4,5,6-hexol (C6H8(OH)6) is an osmotic diuretic agent and a weak renal vasodilator. It is a sorbitol isomer.",False,https://orcid.org/0000-0002-0736-9199 -17682787,Trimetazidine treats cardiovascular disorder,560,"An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C76590"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C76590"" NCI Thesaurus); An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function.; A vasodilator used in angina of effort or ischemic heart disease.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Trimetazidine treats cardiovascular disorder supported by the sentence An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C76590"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C76590"" NCI Thesaurus); An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function.; A vasodilator used in angina of effort or ischemic heart disease.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/circulatory_system -30645467,Mannitol treats brain edema,724,"Mannitol is a diuretic and renal diagnostic aid related to sorbitol. It has little significant energy value as it is largely eliminated from the body before any metabolism can take place. It can be used to treat oliguria associated with kidney failure or other manifestations of inadequate renal function and has been used for determination of glomerular filtration rate. Mannitol is also commonly used as a research tool in cell biological studies, usually to control osmolarity. Chemically, mannitol is an alcohol and a sugar, or a polyol; it is similar to xylitol or sorbitol. However, mannitol has a tendency to lose a hydrogen ion in aqueous solutions, which causes the solution to become acidic. For this, it is not uncommon to add a substance to adjust its pH, such as sodium bicarbonate. Mannitol is a non-permeating molecule i.e. it cannot cross biological membranes. Mannitol or hexan-1,2,3,4,5,6-hexol (C6H8(OH)6) is an osmotic diuretic agent and a weak renal vasodilator. It is a sorbitol isomer.","Is the triple Mannitol treats brain edema supported by the sentence Mannitol is a diuretic and renal diagnostic aid related to sorbitol. It has little significant energy value as it is largely eliminated from the body before any metabolism can take place. It can be used to treat oliguria associated with kidney failure or other manifestations of inadequate renal function and has been used for determination of glomerular filtration rate. Mannitol is also commonly used as a research tool in cell biological studies, usually to control osmolarity. Chemically, mannitol is an alcohol and a sugar, or a polyol; it is similar to xylitol or sorbitol. However, mannitol has a tendency to lose a hydrogen ion in aqueous solutions, which causes the solution to become acidic. For this, it is not uncommon to add a substance to adjust its pH, such as sodium bicarbonate. Mannitol is a non-permeating molecule i.e. it cannot cross biological membranes. Mannitol or hexan-1,2,3,4,5,6-hexol (C6H8(OH)6) is an osmotic diuretic agent and a weak renal vasodilator. It is a sorbitol isomer.",False,https://en.wikipedia.org/wiki/cerebral_edema -9968932,Acadesine treats B-cell chronic lymphocytic leukemia,562,"A 5-aminoimidazole-4-carboxamide (AICA) riboside, a purine nucleoside analog, and a nucleotide biosynthesis precursor with B cell pro-apoptotic activity. Following cellular uptake, acadesine is phosphorylated to AICA ribotide (ZMP), which mimics 5'-adenosine monophosphate (AMP). Both AMP-activated protein kinase (AMPK) and AMPK kinase (AMPKK) are activated by ZMP, which appears to be necessary for the induction of apoptosis. Acadesine-induced apoptosis also appears to require cytochrome c release from mitochondria and caspase activation and is p53-independent. However, the exact mechanism of acadesine-induced apoptosis is unknown. T cells are significantly less susceptible than B cells to acadesine-induced apoptosis. AMPK regulates several cellular systems including the cellular uptake of glucose, the beta-oxidation of fatty acids, protein synthesis, and the biogenesis of glucose transporter 4 (GLUT4) and mitochondria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C71537"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C71537"" NCI Thesaurus); A 5-aminoimidazole-4-carboxamide (AICA) riboside, a ribnucleoside analog, and a nucleotide biosynthesis precursor with B cell pro-apoptotic activity. Following cellular uptake, acadesine is phosphorylated to AICA ribotide (ZMP), which mimics 5'-adenosine monophosphate (AMP). Both AMP-activated protein kinase (AMPK) and AMPK kinase (AMPKK) are activated by ZMP, which appears to be necessary for the induction of apoptosis. Acadesine-induced apoptosis also appears to require cytochrome c release from mitochondria and caspase activation and is p53-independent. However, the exact mechanism of acadesine-induced apoptosis is unknown. T cells are significantly less susceptible than B cells to acadesine-induced apoptosis. AMPK regulates several cellular systems including the cellular uptake of glucose, the beta-oxidation of fatty acids, protein synthesis, and the biogenesis of glucose transporter 4 (GLUT4) and mitochondria.","Is the triple Acadesine treats B-cell chronic lymphocytic leukemia supported by the sentence A 5-aminoimidazole-4-carboxamide (AICA) riboside, a purine nucleoside analog, and a nucleotide biosynthesis precursor with B cell pro-apoptotic activity. Following cellular uptake, acadesine is phosphorylated to AICA ribotide (ZMP), which mimics 5'-adenosine monophosphate (AMP). Both AMP-activated protein kinase (AMPK) and AMPK kinase (AMPKK) are activated by ZMP, which appears to be necessary for the induction of apoptosis. Acadesine-induced apoptosis also appears to require cytochrome c release from mitochondria and caspase activation and is p53-independent. However, the exact mechanism of acadesine-induced apoptosis is unknown. T cells are significantly less susceptible than B cells to acadesine-induced apoptosis. AMPK regulates several cellular systems including the cellular uptake of glucose, the beta-oxidation of fatty acids, protein synthesis, and the biogenesis of glucose transporter 4 (GLUT4) and mitochondria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C71537"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C71537"" NCI Thesaurus); A 5-aminoimidazole-4-carboxamide (AICA) riboside, a ribnucleoside analog, and a nucleotide biosynthesis precursor with B cell pro-apoptotic activity. Following cellular uptake, acadesine is phosphorylated to AICA ribotide (ZMP), which mimics 5'-adenosine monophosphate (AMP). Both AMP-activated protein kinase (AMPK) and AMPK kinase (AMPKK) are activated by ZMP, which appears to be necessary for the induction of apoptosis. Acadesine-induced apoptosis also appears to require cytochrome c release from mitochondria and caspase activation and is p53-independent. However, the exact mechanism of acadesine-induced apoptosis is unknown. T cells are significantly less susceptible than B cells to acadesine-induced apoptosis. AMPK regulates several cellular systems including the cellular uptake of glucose, the beta-oxidation of fatty acids, protein synthesis, and the biogenesis of glucose transporter 4 (GLUT4) and mitochondria.",True,http://www.cancer.gov/dictionary?cdrid=346545 -17881291,Ranolazine affects type 2 diabetes mellitus,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine affects type 2 diabetes mellitus supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True,http://en.wikipedia.org/wiki/diabetes_mellitus_type_2 -16822044,Ranolazine treats type 2 diabetes mellitus,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine treats type 2 diabetes mellitus supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True,http://en.wikipedia.org/wiki/diabetes_mellitus_type_2 -24441273,Ranolazine treats amyotrophic lateral sclerosis,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine treats amyotrophic lateral sclerosis supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True,http://www.ninds.nih.gov/disorders/amyotrophiclateralsclerosis/detail_als.htm -12975239,Ranolazine treats coronary artery disorder,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine treats coronary artery disorder supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True,PMID:31420554 -10629663,Ranolazine treats Angina pectoris,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine treats Angina pectoris supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True,https://orcid.org/0000-0002-0736-9199 -17475563,Ranolazine prevents Angina pectoris,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine prevents Angina pectoris supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True,https://orcid.org/0000-0002-0736-9199 -15243162,Ranolazine treats diastolic heart failure,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine treats diastolic heart failure supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True, -15199166,Ranolazine affects myocardial ischemia,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine affects myocardial ischemia supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True, -9302562,Ranolazine treats myocardial ischemia,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine treats myocardial ischemia supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True, -14751648,Ranolazine prevents myocardial ischemia,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine prevents myocardial ischemia supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True, -14672486,Ranolazine treats long QT syndrome,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine treats long QT syndrome supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True,http://en.wikipedia.org/wiki/long_qt_syndrome -13317799,Ranolazine causes atrial fibrillation,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine causes atrial fibrillation supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -19002641,Ranolazine affects atrial fibrillation,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine affects atrial fibrillation supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -16599546,Ranolazine affects atrial fibrillation,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine affects atrial fibrillation supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -30353247,Salsalate treats Insulin resistance,774,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Salsalate is a nonsteroidal anti-inflammatory agent for oral administration. Salsalate's mode of action as an anti-inflammatory and antirheumatic agent may be due to inhibition of synthesis and release of prostaglandins. The usefulness of salicylic acid, the active in vivo product of salsalate, in the treatment of arthritic disorders has been established. In contrast to aspirin, salsalate causes no greater fecal gastrointestinal blood loss than placebo. Salsalate is readily soluble in the small intestine where it is partially hydrolyzed to two molecules of salicylic acid. A significant portion of the parent compound is absorbed unchanged and undergoes rapid esterase hydrolysis in the body. The parent compound has an elimination half-life of about 1 hour. Salicylic acid (the active metabolite) biotransformation is saturated at anti-inflammatory doses of salsalate. Such capacity limited biotransformation results in an increase in the half-life of salicylic acid from 3.5 to 16 or more hours.","Is the triple Salsalate treats Insulin resistance supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Salsalate is a nonsteroidal anti-inflammatory agent for oral administration. Salsalate's mode of action as an anti-inflammatory and antirheumatic agent may be due to inhibition of synthesis and release of prostaglandins. The usefulness of salicylic acid, the active in vivo product of salsalate, in the treatment of arthritic disorders has been established. In contrast to aspirin, salsalate causes no greater fecal gastrointestinal blood loss than placebo. Salsalate is readily soluble in the small intestine where it is partially hydrolyzed to two molecules of salicylic acid. A significant portion of the parent compound is absorbed unchanged and undergoes rapid esterase hydrolysis in the body. The parent compound has an elimination half-life of about 1 hour. Salicylic acid (the active metabolite) biotransformation is saturated at anti-inflammatory doses of salsalate. Such capacity limited biotransformation results in an increase in the half-life of salicylic acid from 3.5 to 16 or more hours.",False,https://orcid.org/0000-0002-0736-9199 -13887428,Ranolazine disrupts atrial fibrillation,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine disrupts atrial fibrillation supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -14280230,Ranolazine prevents atrial fibrillation,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine prevents atrial fibrillation supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -45028274,Aspirin treats rheumatoid arthritis,779,"Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).","Is the triple Aspirin treats rheumatoid arthritis supported by the sentence Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).",False,https://orcid.org/0000-0002-0736-9199 -19314329,Ranolazine affects cardiovascular disorder,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine affects cardiovascular disorder supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True,http://en.wikipedia.org/wiki/circulatory_system -9302560,Ranolazine treats cardiovascular disorder,567,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.","Is the triple Ranolazine treats cardiovascular disorder supported by the sentence Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",True,http://en.wikipedia.org/wiki/circulatory_system -19409335,Prednisolone affects sarcoidosis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects sarcoidosis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/sarcoidosis -9135976,Prednisolone treats sarcoidosis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats sarcoidosis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/sarcoidosis -14345678,Prednisolone treats thrombotic thrombocytopenic purpura,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats thrombotic thrombocytopenic purpura supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -12061894,Prednisolone related to West syndrome,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to West syndrome supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:28276060 -8752241,Prednisolone treats West syndrome,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats West syndrome supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:28276060 -9208405,Prednisolone related to Duchenne muscular dystrophy,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to Duchenne muscular dystrophy supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/duchenne_muscular_dystrophy -7603475,Prednisolone treats Duchenne muscular dystrophy,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats Duchenne muscular dystrophy supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/duchenne_muscular_dystrophy -24042094,Prednisolone treats biliary atresia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats biliary atresia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.nlm.nih.gov/medlineplus/ency/article/000215.htm -11810617,Prednisolone treats congenital adrenal hyperplasia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats congenital adrenal hyperplasia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.genome.jp/dbget-bin/www_bget?ds:h00216 -30646159,Aspirin treats migraine disorder,779,"Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).","Is the triple Aspirin treats migraine disorder supported by the sentence Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).",False,http://www.mayoclinic.com/health/migraine-headache/ds00120 -7600829,Prednisolone treats multiple sclerosis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats multiple sclerosis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://ghr.nlm.nih.gov/condition/multiple-sclerosis -10531966,Prednisolone related to allergic disease,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to allergic disease supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://medlineplus.gov/ency/article/000005.htm -21556285,Prednisolone causes allergic disease,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone causes allergic disease supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://medlineplus.gov/ency/article/000005.htm -25790510,Prednisolone affects allergic disease,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects allergic disease supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://medlineplus.gov/ency/article/000005.htm -8906209,Prednisolone treats allergic disease,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats allergic disease supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://medlineplus.gov/ency/article/000005.htm -30378663,Aspirin treats Toothache,779,"Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).","Is the triple Aspirin treats Toothache supported by the sentence Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).",False,https://www.merriam-webster.com/dictionary/toothache -30378661,Aspirin treats arthritic joint disease,779,"Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).","Is the triple Aspirin treats arthritic joint disease supported by the sentence Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).",False,http://www.arthritis.org/ -13988965,Prednisolone related to osteoarthritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to osteoarthritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.mayoclinic.com/health/osteoarthritis/ds00019 -9361682,Prednisolone affects osteoarthritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects osteoarthritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.mayoclinic.com/health/osteoarthritis/ds00019 -10565149,Prednisolone treats osteoarthritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats osteoarthritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.mayoclinic.com/health/osteoarthritis/ds00019 -17312178,Prednisolone treats type 2 diabetes mellitus,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats type 2 diabetes mellitus supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/diabetes_mellitus_type_2 -9464043,Prednisolone causes cataract,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone causes cataract supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:10414631 -17604301,Prednisolone treats cataract,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats cataract supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:10414631 -22130331,Prednisolone treats schizophrenia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats schizophrenia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/schizophrenia -8405261,Prednisolone related to asthma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to asthma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.nhlbi.nih.gov/health/dci/diseases/asthma/asthma_whatis.htm -30368334,Aspirin treats blood coagulation disease,779,"Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).","Is the triple Aspirin treats blood coagulation disease supported by the sentence Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).",False,https://www.cedars-sinai.edu/patients/health-conditions/coagulation-system-disorders.aspx -13564625,Prednisolone affects asthma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects asthma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.nhlbi.nih.gov/health/dci/diseases/asthma/asthma_whatis.htm -7430895,Prednisolone treats asthma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats asthma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.nhlbi.nih.gov/health/dci/diseases/asthma/asthma_whatis.htm -10594561,Prednisolone disrupts asthma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone disrupts asthma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.nhlbi.nih.gov/health/dci/diseases/asthma/asthma_whatis.htm -11858005,Prednisolone prevents asthma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone prevents asthma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.nhlbi.nih.gov/health/dci/diseases/asthma/asthma_whatis.htm -25959730,Prednisolone related to sarcoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to sarcoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/sarcoma -25621708,Prednisolone related to uveitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to uveitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://www.mayoclinic.org/diseases-conditions/uveitis/symptoms-causes/syc-20378734 -26677891,Prednisolone causes uveitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone causes uveitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://www.mayoclinic.org/diseases-conditions/uveitis/symptoms-causes/syc-20378734 -27658451,Prednisolone affects uveitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects uveitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://www.mayoclinic.org/diseases-conditions/uveitis/symptoms-causes/syc-20378734 -7485161,Prednisolone treats uveitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats uveitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://www.mayoclinic.org/diseases-conditions/uveitis/symptoms-causes/syc-20378734 -27206106,Prednisolone disrupts uveitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone disrupts uveitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://www.mayoclinic.org/diseases-conditions/uveitis/symptoms-causes/syc-20378734 -30346282,Aspirin treats vascular disorder,779,"Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).","Is the triple Aspirin treats vascular disorder supported by the sentence Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).",False,https://doi.org/10.1007/978-3-540-78785-3_7 -10335998,Prednisolone treats pemphigus,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats pemphigus supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://rarediseases.info.nih.gov/diseases/7352/pemphigus -11166362,Prednisolone treats lichen planus,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats lichen planus supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/lichen_planus -9013774,Prednisolone treats ocular pemphigoid,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats ocular pemphigoid supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -26365803,Prednisolone related to adrenocortical insufficiency,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to adrenocortical insufficiency supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -21293782,Prednisolone causes adrenocortical insufficiency,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone causes adrenocortical insufficiency supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -10782301,Prednisolone treats adrenocortical insufficiency,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats adrenocortical insufficiency supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -27323391,Prednisolone affects focal segmental glomerulosclerosis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects focal segmental glomerulosclerosis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:16164633 -11813573,Prednisolone treats focal segmental glomerulosclerosis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats focal segmental glomerulosclerosis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:16164633 -9924521,Prednisolone related to colitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to colitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-6601-2165 -30341165,Aspirin treats preeclampsia,779,"Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).","Is the triple Aspirin treats preeclampsia supported by the sentence Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).",False,PMID:24400024 -19824794,Prednisolone affects colitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects colitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-6601-2165 -7704078,Prednisolone treats colitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats colitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-6601-2165 -15809068,Prednisolone prevents colitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone prevents colitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-6601-2165 -20312000,Prednisolone related to chronic primary adrenal insufficiency,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to chronic primary adrenal insufficiency supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/addison%27s_disease -21634207,Prednisolone treats chronic primary adrenal insufficiency,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats chronic primary adrenal insufficiency supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/addison%27s_disease -20512112,Prednisolone related to castration-resistant prostate carcinoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to castration-resistant prostate carcinoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:30324351 -27410586,Prednisolone affects castration-resistant prostate carcinoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects castration-resistant prostate carcinoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:30324351 -12190701,Prednisolone treats castration-resistant prostate carcinoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats castration-resistant prostate carcinoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:30324351 -24523226,Prednisolone related to glomerulonephritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to glomerulonephritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-6601-2165 -25165576,Prednisolone affects glomerulonephritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects glomerulonephritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-6601-2165 -9729887,Prednisolone treats glomerulonephritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats glomerulonephritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-6601-2165 -9668241,Prednisolone treats pure red-cell aplasia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats pure red-cell aplasia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -10649036,Prednisolone affects chorioretinitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects chorioretinitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:16196117 -10574409,Prednisolone treats epicondylitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats epicondylitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/epicondylitis -20612701,Prednisolone treats myocarditis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats myocarditis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/myocarditis -14373522,Prednisolone causes exfoliative dermatitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone causes exfoliative dermatitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -24297743,Prednisolone treats exfoliative dermatitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats exfoliative dermatitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -10715297,Prednisolone related to keratitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to keratitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.mayoclinic.org/diseases-conditions/keratitis/basics/definition/con-20035288 -11808057,Prednisolone treats keratitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats keratitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.mayoclinic.org/diseases-conditions/keratitis/basics/definition/con-20035288 -26194122,Prednisolone related to synovitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to synovitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=synovitis -10574410,Prednisolone treats synovitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats synovitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=synovitis -26227245,Prednisolone prevents synovitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone prevents synovitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=synovitis -10736101,Prednisolone related to Graves disease,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to Graves disease supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0009-0006-4530-3154 -9538921,Prednisolone treats Graves disease,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats Graves disease supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0009-0006-4530-3154 -22194722,Prednisolone related to pulmonary eosinophilia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to pulmonary eosinophilia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:19618037 -27042309,Prednisolone affects pulmonary eosinophilia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects pulmonary eosinophilia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:19618037 -30345280,ATROPINE treats myopia,839,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Atropine is an alkaloid originally synthesized from Atropa belladonna. It is a racemic mixture of d-and l-hyoscyamine, of which only l-hyoscyamine is pharmacologically active.[A251670,L42835] Atropine is generally available as a sulfate salt and can be administered by intravenous, subcutaneous, intramuscular, intraosseous, endotracheal and ophthalmic methods. Oral atropine is only available in combination products.[A251660,L42840] Atropine is a competitive, reversible antagonist of muscarinic receptors that blocks the effects of acetylcholine and other choline esters.[A251660,L42815,L42825,L42835] It has a variety of therapeutic applications, including pupil dilation and the treatment of anticholinergic poisoning and symptomatic bradycardia in the absence of reversible causes.[A251660] Atropine is a relatively inexpensive drug and is included in the World Health Organization List of Essential Medicines.[A251675]","Is the triple ATROPINE treats myopia supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Atropine is an alkaloid originally synthesized from Atropa belladonna. It is a racemic mixture of d-and l-hyoscyamine, of which only l-hyoscyamine is pharmacologically active.[A251670,L42835] Atropine is generally available as a sulfate salt and can be administered by intravenous, subcutaneous, intramuscular, intraosseous, endotracheal and ophthalmic methods. Oral atropine is only available in combination products.[A251660,L42840] Atropine is a competitive, reversible antagonist of muscarinic receptors that blocks the effects of acetylcholine and other choline esters.[A251660,L42815,L42825,L42835] It has a variety of therapeutic applications, including pupil dilation and the treatment of anticholinergic poisoning and symptomatic bradycardia in the absence of reversible causes.[A251660] Atropine is a relatively inexpensive drug and is included in the World Health Organization List of Essential Medicines.[A251675]",False,https://orcid.org/0000-0002-0736-9199 -17143213,Prednisolone related to temporal arteritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to temporal arteritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://www.mayoclinic.org/diseases-conditions/giant-cell-arteritis/symptoms-causes/syc-20372758 -7900660,Prednisolone treats temporal arteritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats temporal arteritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://www.mayoclinic.org/diseases-conditions/giant-cell-arteritis/symptoms-causes/syc-20372758 -21911849,Prednisolone related to habitual spontaneous abortion,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to habitual spontaneous abortion supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -14676056,Prednisolone treats habitual spontaneous abortion,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats habitual spontaneous abortion supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -10949449,Prednisolone related to polymyalgia rheumatica,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to polymyalgia rheumatica supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://medlineplus.gov/polymyalgiarheumatica.htm -7900659,Prednisolone treats polymyalgia rheumatica,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats polymyalgia rheumatica supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://medlineplus.gov/polymyalgiarheumatica.htm -24291326,Prednisolone treats Anti-neutrophil cytoplasmic antibody-associated vasculitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats Anti-neutrophil cytoplasmic antibody-associated vasculitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -12510603,Prednisolone related to membranous glomerulonephritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to membranous glomerulonephritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -8939337,Prednisolone treats membranous glomerulonephritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats membranous glomerulonephritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -9046445,Prednisolone treats systemic sclerosis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats systemic sclerosis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://ghr.nlm.nih.gov/condition/systemic-scleroderma -27055840,Prednisolone causes glaucoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone causes glaucoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://en.wikipedia.org/wiki/glaucoma -12496746,Prednisolone related to neoplasm,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to neoplasm supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-6601-2165 -8533593,Prednisolone affects neoplasm,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects neoplasm supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-6601-2165 -30648398,Capsaicin treats neuralgia,886,"Capsaicin is identified as the primary pungent principle in Capsicum fruits. Hot chili peppers that belong to the plant genus Capsicum (family Solanaceae) are among the most heavily consumed spices throughout the world. The capsaicin content of green and red peppers ranges from 0.1 to 1%. Capsaicin evokes numerous biological effects and thus has been the target of extensive., investigations since its initial identification in 1919. One of the most recognized physiological properties of capsaicin is its selective effects on the peripheral part of the sensory nervous system, particularly on the primary afferent neurons. The compound is known to deplete the neurotransmitter of painful impulses known as substance P from the sensory nerve terminals, which provides a rationale for its use as a versatile experimental tool for studying pain mechanisms and also for pharmacotherapy to treat some peripheral painful states, such as rheumatoid arthritis, post-herpetic neuralgia, post-mastectomy pain syndrome and diabetic neuropathy. Considering the frequent consumption of capsaicin as a food additive and its current therapeutic application, correct assessment of any harmful effects of this compound is important from the public health standpoint. Ingestion of large amounts of capsaicin has been reported to cause histopathological and biochemical changes, including erosion of gastric mucosa and hepatic necrosis. However, there are contradictory data on the mutagenicity of capsaicin. A recent epidemiological study conducted in Mexico revealed that consumers of chili pepper were at higher risk for gastric cancer than non-consumers. However, it remains unclear whether capsaicin present in hot chili pepper is a major causative factor in the aetiology of gastric cancer in humans. A growing number of recent studies have focused on anticarcinogenic or antimutagenic phytochemicals, particularly those included in human diet. In summary, capsaicin has dual effects on chemically induced carcinogenesis and mutagenesis. Although a minute amount of capsaicin displays few or no deleterious effects, heavy ingestion of the compound has been associated with necrosis, ulceration and even carcinogenesis. Capsaicin is considered to be metabolized by cytochrome P-450-dependent mixed-function oxidases to reactive species. (PMID: 8621114).","Is the triple Capsaicin treats neuralgia supported by the sentence Capsaicin is identified as the primary pungent principle in Capsicum fruits. Hot chili peppers that belong to the plant genus Capsicum (family Solanaceae) are among the most heavily consumed spices throughout the world. The capsaicin content of green and red peppers ranges from 0.1 to 1%. Capsaicin evokes numerous biological effects and thus has been the target of extensive., investigations since its initial identification in 1919. One of the most recognized physiological properties of capsaicin is its selective effects on the peripheral part of the sensory nervous system, particularly on the primary afferent neurons. The compound is known to deplete the neurotransmitter of painful impulses known as substance P from the sensory nerve terminals, which provides a rationale for its use as a versatile experimental tool for studying pain mechanisms and also for pharmacotherapy to treat some peripheral painful states, such as rheumatoid arthritis, post-herpetic neuralgia, post-mastectomy pain syndrome and diabetic neuropathy. Considering the frequent consumption of capsaicin as a food additive and its current therapeutic application, correct assessment of any harmful effects of this compound is important from the public health standpoint. Ingestion of large amounts of capsaicin has been reported to cause histopathological and biochemical changes, including erosion of gastric mucosa and hepatic necrosis. However, there are contradictory data on the mutagenicity of capsaicin. A recent epidemiological study conducted in Mexico revealed that consumers of chili pepper were at higher risk for gastric cancer than non-consumers. However, it remains unclear whether capsaicin present in hot chili pepper is a major causative factor in the aetiology of gastric cancer in humans. A growing number of recent studies have focused on anticarcinogenic or antimutagenic phytochemicals, particularly those included in human diet. In summary, capsaicin has dual effects on chemically induced carcinogenesis and mutagenesis. Although a minute amount of capsaicin displays few or no deleterious effects, heavy ingestion of the compound has been associated with necrosis, ulceration and even carcinogenesis. Capsaicin is considered to be metabolized by cytochrome P-450-dependent mixed-function oxidases to reactive species. (PMID: 8621114).",False, -26515767,Prednisolone disrupts neoplasm,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone disrupts neoplasm supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-6601-2165 -16706850,Prednisolone prevents neoplasm,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone prevents neoplasm supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-6601-2165 -25753407,Prednisolone predisposes neoplasm,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone predisposes neoplasm supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-6601-2165 -10496403,Prednisolone related to Inflammation,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to Inflammation supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,ISBN:0198506732 -9735520,Prednisolone affects Inflammation,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects Inflammation supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,ISBN:0198506732 -9848677,Prednisolone treats Inflammation,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats Inflammation supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,ISBN:0198506732 -8854473,Prednisolone disrupts Inflammation,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone disrupts Inflammation supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,ISBN:0198506732 -10240036,Prednisolone prevents Inflammation,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone prevents Inflammation supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,ISBN:0198506732 -17230021,Prednisolone causes Headache,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone causes Headache supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=headache -11166436,Prednisolone affects Headache,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects Headache supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=headache -10671990,Prednisolone treats Headache,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats Headache supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=headache -10757066,Prednisolone treats atopic eczema,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats atopic eczema supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/atopic_dermatitis -9222009,Prednisolone related to hypereosinophilic syndrome,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to hypereosinophilic syndrome supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://en.wikipedia.org/wiki/hypereosinophilic_syndrome -12949384,Prednisolone affects hypereosinophilic syndrome,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects hypereosinophilic syndrome supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://en.wikipedia.org/wiki/hypereosinophilic_syndrome -8755027,Prednisolone treats hypereosinophilic syndrome,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats hypereosinophilic syndrome supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://en.wikipedia.org/wiki/hypereosinophilic_syndrome -14331279,Prednisolone disrupts hypereosinophilic syndrome,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone disrupts hypereosinophilic syndrome supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://en.wikipedia.org/wiki/hypereosinophilic_syndrome -30648889,Alendronic acid treats osteoporosis,929,"Alendronic acid, also known as alendronate or acido alendronico, belongs to the class of organic compounds known as bisphosphonates. These are organic compounds containing two phosphonate groups linked together through a carbon atoms. Alendronic acid is a drug which is used for the treatment and prevention of osteoporosis in women and paget's disease of bone in both men and women. Alendronic acid exists as a solid, soluble (in water), and an extremely strong acidic compound (based on its pKa). Alendronic acid has been found in human prostate and intestine tissues. Within the cell, alendronic acid is primarily located in the cytoplasm. In humans, alendronic acid is involved in the alendronate action pathway. Alendronic acid is a potentially toxic compound. Alendronate (Fosamax, Merck) is a bisphosphonate drug used for osteoporosis and several other bone diseases. It is marketed alone as well as in combination with vitamin D (2,800 U, under the name Fosavance).","Is the triple Alendronic acid treats osteoporosis supported by the sentence Alendronic acid, also known as alendronate or acido alendronico, belongs to the class of organic compounds known as bisphosphonates. These are organic compounds containing two phosphonate groups linked together through a carbon atoms. Alendronic acid is a drug which is used for the treatment and prevention of osteoporosis in women and paget's disease of bone in both men and women. Alendronic acid exists as a solid, soluble (in water), and an extremely strong acidic compound (based on its pKa). Alendronic acid has been found in human prostate and intestine tissues. Within the cell, alendronic acid is primarily located in the cytoplasm. In humans, alendronic acid is involved in the alendronate action pathway. Alendronic acid is a potentially toxic compound. Alendronate (Fosamax, Merck) is a bisphosphonate drug used for osteoporosis and several other bone diseases. It is marketed alone as well as in combination with vitamin D (2,800 U, under the name Fosavance).",False,http://www.niams.nih.gov/health_info/bone/default.asp -21254689,Prednisolone treats hypersensitivity pneumonitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats hypersensitivity pneumonitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:15316440 -8540122,Prednisolone treats autoimmune hemolytic anemia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats autoimmune hemolytic anemia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/autoimmune_hemolytic_anemia -27475554,Prednisolone treats microscopic polyangiitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats microscopic polyangiitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -12428137,Prednisolone related to croup,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to croup supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://books.google.com/books?id=g6k0tppmrsic&pg=pa254&lpg=pa254&dq#v=onepage&q=&f=false -17184322,Prednisolone treats croup,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats croup supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://books.google.com/books?id=g6k0tppmrsic&pg=pa254&lpg=pa254&dq#v=onepage&q=&f=false -11638013,Prednisolone related to eosinophilic granulomatosis with polyangiitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to eosinophilic granulomatosis with polyangiitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.mayoclinic.com/health/churg-strauss-syndrome/ds00855 -7800931,Prednisolone treats autoimmune thrombocytopenic purpura,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats autoimmune thrombocytopenic purpura supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://rarediseases.org/rare-diseases/immune-thrombocytopenia/ -20106181,Prednisolone related to allergic bronchopulmonary aspergillosis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to allergic bronchopulmonary aspergillosis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.nlm.nih.gov/medlineplus/ency/article/000070.htm -22922261,Prednisolone affects allergic bronchopulmonary aspergillosis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects allergic bronchopulmonary aspergillosis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.nlm.nih.gov/medlineplus/ency/article/000070.htm -13327146,Prednisolone treats allergic bronchopulmonary aspergillosis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats allergic bronchopulmonary aspergillosis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.nlm.nih.gov/medlineplus/ency/article/000070.htm -45045094,Midazolam treats status epilepticus,953,"The hydrochloride salt of a short-acting benzodiazepine derivative with an imidazole structure and anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam binds to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS), resulting in increases in the opening of chloride channels, membrane hyperpolarization, and the inhibitory effect of GABA. This agent may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C654"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C654"" NCI Thesaurus); A short-acting benzodiazepine derivative with an imidazole structure and with anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam exerts its effect by binding to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS). This leads to an increase in the opening of chloride channels, membrane hyperpolarization and increases the inhibitory effect of GABA in the CNS. Midazolam may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft.; The hydrochloride salt of a short-acting benzodiazepine derivative with an imidazole structure and anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam binds to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS), resulting in increases in the opening of chloride channels, membrane hyperpolarization, and the inhibitory effect of GABA. This agent may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft.; A short-acting hypnotic-sedative drug with anxiolytic and amnestic properties. It is used in dentistry, cardiac surgery, endoscopic procedures, as preanesthetic medication, and as an adjunct to local anesthesia. The short duration and cardiorespiratory stability makes it useful in poor-risk, elderly, and cardiac patients. It is water-soluble at pH less than 4 and lipid-soluble at physiological pH.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Midazolam treats status epilepticus supported by the sentence The hydrochloride salt of a short-acting benzodiazepine derivative with an imidazole structure and anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam binds to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS), resulting in increases in the opening of chloride channels, membrane hyperpolarization, and the inhibitory effect of GABA. This agent may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C654"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C654"" NCI Thesaurus); A short-acting benzodiazepine derivative with an imidazole structure and with anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam exerts its effect by binding to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS). This leads to an increase in the opening of chloride channels, membrane hyperpolarization and increases the inhibitory effect of GABA in the CNS. Midazolam may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft.; The hydrochloride salt of a short-acting benzodiazepine derivative with an imidazole structure and anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam binds to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS), resulting in increases in the opening of chloride channels, membrane hyperpolarization, and the inhibitory effect of GABA. This agent may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft.; A short-acting hypnotic-sedative drug with anxiolytic and amnestic properties. It is used in dentistry, cardiac surgery, endoscopic procedures, as preanesthetic medication, and as an adjunct to local anesthesia. The short duration and cardiorespiratory stability makes it useful in poor-risk, elderly, and cardiac patients. It is water-soluble at pH less than 4 and lipid-soluble at physiological pH.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,PMID:28276060 -7990669,Prednisolone treats non-Hodgkin lymphoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats non-Hodgkin lymphoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/non-hodgkin_lymphoma -11142916,Prednisolone related to lupus nephritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to lupus nephritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://medlineplus.gov/ency/article/000481.htm -8499057,Prednisolone treats lupus nephritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats lupus nephritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://medlineplus.gov/ency/article/000481.htm -11037266,Prednisolone related to granulomatosis with polyangiitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to granulomatosis with polyangiitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://en.wikipedia.org/wiki/granulomatosis_with_polyangiitis -7941298,Prednisolone treats granulomatosis with polyangiitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats granulomatosis with polyangiitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://en.wikipedia.org/wiki/granulomatosis_with_polyangiitis -16169223,Prednisolone related to mucocutaneous lymph node syndrome,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to mucocutaneous lymph node syndrome supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/kawasaki_disease -11889996,Prednisolone treats mucocutaneous lymph node syndrome,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats mucocutaneous lymph node syndrome supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/kawasaki_disease -30363840,Midazolam treats delirium,953,"The hydrochloride salt of a short-acting benzodiazepine derivative with an imidazole structure and anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam binds to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS), resulting in increases in the opening of chloride channels, membrane hyperpolarization, and the inhibitory effect of GABA. This agent may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C654"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C654"" NCI Thesaurus); A short-acting benzodiazepine derivative with an imidazole structure and with anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam exerts its effect by binding to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS). This leads to an increase in the opening of chloride channels, membrane hyperpolarization and increases the inhibitory effect of GABA in the CNS. Midazolam may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft.; The hydrochloride salt of a short-acting benzodiazepine derivative with an imidazole structure and anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam binds to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS), resulting in increases in the opening of chloride channels, membrane hyperpolarization, and the inhibitory effect of GABA. This agent may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft.; A short-acting hypnotic-sedative drug with anxiolytic and amnestic properties. It is used in dentistry, cardiac surgery, endoscopic procedures, as preanesthetic medication, and as an adjunct to local anesthesia. The short duration and cardiorespiratory stability makes it useful in poor-risk, elderly, and cardiac patients. It is water-soluble at pH less than 4 and lipid-soluble at physiological pH.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Midazolam treats delirium supported by the sentence The hydrochloride salt of a short-acting benzodiazepine derivative with an imidazole structure and anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam binds to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS), resulting in increases in the opening of chloride channels, membrane hyperpolarization, and the inhibitory effect of GABA. This agent may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C654"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C654"" NCI Thesaurus); A short-acting benzodiazepine derivative with an imidazole structure and with anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam exerts its effect by binding to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS). This leads to an increase in the opening of chloride channels, membrane hyperpolarization and increases the inhibitory effect of GABA in the CNS. Midazolam may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft.; The hydrochloride salt of a short-acting benzodiazepine derivative with an imidazole structure and anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam binds to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS), resulting in increases in the opening of chloride channels, membrane hyperpolarization, and the inhibitory effect of GABA. This agent may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft.; A short-acting hypnotic-sedative drug with anxiolytic and amnestic properties. It is used in dentistry, cardiac surgery, endoscopic procedures, as preanesthetic medication, and as an adjunct to local anesthesia. The short duration and cardiorespiratory stability makes it useful in poor-risk, elderly, and cardiac patients. It is water-soluble at pH less than 4 and lipid-soluble at physiological pH.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=delirium -25953223,Prednisolone causes kidney disorder,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone causes kidney disorder supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.nlm.nih.gov/medlineplus/kidneydiseases.htm -30358534,Midazolam treats hypotensive disorder,953,"The hydrochloride salt of a short-acting benzodiazepine derivative with an imidazole structure and anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam binds to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS), resulting in increases in the opening of chloride channels, membrane hyperpolarization, and the inhibitory effect of GABA. This agent may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C654"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C654"" NCI Thesaurus); A short-acting benzodiazepine derivative with an imidazole structure and with anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam exerts its effect by binding to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS). This leads to an increase in the opening of chloride channels, membrane hyperpolarization and increases the inhibitory effect of GABA in the CNS. Midazolam may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft.; The hydrochloride salt of a short-acting benzodiazepine derivative with an imidazole structure and anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam binds to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS), resulting in increases in the opening of chloride channels, membrane hyperpolarization, and the inhibitory effect of GABA. This agent may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft.; A short-acting hypnotic-sedative drug with anxiolytic and amnestic properties. It is used in dentistry, cardiac surgery, endoscopic procedures, as preanesthetic medication, and as an adjunct to local anesthesia. The short duration and cardiorespiratory stability makes it useful in poor-risk, elderly, and cardiac patients. It is water-soluble at pH less than 4 and lipid-soluble at physiological pH.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Midazolam treats hypotensive disorder supported by the sentence The hydrochloride salt of a short-acting benzodiazepine derivative with an imidazole structure and anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam binds to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS), resulting in increases in the opening of chloride channels, membrane hyperpolarization, and the inhibitory effect of GABA. This agent may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C654"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C654"" NCI Thesaurus); A short-acting benzodiazepine derivative with an imidazole structure and with anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam exerts its effect by binding to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS). This leads to an increase in the opening of chloride channels, membrane hyperpolarization and increases the inhibitory effect of GABA in the CNS. Midazolam may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft.; The hydrochloride salt of a short-acting benzodiazepine derivative with an imidazole structure and anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam binds to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS), resulting in increases in the opening of chloride channels, membrane hyperpolarization, and the inhibitory effect of GABA. This agent may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft.; A short-acting hypnotic-sedative drug with anxiolytic and amnestic properties. It is used in dentistry, cardiac surgery, endoscopic procedures, as preanesthetic medication, and as an adjunct to local anesthesia. The short duration and cardiorespiratory stability makes it useful in poor-risk, elderly, and cardiac patients. It is water-soluble at pH less than 4 and lipid-soluble at physiological pH.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-0736-9199 -11526277,Prednisolone treats kidney disorder,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats kidney disorder supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.nlm.nih.gov/medlineplus/kidneydiseases.htm -16371065,Prednisolone related to celiac disease,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to celiac disease supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.mayoclinic.com/health/celiac-disease/ds00319 -10513879,Prednisolone treats celiac disease,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats celiac disease supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.mayoclinic.com/health/celiac-disease/ds00319 -45032474,Celiprolol treats hypertensive disorder,993,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Celiprolol is indicated for the management of mild to moderate hypertension and effort-induced angina pectoris. It is simultaneously a selective β1 receptor antagonist, a β2 receptor partial agonist and a weak α2 receptor antagonist. In 2010 a clinical trial has suggested a use for this medication in the prevention of vascular complications of a rare inherited disease called vascular Ehlers–Danlos syndrome. This study demonstrated decreased incidence of arterial rupture or dissection (a specific type of arterial rupture in which the layers of the vessel separate prior to complete failure of the artery wall). Celiprolol is not approved for use by the FDA in the treatment of vascular Ehlers–Danlos syndrome.","Is the triple Celiprolol treats hypertensive disorder supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Celiprolol is indicated for the management of mild to moderate hypertension and effort-induced angina pectoris. It is simultaneously a selective β1 receptor antagonist, a β2 receptor partial agonist and a weak α2 receptor antagonist. In 2010 a clinical trial has suggested a use for this medication in the prevention of vascular complications of a rare inherited disease called vascular Ehlers–Danlos syndrome. This study demonstrated decreased incidence of arterial rupture or dissection (a specific type of arterial rupture in which the layers of the vessel separate prior to complete failure of the artery wall). Celiprolol is not approved for use by the FDA in the treatment of vascular Ehlers–Danlos syndrome.",False,PMID:24352797 -12983495,Prednisolone related to prostate cancer,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to prostate cancer supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.cancer.gov/dictionary?cdrid=445079 -11373326,Prednisolone treats prostate cancer,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats prostate cancer supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.cancer.gov/dictionary?cdrid=445079 -10748640,Prednisolone related to infertility disorder,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to infertility disorder supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/infertility -15365269,Prednisolone causes infertility disorder,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone causes infertility disorder supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/infertility -30643281,Esmolol treats atrial fibrillation,997,"The hydrochloride salt form of esmolol, a short, rapid-acting, selective beta-adrenergic receptor blocker, devoid of intrinsic sympathomimetic activity, and with anti-arrhythmic, antihypertensive and potential analgesic activities. Upon intravenous administration, esmolol binds to and blocks the beta-1 receptor in the myocardium thereby preventing the action of epinephrine and norepinephrine. This leads to a reduction in the force and rate of cardiac contractions and thereby preventing tachycardia, arrythmias and/or hypertension. At higher doses, esmolol also blocks beta-2 receptors located in bronchial and vascular smooth muscle, thereby leading to smooth muscle relaxation. In addition, esmolol exerts a peripheral analgesic effect and intraoperative use of this agent may decrease the amount of opioid administration postoperatively. As the ester moiety in esmolol is rapidly hydrolyzed byplasma esterases, this agent has a very short half-life. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C72617"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C72617"" NCI Thesaurus)","Is the triple Esmolol treats atrial fibrillation supported by the sentence The hydrochloride salt form of esmolol, a short, rapid-acting, selective beta-adrenergic receptor blocker, devoid of intrinsic sympathomimetic activity, and with anti-arrhythmic, antihypertensive and potential analgesic activities. Upon intravenous administration, esmolol binds to and blocks the beta-1 receptor in the myocardium thereby preventing the action of epinephrine and norepinephrine. This leads to a reduction in the force and rate of cardiac contractions and thereby preventing tachycardia, arrythmias and/or hypertension. At higher doses, esmolol also blocks beta-2 receptors located in bronchial and vascular smooth muscle, thereby leading to smooth muscle relaxation. In addition, esmolol exerts a peripheral analgesic effect and intraoperative use of this agent may decrease the amount of opioid administration postoperatively. As the ester moiety in esmolol is rapidly hydrolyzed byplasma esterases, this agent has a very short half-life. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C72617"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C72617"" NCI Thesaurus)",False,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -30358140,Esmolol treats atrial fibrillation,997,"The hydrochloride salt form of esmolol, a short, rapid-acting, selective beta-adrenergic receptor blocker, devoid of intrinsic sympathomimetic activity, and with anti-arrhythmic, antihypertensive and potential analgesic activities. Upon intravenous administration, esmolol binds to and blocks the beta-1 receptor in the myocardium thereby preventing the action of epinephrine and norepinephrine. This leads to a reduction in the force and rate of cardiac contractions and thereby preventing tachycardia, arrythmias and/or hypertension. At higher doses, esmolol also blocks beta-2 receptors located in bronchial and vascular smooth muscle, thereby leading to smooth muscle relaxation. In addition, esmolol exerts a peripheral analgesic effect and intraoperative use of this agent may decrease the amount of opioid administration postoperatively. As the ester moiety in esmolol is rapidly hydrolyzed byplasma esterases, this agent has a very short half-life. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C72617"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C72617"" NCI Thesaurus)","Is the triple Esmolol treats atrial fibrillation supported by the sentence The hydrochloride salt form of esmolol, a short, rapid-acting, selective beta-adrenergic receptor blocker, devoid of intrinsic sympathomimetic activity, and with anti-arrhythmic, antihypertensive and potential analgesic activities. Upon intravenous administration, esmolol binds to and blocks the beta-1 receptor in the myocardium thereby preventing the action of epinephrine and norepinephrine. This leads to a reduction in the force and rate of cardiac contractions and thereby preventing tachycardia, arrythmias and/or hypertension. At higher doses, esmolol also blocks beta-2 receptors located in bronchial and vascular smooth muscle, thereby leading to smooth muscle relaxation. In addition, esmolol exerts a peripheral analgesic effect and intraoperative use of this agent may decrease the amount of opioid administration postoperatively. As the ester moiety in esmolol is rapidly hydrolyzed byplasma esterases, this agent has a very short half-life. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C72617"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C72617"" NCI Thesaurus)",False,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -11988157,Prednisolone treats diffuse large B-cell lymphoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats diffuse large B-cell lymphoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:28487884 -26295217,Prednisolone related to angioimmunoblastic T-cell lymphoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to angioimmunoblastic T-cell lymphoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:22700722 -14012190,Prednisolone treats angioimmunoblastic T-cell lymphoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats angioimmunoblastic T-cell lymphoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:22700722 -10527508,Prednisolone related to acute myeloid leukemia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to acute myeloid leukemia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.cancer.gov/dictionary?cdrid=44363 -7866839,Prednisolone treats acute myeloid leukemia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats acute myeloid leukemia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.cancer.gov/dictionary?cdrid=44363 -14564343,Prednisolone related to acute lymphoblastic leukemia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to acute lymphoblastic leukemia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.cancer.gov/dictionary?cdrid=46332 -26879702,Prednisolone has part acute lymphoblastic leukemia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone has part acute lymphoblastic leukemia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.cancer.gov/dictionary?cdrid=46332 -7800426,Prednisolone affects acute lymphoblastic leukemia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects acute lymphoblastic leukemia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.cancer.gov/dictionary?cdrid=46332 -7985554,Prednisolone treats acute lymphoblastic leukemia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats acute lymphoblastic leukemia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.cancer.gov/dictionary?cdrid=46332 -16852549,Prednisolone treats mature T-cell and NK-cell non-Hodgkin lymphoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats mature T-cell and NK-cell non-Hodgkin lymphoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:21919697 -16983852,Prednisolone related to Hodgkins lymphoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to Hodgkins lymphoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://en.wikipedia.org/wiki/hodgkin%27s_lymphoma -10020250,Prednisolone treats Hodgkins lymphoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats Hodgkins lymphoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://en.wikipedia.org/wiki/hodgkin%27s_lymphoma -10687782,Prednisolone related to hepatocellular carcinoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to hepatocellular carcinoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/liver_cance -10509017,Prednisolone treats hepatocellular carcinoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats hepatocellular carcinoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/liver_cance -13151962,Prednisolone related to follicular lymphoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to follicular lymphoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/follicular_lymphoma -30369213,Metoprolol treats cardiac rhythm disease,1000,"A cardioselective competitive beta-1 adrenergic receptor antagonist with antihypertensive properties and devoid of intrinsic sympathomimetic activity. Metoprolol antagonizes beta 1-adrenergic receptors in the myocardium, thereby reducing the rate and force of myocardial contraction leading to a reduction in cardiac output. This agent may also reduce the secretion of renin with subsequent reduction in levels of angiotensin II thereby preventing vasoconstriction and aldosterone secretion. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C61845"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C61845"" NCI Thesaurus); A cardioselective competitive beta-1 adrenergic receptor antagonist with antihypertensive properties and devoid of intrinsic sympathomimetic activity. Metoprolol antagonizes beta 1-adrenergic receptors in the myocardium, thereby reducing the rate and force of myocardial contraction leading to a reduction in cardiac output. This agent may also reduce the secretion of renin with subsequent reduction in levels of angiotensin II thereby preventing vasoconstriction and aldosterone secretion.; A selective adrenergic beta-1 blocking agent that is commonly used to treat ANGINA PECTORIS; HYPERTENSION; and CARDIAC ARRHYTHMIAS.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Metoprolol treats cardiac rhythm disease supported by the sentence A cardioselective competitive beta-1 adrenergic receptor antagonist with antihypertensive properties and devoid of intrinsic sympathomimetic activity. Metoprolol antagonizes beta 1-adrenergic receptors in the myocardium, thereby reducing the rate and force of myocardial contraction leading to a reduction in cardiac output. This agent may also reduce the secretion of renin with subsequent reduction in levels of angiotensin II thereby preventing vasoconstriction and aldosterone secretion. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C61845"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C61845"" NCI Thesaurus); A cardioselective competitive beta-1 adrenergic receptor antagonist with antihypertensive properties and devoid of intrinsic sympathomimetic activity. Metoprolol antagonizes beta 1-adrenergic receptors in the myocardium, thereby reducing the rate and force of myocardial contraction leading to a reduction in cardiac output. This agent may also reduce the secretion of renin with subsequent reduction in levels of angiotensin II thereby preventing vasoconstriction and aldosterone secretion.; A selective adrenergic beta-1 blocking agent that is commonly used to treat ANGINA PECTORIS; HYPERTENSION; and CARDIAC ARRHYTHMIAS.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,PMID:19063792 -11179224,Prednisolone related to alcoholic hepatitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to alcoholic hepatitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -8573433,Prednisolone treats alcoholic hepatitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats alcoholic hepatitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -22580782,Prednisolone treats interstitial lung disease 2,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats interstitial lung disease 2 supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:26666486 -13234063,Prednisolone affects pericarditis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects pericarditis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -30367885,Carbon Dioxide treats respiratory failure,1009,"Carbon dioxide is a colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. Carbon dioxide is produced during respiration by all animals, fungi and microorganisms that depend on living and decaying plants for food, either directly or indirectly. It is, therefore, a major component of the carbon cycle. Additionally, carbon dioxide is used by plants during photosynthesis to make sugars which may either be consumed again in respiration or used as the raw material to produce polysaccharides such as starch and cellulose, proteins and the wide variety of other organic compounds required for plant growth and development. When inhaled at concentrations much higher than usual atmospheric levels, it can produce a sour taste in the mouth and a stinging sensation in the nose and throat. These effects result from the gas dissolving in the mucous membranes and saliva, forming a weak solution of carbonic acid. Carbon dioxide is used by the food industry, the oil industry, and the chemical industry. Carbon dioxide is used to produce carbonated soft drinks and soda water. Traditionally, the carbonation in beer and sparkling wine comes about through natural fermentation, but some manufacturers carbonate these drinks artificially.","Is the triple Carbon Dioxide treats respiratory failure supported by the sentence Carbon dioxide is a colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. Carbon dioxide is produced during respiration by all animals, fungi and microorganisms that depend on living and decaying plants for food, either directly or indirectly. It is, therefore, a major component of the carbon cycle. Additionally, carbon dioxide is used by plants during photosynthesis to make sugars which may either be consumed again in respiration or used as the raw material to produce polysaccharides such as starch and cellulose, proteins and the wide variety of other organic compounds required for plant growth and development. When inhaled at concentrations much higher than usual atmospheric levels, it can produce a sour taste in the mouth and a stinging sensation in the nose and throat. These effects result from the gas dissolving in the mucous membranes and saliva, forming a weak solution of carbonic acid. Carbon dioxide is used by the food industry, the oil industry, and the chemical industry. Carbon dioxide is used to produce carbonated soft drinks and soda water. Traditionally, the carbonation in beer and sparkling wine comes about through natural fermentation, but some manufacturers carbonate these drinks artificially.",False,https://www.nhlbi.nih.gov/health/respiratory-failure -7676165,Prednisolone treats hypercalcemia disease,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats hypercalcemia disease supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -9282196,Prednisolone related to IgA glomerulonephritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to IgA glomerulonephritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.nlm.nih.gov/medlineplus/ency/article/000466.htm -30347985,Cefepime treats toxic shock syndrome,1029,"The hydrochoride salt of a semi-synthetic, beta-lactamase-resistant, fourth-generation cephalosporin antibiotic derived from an Acremonium fungal species with broad-spectrum bactericidal activity. Administered parenterally, cefipime inhibits bacterial cell wall synthesis by binding to and inactivating penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity, resulting in a reduction of bacterial cell wall stability and cell lysis. This agent is more active against a variety of Gram-positive pathogens compared to third-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1041"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1041"" NCI Thesaurus); The hydrochloride salt of a semi-synthetic, beta-lactamase-resistant, fourth-generation cephalosporin antibiotic derived from an Acremonium fungal species with broad-spectrum bactericidal activity. Administered parenterally, cefepime inhibits bacterial cell wall synthesis by binding to and inactivating penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity, resulting in a reduction of bacterial cell wall stability and cell lysis. This agent is more active against a variety of Gram-positive pathogens compared to third-generation cephalosporins.; A semisynthetic, broad-spectrum, fourth-generation cephalosporin with antibacterial activity. Cefepime binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.; A fourth-generation cephalosporin antibacterial agent that is used in the treatment of infections, including those of the abdomen, urinary tract, respiratory tract, and skin. It is effective against PSEUDOMONAS AERUGINOSA and may also be used in the empiric treatment of FEBRILE NEUTROPENIA.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefepime treats toxic shock syndrome supported by the sentence The hydrochoride salt of a semi-synthetic, beta-lactamase-resistant, fourth-generation cephalosporin antibiotic derived from an Acremonium fungal species with broad-spectrum bactericidal activity. Administered parenterally, cefipime inhibits bacterial cell wall synthesis by binding to and inactivating penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity, resulting in a reduction of bacterial cell wall stability and cell lysis. This agent is more active against a variety of Gram-positive pathogens compared to third-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1041"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1041"" NCI Thesaurus); The hydrochloride salt of a semi-synthetic, beta-lactamase-resistant, fourth-generation cephalosporin antibiotic derived from an Acremonium fungal species with broad-spectrum bactericidal activity. Administered parenterally, cefepime inhibits bacterial cell wall synthesis by binding to and inactivating penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity, resulting in a reduction of bacterial cell wall stability and cell lysis. This agent is more active against a variety of Gram-positive pathogens compared to third-generation cephalosporins.; A semisynthetic, broad-spectrum, fourth-generation cephalosporin with antibacterial activity. Cefepime binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.; A fourth-generation cephalosporin antibacterial agent that is used in the treatment of infections, including those of the abdomen, urinary tract, respiratory tract, and skin. It is effective against PSEUDOMONAS AERUGINOSA and may also be used in the empiric treatment of FEBRILE NEUTROPENIA.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",False,http://en.wikipedia.org/wiki/toxic_shock_syndrome -8268574,Prednisolone treats thrombocytopenia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats thrombocytopenia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -9717382,Prednisolone treats hemangioma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats hemangioma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0001-6908-9849 -23496152,Prednisolone related to subacute thyroiditis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to subacute thyroiditis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -8865745,Prednisolone treats subacute thyroiditis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats subacute thyroiditis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -8819323,Prednisolone treats meningeal tuberculosis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats meningeal tuberculosis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -12767794,Prednisolone treats pneumonia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats pneumonia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/pneumonia -30350207,Isotretinoin treats neoplasm,1066,"A naturally-occurring retinoic acid with potential antineoplastic activity. Isotretinoin binds to and activates nuclear retinoic acid receptors (RARs); activated RARs serve as transcription factors that promote cell differentiation and apoptosis. This agent also exhibits immunomodulatory and anti-inflammatory responses and inhibits ornithine decarboxylase, thereby decreasing polyamine synthesis and keratinization. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C603"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C603"" NCI Thesaurus); An orally- and topically-active naturally-occurring retinoic acid with antineoplastic, chemopreventive, teratogenic, and embryotoxic activities. Alitretinoin binds to and activates nuclear retinoic acid receptors (RAR) and retinoid X receptors (RXR); these activated receptors act as transcription factors, regulating gene expression that results in the inhibition of cell proliferation, induction of cell differentiation, and apoptosis of both normal cells and tumor cells. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1574"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1574"" NCI Thesaurus); An orally- and topically-active naturally-occurring retinoic acid with antineoplastic, chemopreventive, teratogenic, and embryotoxic activities. Alitretinoin binds to and activates nuclear retinoic acid receptors (RAR) and retinoid X receptors (RXR); these activated receptors act as transcription factors, regulating gene expression that results in the inhibition of cell proliferation, induction of cell differentiation, and apoptosis of both normal cells and tumor cells.; A naturally-occurring retinoic acid with potential antineoplastic activity. Isotretinoin binds to and activates nuclear retinoic acid receptors (RARs); activated RARs serve as transcription factors that promote cell differentiation and apoptosis. This agent also exhibits immunomodulatory and anti-inflammatory responses and inhibits ornithine decarboxylase, thereby decreasing polyamine synthesis and keratinization.; A topical dermatologic agent that is used in the treatment of ACNE VULGARIS and several other skin diseases. The drug has teratogenic and other adverse effects.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Isotretinoin treats neoplasm supported by the sentence A naturally-occurring retinoic acid with potential antineoplastic activity. Isotretinoin binds to and activates nuclear retinoic acid receptors (RARs); activated RARs serve as transcription factors that promote cell differentiation and apoptosis. This agent also exhibits immunomodulatory and anti-inflammatory responses and inhibits ornithine decarboxylase, thereby decreasing polyamine synthesis and keratinization. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C603"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C603"" NCI Thesaurus); An orally- and topically-active naturally-occurring retinoic acid with antineoplastic, chemopreventive, teratogenic, and embryotoxic activities. Alitretinoin binds to and activates nuclear retinoic acid receptors (RAR) and retinoid X receptors (RXR); these activated receptors act as transcription factors, regulating gene expression that results in the inhibition of cell proliferation, induction of cell differentiation, and apoptosis of both normal cells and tumor cells. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1574"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1574"" NCI Thesaurus); An orally- and topically-active naturally-occurring retinoic acid with antineoplastic, chemopreventive, teratogenic, and embryotoxic activities. Alitretinoin binds to and activates nuclear retinoic acid receptors (RAR) and retinoid X receptors (RXR); these activated receptors act as transcription factors, regulating gene expression that results in the inhibition of cell proliferation, induction of cell differentiation, and apoptosis of both normal cells and tumor cells.; A naturally-occurring retinoic acid with potential antineoplastic activity. Isotretinoin binds to and activates nuclear retinoic acid receptors (RARs); activated RARs serve as transcription factors that promote cell differentiation and apoptosis. This agent also exhibits immunomodulatory and anti-inflammatory responses and inhibits ornithine decarboxylase, thereby decreasing polyamine synthesis and keratinization.; A topical dermatologic agent that is used in the treatment of ACNE VULGARIS and several other skin diseases. The drug has teratogenic and other adverse effects.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-6601-2165 -30341297,Isotretinoin treats acne,1066,"A naturally-occurring retinoic acid with potential antineoplastic activity. Isotretinoin binds to and activates nuclear retinoic acid receptors (RARs); activated RARs serve as transcription factors that promote cell differentiation and apoptosis. This agent also exhibits immunomodulatory and anti-inflammatory responses and inhibits ornithine decarboxylase, thereby decreasing polyamine synthesis and keratinization. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C603"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C603"" NCI Thesaurus); An orally- and topically-active naturally-occurring retinoic acid with antineoplastic, chemopreventive, teratogenic, and embryotoxic activities. Alitretinoin binds to and activates nuclear retinoic acid receptors (RAR) and retinoid X receptors (RXR); these activated receptors act as transcription factors, regulating gene expression that results in the inhibition of cell proliferation, induction of cell differentiation, and apoptosis of both normal cells and tumor cells. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1574"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1574"" NCI Thesaurus); An orally- and topically-active naturally-occurring retinoic acid with antineoplastic, chemopreventive, teratogenic, and embryotoxic activities. Alitretinoin binds to and activates nuclear retinoic acid receptors (RAR) and retinoid X receptors (RXR); these activated receptors act as transcription factors, regulating gene expression that results in the inhibition of cell proliferation, induction of cell differentiation, and apoptosis of both normal cells and tumor cells.; A naturally-occurring retinoic acid with potential antineoplastic activity. Isotretinoin binds to and activates nuclear retinoic acid receptors (RARs); activated RARs serve as transcription factors that promote cell differentiation and apoptosis. This agent also exhibits immunomodulatory and anti-inflammatory responses and inhibits ornithine decarboxylase, thereby decreasing polyamine synthesis and keratinization.; A topical dermatologic agent that is used in the treatment of ACNE VULGARIS and several other skin diseases. The drug has teratogenic and other adverse effects.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Isotretinoin treats acne supported by the sentence A naturally-occurring retinoic acid with potential antineoplastic activity. Isotretinoin binds to and activates nuclear retinoic acid receptors (RARs); activated RARs serve as transcription factors that promote cell differentiation and apoptosis. This agent also exhibits immunomodulatory and anti-inflammatory responses and inhibits ornithine decarboxylase, thereby decreasing polyamine synthesis and keratinization. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C603"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C603"" NCI Thesaurus); An orally- and topically-active naturally-occurring retinoic acid with antineoplastic, chemopreventive, teratogenic, and embryotoxic activities. Alitretinoin binds to and activates nuclear retinoic acid receptors (RAR) and retinoid X receptors (RXR); these activated receptors act as transcription factors, regulating gene expression that results in the inhibition of cell proliferation, induction of cell differentiation, and apoptosis of both normal cells and tumor cells. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1574"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1574"" NCI Thesaurus); An orally- and topically-active naturally-occurring retinoic acid with antineoplastic, chemopreventive, teratogenic, and embryotoxic activities. Alitretinoin binds to and activates nuclear retinoic acid receptors (RAR) and retinoid X receptors (RXR); these activated receptors act as transcription factors, regulating gene expression that results in the inhibition of cell proliferation, induction of cell differentiation, and apoptosis of both normal cells and tumor cells.; A naturally-occurring retinoic acid with potential antineoplastic activity. Isotretinoin binds to and activates nuclear retinoic acid receptors (RARs); activated RARs serve as transcription factors that promote cell differentiation and apoptosis. This agent also exhibits immunomodulatory and anti-inflammatory responses and inhibits ornithine decarboxylase, thereby decreasing polyamine synthesis and keratinization.; A topical dermatologic agent that is used in the treatment of ACNE VULGARIS and several other skin diseases. The drug has teratogenic and other adverse effects.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,http://en.wikipedia.org/wiki/sebaceous_gland#clinical_significance -11013570,Prednisolone related to leukemia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to leukemia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/leukemia -10623724,Prednisolone related to hemolytic anemia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to hemolytic anemia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -10502737,Prednisolone treats hemolytic anemia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats hemolytic anemia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -16960031,Prednisolone related to psoriatic arthritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to psoriatic arthritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/psoriatic_arthropathy -9109448,Prednisolone treats psoriatic arthritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats psoriatic arthritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/psoriatic_arthropathy -14742554,Prednisolone treats psoriasis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats psoriasis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -45047885,Pentobarbital treats insomnia,1156,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; A short-acting barbiturate that is effective as a sedative and hypnotic (but not as an anti-anxiety) agent and is usually given orally. It is prescribed more frequently for sleep induction than for sedation but, like similar agents, may lose its effectiveness by the second week of continued administration. (From AMA Drug Evaluations Annual, 1994, p236)","Is the triple Pentobarbital treats insomnia supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; A short-acting barbiturate that is effective as a sedative and hypnotic (but not as an anti-anxiety) agent and is usually given orally. It is prescribed more frequently for sleep induction than for sedation but, like similar agents, may lose its effectiveness by the second week of continued administration. (From AMA Drug Evaluations Annual, 1994, p236)",False,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=insomnia -45047883,Pentobarbital treats epilepsy,1156,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; A short-acting barbiturate that is effective as a sedative and hypnotic (but not as an anti-anxiety) agent and is usually given orally. It is prescribed more frequently for sleep induction than for sedation but, like similar agents, may lose its effectiveness by the second week of continued administration. (From AMA Drug Evaluations Annual, 1994, p236)","Is the triple Pentobarbital treats epilepsy supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; A short-acting barbiturate that is effective as a sedative and hypnotic (but not as an anti-anxiety) agent and is usually given orally. It is prescribed more frequently for sleep induction than for sedation but, like similar agents, may lose its effectiveness by the second week of continued administration. (From AMA Drug Evaluations Annual, 1994, p236)",False,http://www.merriam-webster.com/medlineplus/epilepsy -13758030,Prednisolone treats optic neuritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats optic neuritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://www.mayoclinic.org/diseases-conditions/optic-neuritis/symptoms-causes/syc-20354953 -10503828,Prednisolone related to seasonal allergic rhinitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to seasonal allergic rhinitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:11449200 -16502712,Prednisolone related to aplastic anemia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to aplastic anemia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.nhlbi.nih.gov/health/health-topics/topics/aplastic/ -14992803,Prednisolone treats aplastic anemia,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats aplastic anemia supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.nhlbi.nih.gov/health/health-topics/topics/aplastic/ -10576837,Prednisolone related to juvenile idiopathic arthritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to juvenile idiopathic arthritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0001-5208-3432 -20836940,Prednisolone treats juvenile idiopathic arthritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats juvenile idiopathic arthritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0001-5208-3432 -30648683,Moxisylyte treats erectile dysfunction,1179,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Moxisylyte, denominated as thymoxamine in the UK, is a specific and orally active α1-adrenergic antagonist.[T45] According to the WHO, moxisylyte is approved since 1987[T91] and in the same year, it acquired the denomination of orphan product by the FDA.[L1172] This drug was developed by the Japanese company Fujirebio and also by the American company Iolab in the late 80s.","Is the triple Moxisylyte treats erectile dysfunction supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Moxisylyte, denominated as thymoxamine in the UK, is a specific and orally active α1-adrenergic antagonist.[T45] According to the WHO, moxisylyte is approved since 1987[T91] and in the same year, it acquired the denomination of orphan product by the FDA.[L1172] This drug was developed by the Japanese company Fujirebio and also by the American company Iolab in the late 80s.",False,https://orcid.org/0000-0002-6601-2165 -30370500,Moxisylyte treats erectile dysfunction,1179,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Moxisylyte, denominated as thymoxamine in the UK, is a specific and orally active α1-adrenergic antagonist.[T45] According to the WHO, moxisylyte is approved since 1987[T91] and in the same year, it acquired the denomination of orphan product by the FDA.[L1172] This drug was developed by the Japanese company Fujirebio and also by the American company Iolab in the late 80s.","Is the triple Moxisylyte treats erectile dysfunction supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Moxisylyte, denominated as thymoxamine in the UK, is a specific and orally active α1-adrenergic antagonist.[T45] According to the WHO, moxisylyte is approved since 1987[T91] and in the same year, it acquired the denomination of orphan product by the FDA.[L1172] This drug was developed by the Japanese company Fujirebio and also by the American company Iolab in the late 80s.",False,https://orcid.org/0000-0002-6601-2165 -9077262,Prednisolone treats lymphoma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats lymphoma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -16192798,Prednisolone related to dermatomyositis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to dermatomyositis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/dermatomyositis -24270725,Prednisolone affects dermatomyositis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects dermatomyositis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/dermatomyositis -9061500,Prednisolone treats dermatomyositis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats dermatomyositis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/dermatomyositis -11663099,Prednisolone related to Crohn disease,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to Crohn disease supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/chron%27s_disease -12057849,Prednisolone affects Crohn disease,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects Crohn disease supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/chron%27s_disease -7986379,Prednisolone treats Crohn disease,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats Crohn disease supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/chron%27s_disease -10703266,Prednisolone related to ulcerative colitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to ulcerative colitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://meshb.nlm.nih.gov/record/ui?ui=d003093 -20789636,Prednisolone causes ulcerative colitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone causes ulcerative colitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://meshb.nlm.nih.gov/record/ui?ui=d003093 -30368317,Amisulpride treats psychotic disorder,1221,"Amisulpride (trade name Solian) is an antipsychotic drug sold by Sanofi-Aventis. It is not approved for use in the United States, but is approved for use in Europe and Australia for the treatment of psychoses and schizophrenia. Additionally, it is approved in Italy for the treatment of dysthymia (under the brand name Deniban). Amisulpride is a selective dopamine antagonist.","Is the triple Amisulpride treats psychotic disorder supported by the sentence Amisulpride (trade name Solian) is an antipsychotic drug sold by Sanofi-Aventis. It is not approved for use in the United States, but is approved for use in Europe and Australia for the treatment of psychoses and schizophrenia. Additionally, it is approved in Italy for the treatment of dysthymia (under the brand name Deniban). Amisulpride is a selective dopamine antagonist.",False,http://www.nlm.nih.gov/medlineplus/psychoticdisorders.htm -7586864,Prednisolone treats ulcerative colitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats ulcerative colitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://meshb.nlm.nih.gov/record/ui?ui=d003093 -45046273,Nitroglycerin treats Angina pectoris,1261,"An organic nitrate with vasodilator activity. Nitroglycerin is converted into nitric oxide (NO) in smooth muscle and activates guanylyl cyclase, thereby increasing cGMP concentration, and resulting in smooth muscle relaxation. Dilatation of the veins results in decreased venous return to the heart, thereby decreasing left ventricular volume (reduced preload) and decreasing myocardial oxygen requirements. Arteriolar relaxation reduces arteriolar resistance (reduced afterload), thereby decreasing myocardial oxygen demands. In addition, nitroglycerin causes coronary artery dilatation, thereby improving myocardial blood distribution. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29294"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29294"" NCI Thesaurus); An organic nitrate with vasodilator activity. Nitroglycerin is converted into nitric oxide (NO) in smooth muscle and activates guanylyl cyclase, thereby increasing cGMP concentration, and resulting in smooth muscle relaxation. Dilatation of the veins results in decreased venous return to the heart, thereby decreasing left ventricular volume (reduced preload) and decreasing myocardial oxygen requirements. Arteriolar relaxation reduces arteriolar resistance (reduced afterload), thereby decreasing myocardial oxygen demands. In addition, nitroglycerine causes coronary artery dilatation, thereby improving myocardial blood distribution.; A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Nitroglycerin treats Angina pectoris supported by the sentence An organic nitrate with vasodilator activity. Nitroglycerin is converted into nitric oxide (NO) in smooth muscle and activates guanylyl cyclase, thereby increasing cGMP concentration, and resulting in smooth muscle relaxation. Dilatation of the veins results in decreased venous return to the heart, thereby decreasing left ventricular volume (reduced preload) and decreasing myocardial oxygen requirements. Arteriolar relaxation reduces arteriolar resistance (reduced afterload), thereby decreasing myocardial oxygen demands. In addition, nitroglycerin causes coronary artery dilatation, thereby improving myocardial blood distribution. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29294"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29294"" NCI Thesaurus); An organic nitrate with vasodilator activity. Nitroglycerin is converted into nitric oxide (NO) in smooth muscle and activates guanylyl cyclase, thereby increasing cGMP concentration, and resulting in smooth muscle relaxation. Dilatation of the veins results in decreased venous return to the heart, thereby decreasing left ventricular volume (reduced preload) and decreasing myocardial oxygen requirements. Arteriolar relaxation reduces arteriolar resistance (reduced afterload), thereby decreasing myocardial oxygen demands. In addition, nitroglycerine causes coronary artery dilatation, thereby improving myocardial blood distribution.; A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-0736-9199 -30360377,Nitroglycerin treats Angina pectoris,1261,"An organic nitrate with vasodilator activity. Nitroglycerin is converted into nitric oxide (NO) in smooth muscle and activates guanylyl cyclase, thereby increasing cGMP concentration, and resulting in smooth muscle relaxation. Dilatation of the veins results in decreased venous return to the heart, thereby decreasing left ventricular volume (reduced preload) and decreasing myocardial oxygen requirements. Arteriolar relaxation reduces arteriolar resistance (reduced afterload), thereby decreasing myocardial oxygen demands. In addition, nitroglycerin causes coronary artery dilatation, thereby improving myocardial blood distribution. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29294"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29294"" NCI Thesaurus); An organic nitrate with vasodilator activity. Nitroglycerin is converted into nitric oxide (NO) in smooth muscle and activates guanylyl cyclase, thereby increasing cGMP concentration, and resulting in smooth muscle relaxation. Dilatation of the veins results in decreased venous return to the heart, thereby decreasing left ventricular volume (reduced preload) and decreasing myocardial oxygen requirements. Arteriolar relaxation reduces arteriolar resistance (reduced afterload), thereby decreasing myocardial oxygen demands. In addition, nitroglycerine causes coronary artery dilatation, thereby improving myocardial blood distribution.; A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Nitroglycerin treats Angina pectoris supported by the sentence An organic nitrate with vasodilator activity. Nitroglycerin is converted into nitric oxide (NO) in smooth muscle and activates guanylyl cyclase, thereby increasing cGMP concentration, and resulting in smooth muscle relaxation. Dilatation of the veins results in decreased venous return to the heart, thereby decreasing left ventricular volume (reduced preload) and decreasing myocardial oxygen requirements. Arteriolar relaxation reduces arteriolar resistance (reduced afterload), thereby decreasing myocardial oxygen demands. In addition, nitroglycerin causes coronary artery dilatation, thereby improving myocardial blood distribution. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29294"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29294"" NCI Thesaurus); An organic nitrate with vasodilator activity. Nitroglycerin is converted into nitric oxide (NO) in smooth muscle and activates guanylyl cyclase, thereby increasing cGMP concentration, and resulting in smooth muscle relaxation. Dilatation of the veins results in decreased venous return to the heart, thereby decreasing left ventricular volume (reduced preload) and decreasing myocardial oxygen requirements. Arteriolar relaxation reduces arteriolar resistance (reduced afterload), thereby decreasing myocardial oxygen demands. In addition, nitroglycerine causes coronary artery dilatation, thereby improving myocardial blood distribution.; A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-0736-9199 -13029310,Prednisolone affects chronic obstructive pulmonary disease,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects chronic obstructive pulmonary disease supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://www.nhlbi.nih.gov/health-topics/copd -8455402,Prednisolone treats chronic obstructive pulmonary disease,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats chronic obstructive pulmonary disease supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://www.nhlbi.nih.gov/health-topics/copd -16360878,Prednisolone treats ophthalmic herpes zoster,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats ophthalmic herpes zoster supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -10735861,Prednisolone causes contact dermatitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone causes contact dermatitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -26379811,Prednisolone disrupts contact dermatitis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone disrupts contact dermatitis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -10744705,"Prednisolone related to dermatitis, atopic",568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to dermatitis, atopic supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:27904186 -11527350,"Prednisolone treats dermatitis, atopic",568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats dermatitis, atopic supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:27904186 -9437304,Prednisolone related to systemic lupus erythematosus,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to systemic lupus erythematosus supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/systemic_lupus_erythematosus -8757881,Prednisolone causes systemic lupus erythematosus,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone causes systemic lupus erythematosus supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/systemic_lupus_erythematosus -7395227,Prednisolone affects systemic lupus erythematosus,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects systemic lupus erythematosus supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/systemic_lupus_erythematosus -7819165,Prednisolone treats systemic lupus erythematosus,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats systemic lupus erythematosus supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/systemic_lupus_erythematosus -16114172,Prednisolone related to plasma cell myeloma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to plasma cell myeloma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.cancer.gov/dictionary?cdrid=411384 -26670577,Prednisolone has part plasma cell myeloma,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone has part plasma cell myeloma supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.cancer.gov/dictionary?cdrid=411384 -11213963,Prednisolone related to leprosy,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to leprosy supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/leprosy -8583398,Prednisolone treats leprosy,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats leprosy supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/leprosy -10983909,Prednisolone prevents leprosy,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone prevents leprosy supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/leprosy -7262473,Prednisolone related to rheumatoid arthritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to rheumatoid arthritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -15888410,Prednisolone affects rheumatoid arthritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects rheumatoid arthritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -7158230,Prednisolone treats rheumatoid arthritis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats rheumatoid arthritis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://orcid.org/0000-0002-0736-9199 -10565620,Prednisolone related to nephrotic syndrome,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to nephrotic syndrome supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://www.niddk.nih.gov/health-information/kidney-disease/nephrotic-syndrome-adults -30383659,Sodium Chloride treats periodontitis,1300,"A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197","Is the triple Sodium Chloride treats periodontitis supported by the sentence A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197",False,https://orcid.org/0000-0001-5889-4463 -7927983,Prednisolone treats nephrotic syndrome,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats nephrotic syndrome supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,https://www.niddk.nih.gov/health-information/kidney-disease/nephrotic-syndrome-adults -26307899,Prednisolone treats eye disorder,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats eye disorder supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://en.wikipedia.org/wiki/eye_disease -23981131,Prednisolone treats mycosis fungoides,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats mycosis fungoides supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True, -11166361,Prednisolone treats erythema multiforme,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats erythema multiforme supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,http://www.nlm.nih.gov/medlineplus/ency/article/000851.htm -10555139,Prednisolone affects peptic ulcer disease,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects peptic ulcer disease supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:28242110 -30370768,Sodium Chloride treats intervertebral disc degenerative disorder,1300,"A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197","Is the triple Sodium Chloride treats intervertebral disc degenerative disorder supported by the sentence A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197",False,http://www.cedars-sinai.edu/patients/health-conditions/degenerative-disc-disease.aspx -30370766,Sodium Chloride treats Low back pain,1300,"A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197","Is the triple Sodium Chloride treats Low back pain supported by the sentence A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197",False, -7206314,Prednisolone related to pulmonary tuberculosis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone related to pulmonary tuberculosis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:30345099 -10545904,Prednisolone causes pulmonary tuberculosis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone causes pulmonary tuberculosis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:30345099 -8647269,Prednisolone treats pulmonary tuberculosis,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats pulmonary tuberculosis supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:30345099 -11166363,Prednisolone treats canker sore,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone treats canker sore supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:25346356 -30362731,Sodium Chloride treats Dyspnea,1300,"A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197","Is the triple Sodium Chloride treats Dyspnea supported by the sentence A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197",False,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=dyspnea -30362729,Sodium Chloride treats Fever,1300,"A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197","Is the triple Sodium Chloride treats Fever supported by the sentence A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197",False,PMID:9759682 -18935086,Prednisolone coexists with Prednisone,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone coexists with Prednisone supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:32422522 -9296680,Prednisolone derives from Prednisone,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone derives from Prednisone supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:32422522 -30362717,Sodium Chloride treats multiple organ dysfunction syndrome,1300,"A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197","Is the triple Sodium Chloride treats multiple organ dysfunction syndrome supported by the sentence A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197",False,https://www.ncbi.nlm.nih.gov/books/nbk6868/ -14808035,Prednisolone physically interacts with Prednisone,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone physically interacts with Prednisone supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:32422522 -9296682,Prednisolone physically interacts with Prednisone,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone physically interacts with Prednisone supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:32422522 -17668631,Prednisolone affects Prednisone,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone affects Prednisone supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:32422522 -30362703,Sodium Chloride treats cardiac arrest,1300,"A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197","Is the triple Sodium Chloride treats cardiac arrest supported by the sentence A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197",False,http://www.nlm.nih.gov/medlineplus/cardiacarrest.htm -9655099,Prednisolone has input Prednisone,568,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.","Is the triple Prednisolone has input Prednisone supported by the sentence Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",True,PMID:32422522 -14483328,Hydrocortisone related to bronchopulmonary dysplasia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to bronchopulmonary dysplasia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://www.nhlbi.nih.gov/health/bronchopulmonary-dysplasia -8632826,Hydrocortisone treats bronchopulmonary dysplasia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats bronchopulmonary dysplasia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://www.nhlbi.nih.gov/health/bronchopulmonary-dysplasia -14020540,Hydrocortisone prevents bronchopulmonary dysplasia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone prevents bronchopulmonary dysplasia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://www.nhlbi.nih.gov/health/bronchopulmonary-dysplasia -11888652,Hydrocortisone related to congenital adrenal hyperplasia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to congenital adrenal hyperplasia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.genome.jp/dbget-bin/www_bget?ds:h00216 -18446972,Hydrocortisone causes congenital adrenal hyperplasia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes congenital adrenal hyperplasia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.genome.jp/dbget-bin/www_bget?ds:h00216 -26997315,Hydrocortisone affects congenital adrenal hyperplasia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects congenital adrenal hyperplasia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.genome.jp/dbget-bin/www_bget?ds:h00216 -13999195,Hydrocortisone affects congenital adrenal hyperplasia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects congenital adrenal hyperplasia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.genome.jp/dbget-bin/www_bget?ds:h00216 -30355210,Sodium Chloride treats pulmonary edema,1300,"A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197","Is the triple Sodium Chloride treats pulmonary edema supported by the sentence A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197",False,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=pulmonary%20edema -23738730,Hydrocortisone produces congenital adrenal hyperplasia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces congenital adrenal hyperplasia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.genome.jp/dbget-bin/www_bget?ds:h00216 -19793698,Hydrocortisone related to alcohol abuse,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to alcohol abuse supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://www.niaaa.nih.gov/alcohol-health/overview-alcohol-consumption/alcohol-use-disorders -10522181,Hydrocortisone related to osteoarthritis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to osteoarthritis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.mayoclinic.com/health/osteoarthritis/ds00019 -21274202,Hydrocortisone affects osteoarthritis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects osteoarthritis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.mayoclinic.com/health/osteoarthritis/ds00019 -10492262,Hydrocortisone treats osteoarthritis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats osteoarthritis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.mayoclinic.com/health/osteoarthritis/ds00019 -9235597,Hydrocortisone related to type 1 diabetes mellitus,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to type 1 diabetes mellitus supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/diabetes_mellitus_type_1 -9175521,Hydrocortisone treats type 1 diabetes mellitus,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats type 1 diabetes mellitus supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/diabetes_mellitus_type_1 -16473285,Hydrocortisone produces type 1 diabetes mellitus,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces type 1 diabetes mellitus supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/diabetes_mellitus_type_1 -8615164,Hydrocortisone related to asthma,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to asthma supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.nhlbi.nih.gov/health/dci/diseases/asthma/asthma_whatis.htm -13347553,Hydrocortisone affects asthma,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects asthma supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.nhlbi.nih.gov/health/dci/diseases/asthma/asthma_whatis.htm -9120606,Hydrocortisone affects asthma,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects asthma supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.nhlbi.nih.gov/health/dci/diseases/asthma/asthma_whatis.htm -7363431,Hydrocortisone treats asthma,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats asthma supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.nhlbi.nih.gov/health/dci/diseases/asthma/asthma_whatis.htm -13669597,Hydrocortisone produces asthma,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces asthma supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.nhlbi.nih.gov/health/dci/diseases/asthma/asthma_whatis.htm -8552834,Hydrocortisone predisposes asthma,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone predisposes asthma supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.nhlbi.nih.gov/health/dci/diseases/asthma/asthma_whatis.htm -11089023,Hydrocortisone related to pancreatitis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to pancreatitis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://medlineplus.gov/pancreatitis.htm -7432490,Hydrocortisone causes pancreatitis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes pancreatitis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://medlineplus.gov/pancreatitis.htm -7432481,Hydrocortisone treats pancreatitis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats pancreatitis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://medlineplus.gov/pancreatitis.htm -13724762,Hydrocortisone treats severe acute respiratory syndrome,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats severe acute respiratory syndrome supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/severe_acute_respiratory_syndrome -7919367,Hydrocortisone related to adrenocortical insufficiency,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to adrenocortical insufficiency supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -9318796,Hydrocortisone causes adrenocortical insufficiency,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes adrenocortical insufficiency supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -9535781,Hydrocortisone treats adrenocortical insufficiency,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats adrenocortical insufficiency supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -30344592,Sodium Chloride treats hypotensive disorder,1300,"A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197","Is the triple Sodium Chloride treats hypotensive disorder supported by the sentence A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197",False,https://orcid.org/0000-0002-0736-9199 -27711985,Hydrocortisone disrupts adrenocortical insufficiency,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone disrupts adrenocortical insufficiency supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -16963888,Hydrocortisone prevents adrenocortical insufficiency,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone prevents adrenocortical insufficiency supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -7573954,Hydrocortisone related to neoplasm,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to neoplasm supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-6601-2165 -8657746,Hydrocortisone causes neoplasm,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes neoplasm supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-6601-2165 -30372932,ELTROMBOPAG treats anemia,1343,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T116; Eltrombopag is used to treat low blood platelet counts in adults with chronic immune (idiopathic) thrombocytopenia (ITP), when certain other medicines, or surgery to remove the spleen, have not worked well enough. ITP is a condition that may cause unusual bruising or bleeding due to an abnormally low number of platelets in the blood. Eltrombopag has also been recently approved (late 2012) for the treatment of thrombocytopenia (low blood platelet counts) in patients with chronic hepatitis C to allow them to initiate and maintain interferon-based therapy.","Is the triple ELTROMBOPAG treats anemia supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T116; Eltrombopag is used to treat low blood platelet counts in adults with chronic immune (idiopathic) thrombocytopenia (ITP), when certain other medicines, or surgery to remove the spleen, have not worked well enough. ITP is a condition that may cause unusual bruising or bleeding due to an abnormally low number of platelets in the blood. Eltrombopag has also been recently approved (late 2012) for the treatment of thrombocytopenia (low blood platelet counts) in patients with chronic hepatitis C to allow them to initiate and maintain interferon-based therapy.",False,http://www.nhlbi.nih.gov/health/health-topics/topics/anemia/ -12524121,Hydrocortisone treats neoplasm,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats neoplasm supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-6601-2165 -8077250,Hydrocortisone produces neoplasm,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces neoplasm supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-6601-2165 -26389045,Hydrocortisone disrupts neoplasm,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone disrupts neoplasm supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-6601-2165 -30353114,mitomycin C treats sarcoma,1357,"A methylazirinopyrroloindoledione antineoplastic antibiotic isolated from the bacterium Streptomyces caespitosus and other Streptomyces bacterial species. Bioreduced mitomycin C generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis. Preferentially toxic to hypoxic cells, mitomycin C also inhibits RNA and protein synthesis at high concentrations. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1820"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1820"" NCI Thesaurus); A methylazirinopyrroloindoledione antineoplastic antibiotic isolated from the bacterium Streptomyces caespitosus and other Streptomyces bacterial species. Bioreduced mitomycin C generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis. Preferentially toxic to hypoxic cells, mitomycin C also inhibits RNA and protein synthesis at high concentrations. (NCI04); An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple mitomycin C treats sarcoma supported by the sentence A methylazirinopyrroloindoledione antineoplastic antibiotic isolated from the bacterium Streptomyces caespitosus and other Streptomyces bacterial species. Bioreduced mitomycin C generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis. Preferentially toxic to hypoxic cells, mitomycin C also inhibits RNA and protein synthesis at high concentrations. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1820"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1820"" NCI Thesaurus); A methylazirinopyrroloindoledione antineoplastic antibiotic isolated from the bacterium Streptomyces caespitosus and other Streptomyces bacterial species. Bioreduced mitomycin C generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis. Preferentially toxic to hypoxic cells, mitomycin C also inhibits RNA and protein synthesis at high concentrations. (NCI04); An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",False,http://en.wikipedia.org/wiki/sarcoma -13213365,Hydrocortisone related to chronic primary adrenal insufficiency,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to chronic primary adrenal insufficiency supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/addison%27s_disease -30345648,mitomycin C treats carcinoma,1357,"A methylazirinopyrroloindoledione antineoplastic antibiotic isolated from the bacterium Streptomyces caespitosus and other Streptomyces bacterial species. Bioreduced mitomycin C generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis. Preferentially toxic to hypoxic cells, mitomycin C also inhibits RNA and protein synthesis at high concentrations. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1820"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1820"" NCI Thesaurus); A methylazirinopyrroloindoledione antineoplastic antibiotic isolated from the bacterium Streptomyces caespitosus and other Streptomyces bacterial species. Bioreduced mitomycin C generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis. Preferentially toxic to hypoxic cells, mitomycin C also inhibits RNA and protein synthesis at high concentrations. (NCI04); An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple mitomycin C treats carcinoma supported by the sentence A methylazirinopyrroloindoledione antineoplastic antibiotic isolated from the bacterium Streptomyces caespitosus and other Streptomyces bacterial species. Bioreduced mitomycin C generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis. Preferentially toxic to hypoxic cells, mitomycin C also inhibits RNA and protein synthesis at high concentrations. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1820"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1820"" NCI Thesaurus); A methylazirinopyrroloindoledione antineoplastic antibiotic isolated from the bacterium Streptomyces caespitosus and other Streptomyces bacterial species. Bioreduced mitomycin C generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis. Preferentially toxic to hypoxic cells, mitomycin C also inhibits RNA and protein synthesis at high concentrations. (NCI04); An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-0736-9199 -15330155,Hydrocortisone produces chronic primary adrenal insufficiency,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces chronic primary adrenal insufficiency supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/addison%27s_disease -45032043,Cefazolin treats bacterial infectious disease with sepsis,1362,"Cefazolin is only found in individuals that have used or taken this drug. It is a semisynthetic cephalosporin analog with broad-spectrum antibiotic action due to inhibition of bacterial cell wall synthesis. It attains high serum levels and is excreted quickly via the urine. [PubChem]In vitro tests demonstrate that the bactericidal action of cephalosporins results from inhibition of cell wall synthesis. By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, it inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins.","Is the triple Cefazolin treats bacterial infectious disease with sepsis supported by the sentence Cefazolin is only found in individuals that have used or taken this drug. It is a semisynthetic cephalosporin analog with broad-spectrum antibiotic action due to inhibition of bacterial cell wall synthesis. It attains high serum levels and is excreted quickly via the urine. [PubChem]In vitro tests demonstrate that the bactericidal action of cephalosporins results from inhibition of cell wall synthesis. By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, it inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins.",False,PMID:20421654 -14360687,Hydrocortisone related to dermatitis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to dermatitis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.nlm.nih.gov/medlineplus/eczema.htm -20336537,Hydrocortisone affects dermatitis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects dermatitis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.nlm.nih.gov/medlineplus/eczema.htm -45032489,Cephalothin treats osteomyelitis,1363,"A semisynthetic, beta-lactam, first-generation cephalosporin antibiotic with bactericidal activity. Cephalothin binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.; A cephalosporin antibiotic.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cephalothin treats osteomyelitis supported by the sentence A semisynthetic, beta-lactam, first-generation cephalosporin antibiotic with bactericidal activity. Cephalothin binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.; A cephalosporin antibiotic.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-0736-9199 -12576998,Hydrocortisone related to Hypoxemia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to Hypoxemia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0001-5208-3432 -24030854,Hydrocortisone related to Hypoxemia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to Hypoxemia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0001-5208-3432 -20591759,Hydrocortisone causes Hypoxemia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes Hypoxemia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0001-5208-3432 -11695335,Hydrocortisone affects Hypoxemia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects Hypoxemia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0001-5208-3432 -7366981,Hydrocortisone affects Hypoxemia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects Hypoxemia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0001-5208-3432 -15602187,Hydrocortisone treats Hypoxemia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats Hypoxemia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0001-5208-3432 -11989948,Hydrocortisone produces Hypoxemia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces Hypoxemia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0001-5208-3432 -17359303,Hydrocortisone causes influenza,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes influenza supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.merck.com/mmhe/sec17/ch198/ch198d.htm -15155784,Hydrocortisone related to psoriasis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to psoriasis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -45045320,Mitoxantrone treats acute myeloid leukemia,1379,"The hydrochloride salt of an anthracenedione antibiotic with antineoplastic activity. Mitoxantrone intercalates into and crosslinks DNA, thereby disrupting DNA and RNA replication. This agent also binds to topoisomerase II, resulting in DNA strand breaks and inhibition of DNA repair. Mitoxantrone is less cardiotoxic compared to doxorubicin. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C665"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C665"" NCI Thesaurus); An anthracenedione antibiotic with antineoplastic activity. Mitoxantrone intercalates into and crosslinks DNA, thereby disrupting DNA and RNA replication. This agent also binds to topoisomerase II, resulting in DNA strand breaks and inhibition of DNA repair. Mitoxantrone is less cardiotoxic compared to doxorubicin.; An anthracenedione-derived antineoplastic agent.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Mitoxantrone treats acute myeloid leukemia supported by the sentence The hydrochloride salt of an anthracenedione antibiotic with antineoplastic activity. Mitoxantrone intercalates into and crosslinks DNA, thereby disrupting DNA and RNA replication. This agent also binds to topoisomerase II, resulting in DNA strand breaks and inhibition of DNA repair. Mitoxantrone is less cardiotoxic compared to doxorubicin. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C665"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C665"" NCI Thesaurus); An anthracenedione antibiotic with antineoplastic activity. Mitoxantrone intercalates into and crosslinks DNA, thereby disrupting DNA and RNA replication. This agent also binds to topoisomerase II, resulting in DNA strand breaks and inhibition of DNA repair. Mitoxantrone is less cardiotoxic compared to doxorubicin.; An anthracenedione-derived antineoplastic agent.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,http://www.cancer.gov/dictionary?cdrid=44363 -15325707,Hydrocortisone treats psoriasis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats psoriasis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -14450267,Hydrocortisone related to adrenal cortex neoplasm,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to adrenal cortex neoplasm supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -8699464,Hydrocortisone causes adrenal cortex neoplasm,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes adrenal cortex neoplasm supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -16946872,Hydrocortisone treats adrenal cortex neoplasm,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats adrenal cortex neoplasm supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -13796050,Hydrocortisone produces adrenal cortex neoplasm,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces adrenal cortex neoplasm supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -10518203,Hydrocortisone related to otitis externa,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to otitis externa supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/otitis_externa -9145908,Hydrocortisone causes otitis externa,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes otitis externa supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/otitis_externa -7698304,Hydrocortisone treats otitis externa,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats otitis externa supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/otitis_externa -25927636,Hydrocortisone related to cardiac arrest,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to cardiac arrest supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.nlm.nih.gov/medlineplus/cardiacarrest.htm -26940919,Hydrocortisone affects cardiac arrest,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects cardiac arrest supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.nlm.nih.gov/medlineplus/cardiacarrest.htm -30646392,Doxorubicin treats lung cancer,1383,"The hydrochloride salt of doxorubicin, an anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1326"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1326"" NCI Thesaurus); The hydrochloride salt of doxorubicin, an anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.; An anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.; Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Doxorubicin treats lung cancer supported by the sentence The hydrochloride salt of doxorubicin, an anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1326"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1326"" NCI Thesaurus); The hydrochloride salt of doxorubicin, an anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.; An anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.; Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",False,http://en.wikipedia.org/wiki/lung_cance -11866289,Hydrocortisone related to nicotine dependence,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to nicotine dependence supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://en.wikipedia.org/wiki/nicotine_dependence -8625521,Hydrocortisone related to dissociative amnesia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to dissociative amnesia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://www.merckmanuals.com/professional/psychiatric-disorders/dissociative-disorders/dissociative-amnesia -9850315,Hydrocortisone causes dissociative amnesia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes dissociative amnesia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://www.merckmanuals.com/professional/psychiatric-disorders/dissociative-disorders/dissociative-amnesia -7266667,Hydrocortisone affects dissociative amnesia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects dissociative amnesia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://www.merckmanuals.com/professional/psychiatric-disorders/dissociative-disorders/dissociative-amnesia -15753359,Hydrocortisone treats dissociative amnesia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats dissociative amnesia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://www.merckmanuals.com/professional/psychiatric-disorders/dissociative-disorders/dissociative-amnesia -8615556,Hydrocortisone predisposes dissociative amnesia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone predisposes dissociative amnesia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://www.merckmanuals.com/professional/psychiatric-disorders/dissociative-disorders/dissociative-amnesia -25131277,Hydrocortisone related to Crohn disease,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to Crohn disease supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/chron%27s_disease -7584436,Hydrocortisone treats Crohn disease,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats Crohn disease supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/chron%27s_disease -30361635,Doxorubicin treats acute myeloid leukemia,1383,"The hydrochloride salt of doxorubicin, an anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1326"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1326"" NCI Thesaurus); The hydrochloride salt of doxorubicin, an anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.; An anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.; Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Doxorubicin treats acute myeloid leukemia supported by the sentence The hydrochloride salt of doxorubicin, an anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1326"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1326"" NCI Thesaurus); The hydrochloride salt of doxorubicin, an anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.; An anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.; Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",False,http://www.cancer.gov/dictionary?cdrid=44363 -19531871,Hydrocortisone affects atrial fibrillation,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects atrial fibrillation supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -13075196,Hydrocortisone prevents atrial fibrillation,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone prevents atrial fibrillation supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -25411585,Hydrocortisone predisposes atrial fibrillation,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone predisposes atrial fibrillation supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=atrial%20fibrillation -14891361,"Hydrocortisone related to dermatitis, atopic",569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to dermatitis, atopic supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,PMID:27904186 -30343934,Doxorubicin treats sarcoma,1383,"The hydrochloride salt of doxorubicin, an anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1326"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1326"" NCI Thesaurus); The hydrochloride salt of doxorubicin, an anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.; An anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.; Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Doxorubicin treats sarcoma supported by the sentence The hydrochloride salt of doxorubicin, an anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1326"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1326"" NCI Thesaurus); The hydrochloride salt of doxorubicin, an anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.; An anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.; Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",False,http://en.wikipedia.org/wiki/sarcoma -8540090,"Hydrocortisone treats dermatitis, atopic",569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats dermatitis, atopic supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,PMID:27904186 -20514012,"Hydrocortisone produces dermatitis, atopic",569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces dermatitis, atopic supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,PMID:27904186 -8778414,Hydrocortisone related to Inflammation,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to Inflammation supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,ISBN:0198506732 -24445107,Hydrocortisone related to Inflammation,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to Inflammation supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,ISBN:0198506732 -10068843,Hydrocortisone causes Inflammation,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes Inflammation supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,ISBN:0198506732 -15925719,Hydrocortisone affects Inflammation,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects Inflammation supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,ISBN:0198506732 -10431364,Hydrocortisone affects Inflammation,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects Inflammation supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,ISBN:0198506732 -30369697,Sevoflurane treats brain injury,1417,"A fluorinated isopropyl ether with general anesthetic activity. Although the mechanism of action has not been fully elucidated, sevoflurane may interfere with the release and re-uptake of neurotransmitters at post-synaptic terminals, and/or alter ionic conductance following receptor activation by a neurotransmitter. This agent may also interact directly with the lipid matrix of neuronal membranes, thereby affecting gating properties of ion channels. In addition, sevoflurane may activate gamma-aminobutyric acid (GABA) receptors, hyperpolarizing cell membranes and resulting in a general anesthetic effect, a decrease in myocardial contractility and mean arterial pressure, and an increased respiratory rate. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C47717"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C47717"" NCI Thesaurus); A fluorinated isopropyl ether with general anesthetic property. Although the mechanism of action has not been fully elucidated, sevoflurane may act by interfering with the release and re-uptake of neurotransmitters at post-synaptic terminals, and/or alter ionic conductance following receptor activation by a neurotransmitter. Sevoflurane may also interact directly with lipid matrix of neuronal membranes, thereby affecting gating properties of ion channels. In addition, this agent may activate gamma-aminobutyric acid (GABA) receptors hyperpolarizing cell membranes. This results in a general anesthetic effect, a decrease in myocardial contractility and mean arterial pressure as well as an increased respiratory rate.; A non-explosive inhalation anesthetic used in the induction and maintenance of general anesthesia. It does not cause respiratory irritation and may also prevent PLATELET AGGREGATION.","Is the triple Sevoflurane treats brain injury supported by the sentence A fluorinated isopropyl ether with general anesthetic activity. Although the mechanism of action has not been fully elucidated, sevoflurane may interfere with the release and re-uptake of neurotransmitters at post-synaptic terminals, and/or alter ionic conductance following receptor activation by a neurotransmitter. This agent may also interact directly with the lipid matrix of neuronal membranes, thereby affecting gating properties of ion channels. In addition, sevoflurane may activate gamma-aminobutyric acid (GABA) receptors, hyperpolarizing cell membranes and resulting in a general anesthetic effect, a decrease in myocardial contractility and mean arterial pressure, and an increased respiratory rate. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C47717"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C47717"" NCI Thesaurus); A fluorinated isopropyl ether with general anesthetic property. Although the mechanism of action has not been fully elucidated, sevoflurane may act by interfering with the release and re-uptake of neurotransmitters at post-synaptic terminals, and/or alter ionic conductance following receptor activation by a neurotransmitter. Sevoflurane may also interact directly with lipid matrix of neuronal membranes, thereby affecting gating properties of ion channels. In addition, this agent may activate gamma-aminobutyric acid (GABA) receptors hyperpolarizing cell membranes. This results in a general anesthetic effect, a decrease in myocardial contractility and mean arterial pressure as well as an increased respiratory rate.; A non-explosive inhalation anesthetic used in the induction and maintenance of general anesthesia. It does not cause respiratory irritation and may also prevent PLATELET AGGREGATION.",False, -18924640,Hydrocortisone produces Inflammation,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces Inflammation supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,ISBN:0198506732 -30362098,Sevoflurane treats delirium,1417,"A fluorinated isopropyl ether with general anesthetic activity. Although the mechanism of action has not been fully elucidated, sevoflurane may interfere with the release and re-uptake of neurotransmitters at post-synaptic terminals, and/or alter ionic conductance following receptor activation by a neurotransmitter. This agent may also interact directly with the lipid matrix of neuronal membranes, thereby affecting gating properties of ion channels. In addition, sevoflurane may activate gamma-aminobutyric acid (GABA) receptors, hyperpolarizing cell membranes and resulting in a general anesthetic effect, a decrease in myocardial contractility and mean arterial pressure, and an increased respiratory rate. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C47717"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C47717"" NCI Thesaurus); A fluorinated isopropyl ether with general anesthetic property. Although the mechanism of action has not been fully elucidated, sevoflurane may act by interfering with the release and re-uptake of neurotransmitters at post-synaptic terminals, and/or alter ionic conductance following receptor activation by a neurotransmitter. Sevoflurane may also interact directly with lipid matrix of neuronal membranes, thereby affecting gating properties of ion channels. In addition, this agent may activate gamma-aminobutyric acid (GABA) receptors hyperpolarizing cell membranes. This results in a general anesthetic effect, a decrease in myocardial contractility and mean arterial pressure as well as an increased respiratory rate.; A non-explosive inhalation anesthetic used in the induction and maintenance of general anesthesia. It does not cause respiratory irritation and may also prevent PLATELET AGGREGATION.","Is the triple Sevoflurane treats delirium supported by the sentence A fluorinated isopropyl ether with general anesthetic activity. Although the mechanism of action has not been fully elucidated, sevoflurane may interfere with the release and re-uptake of neurotransmitters at post-synaptic terminals, and/or alter ionic conductance following receptor activation by a neurotransmitter. This agent may also interact directly with the lipid matrix of neuronal membranes, thereby affecting gating properties of ion channels. In addition, sevoflurane may activate gamma-aminobutyric acid (GABA) receptors, hyperpolarizing cell membranes and resulting in a general anesthetic effect, a decrease in myocardial contractility and mean arterial pressure, and an increased respiratory rate. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C47717"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C47717"" NCI Thesaurus); A fluorinated isopropyl ether with general anesthetic property. Although the mechanism of action has not been fully elucidated, sevoflurane may act by interfering with the release and re-uptake of neurotransmitters at post-synaptic terminals, and/or alter ionic conductance following receptor activation by a neurotransmitter. Sevoflurane may also interact directly with lipid matrix of neuronal membranes, thereby affecting gating properties of ion channels. In addition, this agent may activate gamma-aminobutyric acid (GABA) receptors hyperpolarizing cell membranes. This results in a general anesthetic effect, a decrease in myocardial contractility and mean arterial pressure as well as an increased respiratory rate.; A non-explosive inhalation anesthetic used in the induction and maintenance of general anesthesia. It does not cause respiratory irritation and may also prevent PLATELET AGGREGATION.",False,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=delirium -15550113,Hydrocortisone prevents Inflammation,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone prevents Inflammation supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,ISBN:0198506732 -11782928,Hydrocortisone predisposes Inflammation,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone predisposes Inflammation supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,ISBN:0198506732 -9238280,Hydrocortisone related to Sepsis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to Sepsis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -27747115,Hydrocortisone causes Sepsis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes Sepsis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -24701128,Hydrocortisone affects Sepsis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects Sepsis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -30358697,Heroin treats heroin dependence,1427,"Heroin, also known as diacetylmorphine or diagesil, belongs to the class of organic compounds known as morphinans. These are polycyclic compounds with a four-ring skeleton with three condensed six-member rings forming a partially hydrogenated phenanthrene moiety, one of which is aromatic while the two others are alicyclic. Heroin is a drug which is used in the treatment of acute pain, myocardial infarction, acute pulmonary oedema, and chronic pain. Heroin exists as a solid and is considered to be practically insoluble (in water) and relatively neutral. Heroin can be biosynthesized from morphine. Heroin is a potentially toxic compound.","Is the triple Heroin treats heroin dependence supported by the sentence Heroin, also known as diacetylmorphine or diagesil, belongs to the class of organic compounds known as morphinans. These are polycyclic compounds with a four-ring skeleton with three condensed six-member rings forming a partially hydrogenated phenanthrene moiety, one of which is aromatic while the two others are alicyclic. Heroin is a drug which is used in the treatment of acute pain, myocardial infarction, acute pulmonary oedema, and chronic pain. Heroin exists as a solid and is considered to be practically insoluble (in water) and relatively neutral. Heroin can be biosynthesized from morphine. Heroin is a potentially toxic compound.",False,PMID:28790493 -12147996,Hydrocortisone produces Sepsis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces Sepsis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -17956690,Hydrocortisone prevents Sepsis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone prevents Sepsis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -14643692,Hydrocortisone exacerbates Sepsis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone exacerbates Sepsis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -19755964,Hydrocortisone predisposes Sepsis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone predisposes Sepsis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -12756660,Hydrocortisone related to borderline personality disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to borderline personality disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/borderline_personality_disorde -8054429,Hydrocortisone treats borderline personality disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats borderline personality disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/borderline_personality_disorde -9718673,Hydrocortisone related to atopic eczema,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to atopic eczema supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/atopic_dermatitis -27073884,Hydrocortisone causes atopic eczema,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes atopic eczema supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/atopic_dermatitis -17910566,Hydrocortisone affects atopic eczema,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects atopic eczema supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/atopic_dermatitis -10221382,Hydrocortisone treats atopic eczema,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats atopic eczema supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/atopic_dermatitis -18705900,Hydrocortisone related to phobic disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to phobic disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/anxiety_disorde -22345112,Hydrocortisone treats oral submucous fibrosis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats oral submucous fibrosis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://en.wikipedia.org/wiki/oral_submucous_fibrosis -15213238,Hydrocortisone treats herpes labialis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats herpes labialis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True, -8570630,Hydrocortisone related to fibromyalgia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to fibromyalgia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,PMID:33024295 -25383174,Hydrocortisone causes fibromyalgia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes fibromyalgia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,PMID:33024295 -20137862,Hydrocortisone affects fibromyalgia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects fibromyalgia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,PMID:33024295 -7402054,Hydrocortisone treats fibromyalgia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats fibromyalgia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,PMID:33024295 -9492934,Hydrocortisone related to opiate dependence,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to opiate dependence supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/opiate_dependency -25205462,Hydrocortisone causes hypotensive disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes hypotensive disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -14533429,Hydrocortisone affects hypotensive disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects hypotensive disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -13180935,Hydrocortisone affects hypotensive disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects hypotensive disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -9459897,Hydrocortisone treats hypotensive disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats hypotensive disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -12533519,Hydrocortisone related to Insulin resistance,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to Insulin resistance supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -8017438,Hydrocortisone related to Insulin resistance,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to Insulin resistance supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -7929803,Hydrocortisone causes Insulin resistance,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes Insulin resistance supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -14970164,Hydrocortisone affects Insulin resistance,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects Insulin resistance supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -7974249,Hydrocortisone affects Insulin resistance,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects Insulin resistance supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -13691671,Hydrocortisone treats Insulin resistance,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats Insulin resistance supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -14100936,Hydrocortisone produces Insulin resistance,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces Insulin resistance supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -12187318,Hydrocortisone prevents Insulin resistance,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone prevents Insulin resistance supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -8002300,Hydrocortisone predisposes Insulin resistance,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone predisposes Insulin resistance supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -27027571,Hydrocortisone related to HIV infectious disease,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to HIV infectious disease supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/hiv -10074536,Hydrocortisone affects HIV infectious disease,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects HIV infectious disease supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/hiv -13951019,Hydrocortisone treats HIV infectious disease,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats HIV infectious disease supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/hiv -27426083,Hydrocortisone produces HIV infectious disease,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces HIV infectious disease supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/hiv -10280121,Hydrocortisone treats melanoma,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats melanoma supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/melanoma -26128287,Hydrocortisone disrupts melanoma,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone disrupts melanoma supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/melanoma -10484611,Hydrocortisone related to ulcerative colitis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to ulcerative colitis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://meshb.nlm.nih.gov/record/ui?ui=d003093 -10518308,Hydrocortisone treats ulcerative colitis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats ulcerative colitis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://meshb.nlm.nih.gov/record/ui?ui=d003093 -11442939,Hydrocortisone related to prostate cancer,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to prostate cancer supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.cancer.gov/dictionary?cdrid=445079 -9665107,Hydrocortisone treats prostate cancer,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats prostate cancer supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.cancer.gov/dictionary?cdrid=445079 -8328567,Hydrocortisone produces prostate cancer,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces prostate cancer supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.cancer.gov/dictionary?cdrid=445079 -10649902,Hydrocortisone related to myocardial infarction,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to myocardial infarction supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -26840479,Hydrocortisone affects myocardial infarction,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects myocardial infarction supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -12881395,Hydrocortisone treats myocardial infarction,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats myocardial infarction supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -30376926,Empagliflozin treats myocardial infarction,1500,"An orally available competitive inhibitor of sodium-glucose co-transporter 2 (SGLT2; SLC5A2) with antihyperglycemic activity. Upon oral administration, empagliflozin selectively and potently inhibits SGLT2 in the kidneys, thereby suppressing the reabsorption of glucose in the proximal tubule. Inhibition of SGLT2 increases urinary glucose excretion by the kidneys, resulting in a reduction of plasma glucose levels in an insulin-independent manner. Inhibition of SGLT2 in the kidneys also suppresses the renal reabsorption of 1,5-anhydroglucitol (1,5AG). This lowers serum 1,5AG and neutrophil 1,5-anhydroglucitol-6-phosphate (1,5AG6P) levels, which may improve neutropenia and neutrophil dysfunction in patients with glycogen storage disease type Ib (GSD Ib). SGLT2, a transport protein exclusively expressed in the proximal renal tubules, mediates approximately 90% of renal glucose reabsorption from tubular fluid.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Empagliflozin treats myocardial infarction supported by the sentence An orally available competitive inhibitor of sodium-glucose co-transporter 2 (SGLT2; SLC5A2) with antihyperglycemic activity. Upon oral administration, empagliflozin selectively and potently inhibits SGLT2 in the kidneys, thereby suppressing the reabsorption of glucose in the proximal tubule. Inhibition of SGLT2 increases urinary glucose excretion by the kidneys, resulting in a reduction of plasma glucose levels in an insulin-independent manner. Inhibition of SGLT2 in the kidneys also suppresses the renal reabsorption of 1,5-anhydroglucitol (1,5AG). This lowers serum 1,5AG and neutrophil 1,5-anhydroglucitol-6-phosphate (1,5AG6P) levels, which may improve neutropenia and neutrophil dysfunction in patients with glycogen storage disease type Ib (GSD Ib). SGLT2, a transport protein exclusively expressed in the proximal renal tubules, mediates approximately 90% of renal glucose reabsorption from tubular fluid.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-0736-9199 -18495054,Hydrocortisone affects lymphoma,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects lymphoma supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -21368080,Hydrocortisone treats lymphoma,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats lymphoma supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -18495053,Hydrocortisone affects leukemia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects leukemia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/leukemia -23769275,Hydrocortisone treats leukemia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats leukemia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/leukemia -26428860,Hydrocortisone disrupts leukemia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone disrupts leukemia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/leukemia -13844584,Hydrocortisone related to acute myeloid leukemia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to acute myeloid leukemia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.cancer.gov/dictionary?cdrid=44363 -10480635,Hydrocortisone treats atopic conjunctivitis,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats atopic conjunctivitis supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/allergic_conjunctivitis -11530989,Hydrocortisone related to pneumonia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to pneumonia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/pneumonia -19555227,Hydrocortisone affects pneumonia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects pneumonia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/pneumonia -9971730,Hydrocortisone treats pneumonia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats pneumonia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/pneumonia -11730055,Hydrocortisone produces pneumonia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces pneumonia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/pneumonia -21020907,Hydrocortisone disrupts pneumonia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone disrupts pneumonia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/pneumonia -15540854,Hydrocortisone prevents pneumonia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone prevents pneumonia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/pneumonia -7960726,Hydrocortisone predisposes pneumonia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone predisposes pneumonia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/pneumonia -7182905,Hydrocortisone related to obesity disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to obesity disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://en.wikipedia.org/wiki/obesity -12645476,Hydrocortisone causes obesity disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes obesity disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://en.wikipedia.org/wiki/obesity -11304252,Hydrocortisone affects obesity disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects obesity disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://en.wikipedia.org/wiki/obesity -8017440,Hydrocortisone affects obesity disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects obesity disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://en.wikipedia.org/wiki/obesity -8412499,Hydrocortisone treats obesity disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats obesity disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://en.wikipedia.org/wiki/obesity -45032471,Celecoxib treats osteoarthritis,1540,"Celecoxib (INN) is a non-steroidal anti-inflammatory drug (NSAID) used in the treatment of osteoarthritis, rheumatoid arthritis, acute pain, painful menstruation and menstrual symptoms, and to reduce numbers of colon and rectum polyps in patients with familial adenomatous polyposis. It is marketed by Pfizer under the brand name Celebrex. In some countries, it is branded Celebra. Celecoxib is a non-steroidal anti-inflammatory drug (NSAID) used in the treatment of osteoarthritis, rheumatoid arthritis, acute pain, painful menstruation and menstrual symptoms, and to reduce numbers of colon and rectum polyps in patients with familial adenomatous polyposis. Celecoxib is a highly selective COX-2 inhibitor and primarily inhibits this isoform of cyclooxygenase, whereas traditional NSAIDs inhibit both COX-1 and COX-2. Celecoxib is approximately 10-20 times more selective for COX-2 inhibition over COX-1. In theory, this specificity allows celecoxib and other COX-2 inhibitors to reduce inflammation (and pain) while minimizing gastrointestinal adverse drug reactions (e.g. stomach ulcers) that are common with non-selective NSAIDs. It also means that it has a reduced effect on platelet aggregation compared to traditional NSAIDs; Celecoxib is a highly selective COX-2 inhibitor and primarily inhibits this isoform of cyclooxygenase, whereas traditional NSAIDs inhibit both COX-1 and COX-2. Celecoxib is approximately 10-20 times more selective for COX-2 inhibition over COX-1. In theory, this specificity allows celecoxib and other COX-2 inhibitors to reduce inflammation (and pain) while minimizing gastrointestinal adverse drug reactions (e.g. stomach ulcers) that are common with non-selective NSAIDs. It also means that it has a reduced effect on platelet aggregation compared to traditional NSAIDs.","Is the triple Celecoxib treats osteoarthritis supported by the sentence Celecoxib (INN) is a non-steroidal anti-inflammatory drug (NSAID) used in the treatment of osteoarthritis, rheumatoid arthritis, acute pain, painful menstruation and menstrual symptoms, and to reduce numbers of colon and rectum polyps in patients with familial adenomatous polyposis. It is marketed by Pfizer under the brand name Celebrex. In some countries, it is branded Celebra. Celecoxib is a non-steroidal anti-inflammatory drug (NSAID) used in the treatment of osteoarthritis, rheumatoid arthritis, acute pain, painful menstruation and menstrual symptoms, and to reduce numbers of colon and rectum polyps in patients with familial adenomatous polyposis. Celecoxib is a highly selective COX-2 inhibitor and primarily inhibits this isoform of cyclooxygenase, whereas traditional NSAIDs inhibit both COX-1 and COX-2. Celecoxib is approximately 10-20 times more selective for COX-2 inhibition over COX-1. In theory, this specificity allows celecoxib and other COX-2 inhibitors to reduce inflammation (and pain) while minimizing gastrointestinal adverse drug reactions (e.g. stomach ulcers) that are common with non-selective NSAIDs. It also means that it has a reduced effect on platelet aggregation compared to traditional NSAIDs; Celecoxib is a highly selective COX-2 inhibitor and primarily inhibits this isoform of cyclooxygenase, whereas traditional NSAIDs inhibit both COX-1 and COX-2. Celecoxib is approximately 10-20 times more selective for COX-2 inhibition over COX-1. In theory, this specificity allows celecoxib and other COX-2 inhibitors to reduce inflammation (and pain) while minimizing gastrointestinal adverse drug reactions (e.g. stomach ulcers) that are common with non-selective NSAIDs. It also means that it has a reduced effect on platelet aggregation compared to traditional NSAIDs.",False,http://www.mayoclinic.com/health/osteoarthritis/ds00019 -15895489,Hydrocortisone disrupts obesity disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone disrupts obesity disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://en.wikipedia.org/wiki/obesity -19342068,Hydrocortisone prevents obesity disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone prevents obesity disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://en.wikipedia.org/wiki/obesity -8122784,Hydrocortisone exacerbates obesity disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone exacerbates obesity disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://en.wikipedia.org/wiki/obesity -10520517,Hydrocortisone predisposes obesity disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone predisposes obesity disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://en.wikipedia.org/wiki/obesity -14075841,Hydrocortisone treats acute lymphoblastic leukemia,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats acute lymphoblastic leukemia supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://www.cancer.gov/dictionary?cdrid=46332 -14387016,Hydrocortisone related to cirrhosis of liver,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to cirrhosis of liver supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -14532907,Hydrocortisone treats cirrhosis of liver,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats cirrhosis of liver supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -24427531,Hydrocortisone produces cirrhosis of liver,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces cirrhosis of liver supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,https://orcid.org/0000-0002-0736-9199 -8977987,Hydrocortisone related to injury,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to injury supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True, -18240145,Hydrocortisone causes injury,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes injury supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True, -14804311,Hydrocortisone affects injury,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects injury supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True, -10523644,Hydrocortisone affects injury,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects injury supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True, -11965490,Hydrocortisone treats injury,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats injury supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True, -15750557,Hydrocortisone disrupts injury,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone disrupts injury supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True, -18758297,Hydrocortisone prevents injury,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone prevents injury supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True, -13712588,Hydrocortisone predisposes injury,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone predisposes injury supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True, -22282269,Hydrocortisone treats Infection,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats Infection supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True, -30643591,Ropinirole treats Parkinson disease,1569,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ropinirole, also known as _ReQuip_, is a non-ergoline dopamine agonist used in Parkinson's disease and restless legs syndrome [FDA label], [A174547]. It is manufactured by GlaxoSmithKline Pharmaceuticals. Ropinirole was initially approved in 1997 by the FDA [FDA label] for the management of Parkinson's disease. In 2005, it was the first drug approved in the US for the management of primary moderate to severe restless legs syndrome [A174547]. In 2008, the extended-release capsules of ropinirole were approved, allowing for less frequent dosing, therefore increased compliance, and offering a similar side effect profile and efficacy to previous formulations of ropinirole [A35711].","Is the triple Ropinirole treats Parkinson disease supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ropinirole, also known as _ReQuip_, is a non-ergoline dopamine agonist used in Parkinson's disease and restless legs syndrome [FDA label], [A174547]. It is manufactured by GlaxoSmithKline Pharmaceuticals. Ropinirole was initially approved in 1997 by the FDA [FDA label] for the management of Parkinson's disease. In 2005, it was the first drug approved in the US for the management of primary moderate to severe restless legs syndrome [A174547]. In 2008, the extended-release capsules of ropinirole were approved, allowing for less frequent dosing, therefore increased compliance, and offering a similar side effect profile and efficacy to previous formulations of ropinirole [A35711].",False,http://en.wikipedia.org/wiki/parkinson%27s_disease -11029944,Hydrocortisone treats eye disorder,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats eye disorder supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/eye_disease -8763179,Hydrocortisone related to toxic shock syndrome,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone related to toxic shock syndrome supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/toxic_shock_syndrome -27747116,Hydrocortisone causes toxic shock syndrome,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone causes toxic shock syndrome supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/toxic_shock_syndrome -18310128,Hydrocortisone affects toxic shock syndrome,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects toxic shock syndrome supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/toxic_shock_syndrome -9872405,Hydrocortisone affects toxic shock syndrome,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone affects toxic shock syndrome supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/toxic_shock_syndrome -7996696,Hydrocortisone treats toxic shock syndrome,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats toxic shock syndrome supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/toxic_shock_syndrome -15760263,Hydrocortisone produces toxic shock syndrome,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone produces toxic shock syndrome supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/toxic_shock_syndrome -19245686,Hydrocortisone prevents toxic shock syndrome,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone prevents toxic shock syndrome supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/toxic_shock_syndrome -12555774,Hydrocortisone predisposes toxic shock syndrome,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone predisposes toxic shock syndrome supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/toxic_shock_syndrome -10516843,Hydrocortisone treats diffuse alopecia areata,569,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.","Is the triple Hydrocortisone treats diffuse alopecia areata supported by the sentence Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",True,http://en.wikipedia.org/wiki/alopecia_areata -30384729,Apomorphine treats Parkinson disease,1577,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Apomorphine is a non-ergoline dopamine D2 agonist indicated to treat hypomobility associated with Parkinson's. It was first synthesized in 1845 and first used in Parkinson's disease in 1884.[A203618] Apomorphine has also been investigated as an emetic, a sedative, a treatment for alcoholism, and a treatment of other movement disorders.[A203597,A203618] Apomorphine was granted FDA approval on 20 April 2004.[L13919]","Is the triple Apomorphine treats Parkinson disease supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Apomorphine is a non-ergoline dopamine D2 agonist indicated to treat hypomobility associated with Parkinson's. It was first synthesized in 1845 and first used in Parkinson's disease in 1884.[A203618] Apomorphine has also been investigated as an emetic, a sedative, a treatment for alcoholism, and a treatment of other movement disorders.[A203597,A203618] Apomorphine was granted FDA approval on 20 April 2004.[L13919]",False,http://en.wikipedia.org/wiki/parkinson%27s_disease -11547088,Methylprednisolone treats thrombotic thrombocytopenic purpura,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats thrombotic thrombocytopenic purpura supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True, -27127545,Methylprednisolone treats lymphoproliferative syndrome,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats lymphoproliferative syndrome supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,PMID:22197273 -9744990,Methylprednisolone prevents ovarian hyperstimulation syndrome,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone prevents ovarian hyperstimulation syndrome supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://www.ncbi.nlm.nih.gov/pmc/articles/pmc3205536/ -7668599,Methylprednisolone related to multiple sclerosis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to multiple sclerosis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://ghr.nlm.nih.gov/condition/multiple-sclerosis -9646753,Methylprednisolone affects multiple sclerosis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone affects multiple sclerosis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://ghr.nlm.nih.gov/condition/multiple-sclerosis -7668594,Methylprednisolone treats multiple sclerosis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats multiple sclerosis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://ghr.nlm.nih.gov/condition/multiple-sclerosis -30644044,Pramipexole treats restless legs syndrome,1580,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Pramipexole is a drug used to treat the symptoms of Parkinson's Disease (PD). It is a _non-ergot dopamine agonist_ drug that is efficacious in treating various Parkinson's symptoms such as tremor, rigidity, and bradykinesia (slow movement) [A176867]. It was first approved by the FDA in 1997 [L5882]. Parkinson's Disease is one of the most common neurodegenerative disorders and causes a high level of disability in patients [A176855], leading to increased difficulty in performing activities of daily living due to symptoms that progress over time [A176858]. The prevalence of Parkinson's Disease worldwide has increased from approximately 2.5 million in 1990 to about 6.1 million in 2016 [A176861]. This increase may be attributed to an aging population along with other contributing factors [A176861]. In addition to the above FDA approval for Parkinson's Disease, pramipexole was also approved by the FDA in 2006 for the treatment of Restless Legs Syndrome (RLS) [A176873]. RLS is a sleep-related disorder characterized by unpleasant sensations in the lower extremities, often accompanied by an uncontrollable urge to move the legs [A176876].","Is the triple Pramipexole treats restless legs syndrome supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Pramipexole is a drug used to treat the symptoms of Parkinson's Disease (PD). It is a _non-ergot dopamine agonist_ drug that is efficacious in treating various Parkinson's symptoms such as tremor, rigidity, and bradykinesia (slow movement) [A176867]. It was first approved by the FDA in 1997 [L5882]. Parkinson's Disease is one of the most common neurodegenerative disorders and causes a high level of disability in patients [A176855], leading to increased difficulty in performing activities of daily living due to symptoms that progress over time [A176858]. The prevalence of Parkinson's Disease worldwide has increased from approximately 2.5 million in 1990 to about 6.1 million in 2016 [A176861]. This increase may be attributed to an aging population along with other contributing factors [A176861]. In addition to the above FDA approval for Parkinson's Disease, pramipexole was also approved by the FDA in 2006 for the treatment of Restless Legs Syndrome (RLS) [A176873]. RLS is a sleep-related disorder characterized by unpleasant sensations in the lower extremities, often accompanied by an uncontrollable urge to move the legs [A176876].",False,http://www.ninds.nih.gov/disorders/restless_legs/detail_restless_legs.htm -18427985,Methylprednisolone treats osteoarthritis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats osteoarthritis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.mayoclinic.com/health/osteoarthritis/ds00019 -30353224,Pramipexole treats obsessive-compulsive disorder,1580,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Pramipexole is a drug used to treat the symptoms of Parkinson's Disease (PD). It is a _non-ergot dopamine agonist_ drug that is efficacious in treating various Parkinson's symptoms such as tremor, rigidity, and bradykinesia (slow movement) [A176867]. It was first approved by the FDA in 1997 [L5882]. Parkinson's Disease is one of the most common neurodegenerative disorders and causes a high level of disability in patients [A176855], leading to increased difficulty in performing activities of daily living due to symptoms that progress over time [A176858]. The prevalence of Parkinson's Disease worldwide has increased from approximately 2.5 million in 1990 to about 6.1 million in 2016 [A176861]. This increase may be attributed to an aging population along with other contributing factors [A176861]. In addition to the above FDA approval for Parkinson's Disease, pramipexole was also approved by the FDA in 2006 for the treatment of Restless Legs Syndrome (RLS) [A176873]. RLS is a sleep-related disorder characterized by unpleasant sensations in the lower extremities, often accompanied by an uncontrollable urge to move the legs [A176876].","Is the triple Pramipexole treats obsessive-compulsive disorder supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Pramipexole is a drug used to treat the symptoms of Parkinson's Disease (PD). It is a _non-ergot dopamine agonist_ drug that is efficacious in treating various Parkinson's symptoms such as tremor, rigidity, and bradykinesia (slow movement) [A176867]. It was first approved by the FDA in 1997 [L5882]. Parkinson's Disease is one of the most common neurodegenerative disorders and causes a high level of disability in patients [A176855], leading to increased difficulty in performing activities of daily living due to symptoms that progress over time [A176858]. The prevalence of Parkinson's Disease worldwide has increased from approximately 2.5 million in 1990 to about 6.1 million in 2016 [A176861]. This increase may be attributed to an aging population along with other contributing factors [A176861]. In addition to the above FDA approval for Parkinson's Disease, pramipexole was also approved by the FDA in 2006 for the treatment of Restless Legs Syndrome (RLS) [A176873]. RLS is a sleep-related disorder characterized by unpleasant sensations in the lower extremities, often accompanied by an uncontrollable urge to move the legs [A176876].",False,https://orcid.org/0000-0002-4422-1708 -30346915,Pramipexole treats restless legs syndrome,1580,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Pramipexole is a drug used to treat the symptoms of Parkinson's Disease (PD). It is a _non-ergot dopamine agonist_ drug that is efficacious in treating various Parkinson's symptoms such as tremor, rigidity, and bradykinesia (slow movement) [A176867]. It was first approved by the FDA in 1997 [L5882]. Parkinson's Disease is one of the most common neurodegenerative disorders and causes a high level of disability in patients [A176855], leading to increased difficulty in performing activities of daily living due to symptoms that progress over time [A176858]. The prevalence of Parkinson's Disease worldwide has increased from approximately 2.5 million in 1990 to about 6.1 million in 2016 [A176861]. This increase may be attributed to an aging population along with other contributing factors [A176861]. In addition to the above FDA approval for Parkinson's Disease, pramipexole was also approved by the FDA in 2006 for the treatment of Restless Legs Syndrome (RLS) [A176873]. RLS is a sleep-related disorder characterized by unpleasant sensations in the lower extremities, often accompanied by an uncontrollable urge to move the legs [A176876].","Is the triple Pramipexole treats restless legs syndrome supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Pramipexole is a drug used to treat the symptoms of Parkinson's Disease (PD). It is a _non-ergot dopamine agonist_ drug that is efficacious in treating various Parkinson's symptoms such as tremor, rigidity, and bradykinesia (slow movement) [A176867]. It was first approved by the FDA in 1997 [L5882]. Parkinson's Disease is one of the most common neurodegenerative disorders and causes a high level of disability in patients [A176855], leading to increased difficulty in performing activities of daily living due to symptoms that progress over time [A176858]. The prevalence of Parkinson's Disease worldwide has increased from approximately 2.5 million in 1990 to about 6.1 million in 2016 [A176861]. This increase may be attributed to an aging population along with other contributing factors [A176861]. In addition to the above FDA approval for Parkinson's Disease, pramipexole was also approved by the FDA in 2006 for the treatment of Restless Legs Syndrome (RLS) [A176873]. RLS is a sleep-related disorder characterized by unpleasant sensations in the lower extremities, often accompanied by an uncontrollable urge to move the legs [A176876].",False,http://www.ninds.nih.gov/disorders/restless_legs/detail_restless_legs.htm -8761529,Methylprednisolone treats asthma,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats asthma supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.nhlbi.nih.gov/health/dci/diseases/asthma/asthma_whatis.htm -45039471,Folic Acid treats homocystinuria,1619,"Folic acid or folate, is a vitamin that belongs to the class of compounds known as pterins. Chemically, folate consists of three distinct chemical moieties linked together. A pterin (2-amino-4-hydroxy-pteridine) linked by a methylene bridge to a p-aminobenzoyl group that in turn is linked through an amide linkage to glutamic acid. It is a member of the vitamin B family and is primarily known as vitamin B9. Folate is required for the body to make DNA and RNA and metabolize amino acids necessary for cell division for the hematopoietic system. As humans cannot make folate, it is required in the diet, making it an essential nutrient (i.e. a vitamin). Folate occurs naturally in many foods including mushrooms, spinach, yeast, green leaves, and grasses (poaceae). Folic acid, being biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by the enzyme known as dihydrofolate reductase. Tetrahydrofolate and methyltetrahydrofolate are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids and generate formic acid. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in babies. Low levels in early pregnancy are believed to be the cause of more than half of babies born with NTDs (PMID: 28097362). Folic acid is also a microbial metabolite produced by Bifidobacterium and Lactobacillus (PMID: 22254078).","Is the triple Folic Acid treats homocystinuria supported by the sentence Folic acid or folate, is a vitamin that belongs to the class of compounds known as pterins. Chemically, folate consists of three distinct chemical moieties linked together. A pterin (2-amino-4-hydroxy-pteridine) linked by a methylene bridge to a p-aminobenzoyl group that in turn is linked through an amide linkage to glutamic acid. It is a member of the vitamin B family and is primarily known as vitamin B9. Folate is required for the body to make DNA and RNA and metabolize amino acids necessary for cell division for the hematopoietic system. As humans cannot make folate, it is required in the diet, making it an essential nutrient (i.e. a vitamin). Folate occurs naturally in many foods including mushrooms, spinach, yeast, green leaves, and grasses (poaceae). Folic acid, being biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by the enzyme known as dihydrofolate reductase. Tetrahydrofolate and methyltetrahydrofolate are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids and generate formic acid. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in babies. Low levels in early pregnancy are believed to be the cause of more than half of babies born with NTDs (PMID: 28097362). Folic acid is also a microbial metabolite produced by Bifidobacterium and Lactobacillus (PMID: 22254078).",False,http://en.wikipedia.org/wiki/homocystinuria -13533673,Methylprednisolone treats macrophage activation syndrome,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats macrophage activation syndrome supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True, -45039464,Folic Acid treats Reduced blood folate concentration,1619,"Folic acid or folate, is a vitamin that belongs to the class of compounds known as pterins. Chemically, folate consists of three distinct chemical moieties linked together. A pterin (2-amino-4-hydroxy-pteridine) linked by a methylene bridge to a p-aminobenzoyl group that in turn is linked through an amide linkage to glutamic acid. It is a member of the vitamin B family and is primarily known as vitamin B9. Folate is required for the body to make DNA and RNA and metabolize amino acids necessary for cell division for the hematopoietic system. As humans cannot make folate, it is required in the diet, making it an essential nutrient (i.e. a vitamin). Folate occurs naturally in many foods including mushrooms, spinach, yeast, green leaves, and grasses (poaceae). Folic acid, being biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by the enzyme known as dihydrofolate reductase. Tetrahydrofolate and methyltetrahydrofolate are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids and generate formic acid. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in babies. Low levels in early pregnancy are believed to be the cause of more than half of babies born with NTDs (PMID: 28097362). Folic acid is also a microbial metabolite produced by Bifidobacterium and Lactobacillus (PMID: 22254078).","Is the triple Folic Acid treats Reduced blood folate concentration supported by the sentence Folic acid or folate, is a vitamin that belongs to the class of compounds known as pterins. Chemically, folate consists of three distinct chemical moieties linked together. A pterin (2-amino-4-hydroxy-pteridine) linked by a methylene bridge to a p-aminobenzoyl group that in turn is linked through an amide linkage to glutamic acid. It is a member of the vitamin B family and is primarily known as vitamin B9. Folate is required for the body to make DNA and RNA and metabolize amino acids necessary for cell division for the hematopoietic system. As humans cannot make folate, it is required in the diet, making it an essential nutrient (i.e. a vitamin). Folate occurs naturally in many foods including mushrooms, spinach, yeast, green leaves, and grasses (poaceae). Folic acid, being biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by the enzyme known as dihydrofolate reductase. Tetrahydrofolate and methyltetrahydrofolate are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids and generate formic acid. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in babies. Low levels in early pregnancy are believed to be the cause of more than half of babies born with NTDs (PMID: 28097362). Folic acid is also a microbial metabolite produced by Bifidobacterium and Lactobacillus (PMID: 22254078).",False,https://orcid.org/0000-0002-0736-9199 -22495912,Methylprednisolone treats myocarditis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats myocarditis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/myocarditis -30651803,Folic Acid treats Inflammation,1619,"Folic acid or folate, is a vitamin that belongs to the class of compounds known as pterins. Chemically, folate consists of three distinct chemical moieties linked together. A pterin (2-amino-4-hydroxy-pteridine) linked by a methylene bridge to a p-aminobenzoyl group that in turn is linked through an amide linkage to glutamic acid. It is a member of the vitamin B family and is primarily known as vitamin B9. Folate is required for the body to make DNA and RNA and metabolize amino acids necessary for cell division for the hematopoietic system. As humans cannot make folate, it is required in the diet, making it an essential nutrient (i.e. a vitamin). Folate occurs naturally in many foods including mushrooms, spinach, yeast, green leaves, and grasses (poaceae). Folic acid, being biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by the enzyme known as dihydrofolate reductase. Tetrahydrofolate and methyltetrahydrofolate are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids and generate formic acid. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in babies. Low levels in early pregnancy are believed to be the cause of more than half of babies born with NTDs (PMID: 28097362). Folic acid is also a microbial metabolite produced by Bifidobacterium and Lactobacillus (PMID: 22254078).","Is the triple Folic Acid treats Inflammation supported by the sentence Folic acid or folate, is a vitamin that belongs to the class of compounds known as pterins. Chemically, folate consists of three distinct chemical moieties linked together. A pterin (2-amino-4-hydroxy-pteridine) linked by a methylene bridge to a p-aminobenzoyl group that in turn is linked through an amide linkage to glutamic acid. It is a member of the vitamin B family and is primarily known as vitamin B9. Folate is required for the body to make DNA and RNA and metabolize amino acids necessary for cell division for the hematopoietic system. As humans cannot make folate, it is required in the diet, making it an essential nutrient (i.e. a vitamin). Folate occurs naturally in many foods including mushrooms, spinach, yeast, green leaves, and grasses (poaceae). Folic acid, being biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by the enzyme known as dihydrofolate reductase. Tetrahydrofolate and methyltetrahydrofolate are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids and generate formic acid. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in babies. Low levels in early pregnancy are believed to be the cause of more than half of babies born with NTDs (PMID: 28097362). Folic acid is also a microbial metabolite produced by Bifidobacterium and Lactobacillus (PMID: 22254078).",False,ISBN:0198506732 -14825096,Methylprednisolone treats West syndrome,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats West syndrome supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,PMID:28276060 -19962298,Methylprednisolone treats Hodgkins lymphoma,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats Hodgkins lymphoma supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://en.wikipedia.org/wiki/hodgkin%27s_lymphoma -8227578,Methylprednisolone treats mucocutaneous lymph node syndrome,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats mucocutaneous lymph node syndrome supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/kawasaki_disease -24273559,Methylprednisolone treats Abdominal pain,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats Abdominal pain supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-0736-9199 -30382356,Folic Acid treats Alzheimer disease,1619,"Folic acid or folate, is a vitamin that belongs to the class of compounds known as pterins. Chemically, folate consists of three distinct chemical moieties linked together. A pterin (2-amino-4-hydroxy-pteridine) linked by a methylene bridge to a p-aminobenzoyl group that in turn is linked through an amide linkage to glutamic acid. It is a member of the vitamin B family and is primarily known as vitamin B9. Folate is required for the body to make DNA and RNA and metabolize amino acids necessary for cell division for the hematopoietic system. As humans cannot make folate, it is required in the diet, making it an essential nutrient (i.e. a vitamin). Folate occurs naturally in many foods including mushrooms, spinach, yeast, green leaves, and grasses (poaceae). Folic acid, being biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by the enzyme known as dihydrofolate reductase. Tetrahydrofolate and methyltetrahydrofolate are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids and generate formic acid. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in babies. Low levels in early pregnancy are believed to be the cause of more than half of babies born with NTDs (PMID: 28097362). Folic acid is also a microbial metabolite produced by Bifidobacterium and Lactobacillus (PMID: 22254078).","Is the triple Folic Acid treats Alzheimer disease supported by the sentence Folic acid or folate, is a vitamin that belongs to the class of compounds known as pterins. Chemically, folate consists of three distinct chemical moieties linked together. A pterin (2-amino-4-hydroxy-pteridine) linked by a methylene bridge to a p-aminobenzoyl group that in turn is linked through an amide linkage to glutamic acid. It is a member of the vitamin B family and is primarily known as vitamin B9. Folate is required for the body to make DNA and RNA and metabolize amino acids necessary for cell division for the hematopoietic system. As humans cannot make folate, it is required in the diet, making it an essential nutrient (i.e. a vitamin). Folate occurs naturally in many foods including mushrooms, spinach, yeast, green leaves, and grasses (poaceae). Folic acid, being biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by the enzyme known as dihydrofolate reductase. Tetrahydrofolate and methyltetrahydrofolate are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids and generate formic acid. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in babies. Low levels in early pregnancy are believed to be the cause of more than half of babies born with NTDs (PMID: 28097362). Folic acid is also a microbial metabolite produced by Bifidobacterium and Lactobacillus (PMID: 22254078).",False,http://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-fact-sheet -13679356,Methylprednisolone treats hemophagocytic syndrome,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats hemophagocytic syndrome supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.scielo.br/scielo.php?script=sci_arttext&pid=s1516-31801997000500007&lng=pt&nrm=iso -25845844,Methylprednisolone related to breast neoplasm,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to breast neoplasm supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0001-5208-3432 -15407991,Methylprednisolone treats radiculopathy,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats radiculopathy supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://en.wikipedia.org/wiki/radiculopathy -17649050,Methylprednisolone affects optic nerve disorder,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone affects optic nerve disorder supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.nature.com/eye/journal/v18/n11/full/6701575a.htm -13096165,Methylprednisolone treats optic nerve disorder,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats optic nerve disorder supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.nature.com/eye/journal/v18/n11/full/6701575a.htm -23116362,Methylprednisolone treats pneumocystosis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats pneumocystosis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=pneumocystis%20carinii%20pneumonia -30352624,Folic Acid treats male infertility,1619,"Folic acid or folate, is a vitamin that belongs to the class of compounds known as pterins. Chemically, folate consists of three distinct chemical moieties linked together. A pterin (2-amino-4-hydroxy-pteridine) linked by a methylene bridge to a p-aminobenzoyl group that in turn is linked through an amide linkage to glutamic acid. It is a member of the vitamin B family and is primarily known as vitamin B9. Folate is required for the body to make DNA and RNA and metabolize amino acids necessary for cell division for the hematopoietic system. As humans cannot make folate, it is required in the diet, making it an essential nutrient (i.e. a vitamin). Folate occurs naturally in many foods including mushrooms, spinach, yeast, green leaves, and grasses (poaceae). Folic acid, being biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by the enzyme known as dihydrofolate reductase. Tetrahydrofolate and methyltetrahydrofolate are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids and generate formic acid. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in babies. Low levels in early pregnancy are believed to be the cause of more than half of babies born with NTDs (PMID: 28097362). Folic acid is also a microbial metabolite produced by Bifidobacterium and Lactobacillus (PMID: 22254078).","Is the triple Folic Acid treats male infertility supported by the sentence Folic acid or folate, is a vitamin that belongs to the class of compounds known as pterins. Chemically, folate consists of three distinct chemical moieties linked together. A pterin (2-amino-4-hydroxy-pteridine) linked by a methylene bridge to a p-aminobenzoyl group that in turn is linked through an amide linkage to glutamic acid. It is a member of the vitamin B family and is primarily known as vitamin B9. Folate is required for the body to make DNA and RNA and metabolize amino acids necessary for cell division for the hematopoietic system. As humans cannot make folate, it is required in the diet, making it an essential nutrient (i.e. a vitamin). Folate occurs naturally in many foods including mushrooms, spinach, yeast, green leaves, and grasses (poaceae). Folic acid, being biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by the enzyme known as dihydrofolate reductase. Tetrahydrofolate and methyltetrahydrofolate are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids and generate formic acid. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in babies. Low levels in early pregnancy are believed to be the cause of more than half of babies born with NTDs (PMID: 28097362). Folic acid is also a microbial metabolite produced by Bifidobacterium and Lactobacillus (PMID: 22254078).",False, -10341065,Methylprednisolone treats severe acute respiratory syndrome,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats severe acute respiratory syndrome supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/severe_acute_respiratory_syndrome -19340184,Methylprednisolone related to chronic obstructive pulmonary disease,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to chronic obstructive pulmonary disease supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://www.nhlbi.nih.gov/health-topics/copd -9346353,Methylprednisolone affects chronic obstructive pulmonary disease,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone affects chronic obstructive pulmonary disease supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://www.nhlbi.nih.gov/health-topics/copd -13619118,Methylprednisolone treats chronic obstructive pulmonary disease,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats chronic obstructive pulmonary disease supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://www.nhlbi.nih.gov/health-topics/copd -14166179,Methylprednisolone related to cardiac arrest,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to cardiac arrest supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.nlm.nih.gov/medlineplus/cardiacarrest.htm -23772707,Methylprednisolone treats cardiac arrest,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats cardiac arrest supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.nlm.nih.gov/medlineplus/cardiacarrest.htm -15072844,Methylprednisolone related to Edema,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to Edema supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-0736-9199 -24161886,Methylprednisolone causes Edema,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone causes Edema supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-0736-9199 -30345818,Folic Acid treats anemia,1619,"Folic acid or folate, is a vitamin that belongs to the class of compounds known as pterins. Chemically, folate consists of three distinct chemical moieties linked together. A pterin (2-amino-4-hydroxy-pteridine) linked by a methylene bridge to a p-aminobenzoyl group that in turn is linked through an amide linkage to glutamic acid. It is a member of the vitamin B family and is primarily known as vitamin B9. Folate is required for the body to make DNA and RNA and metabolize amino acids necessary for cell division for the hematopoietic system. As humans cannot make folate, it is required in the diet, making it an essential nutrient (i.e. a vitamin). Folate occurs naturally in many foods including mushrooms, spinach, yeast, green leaves, and grasses (poaceae). Folic acid, being biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by the enzyme known as dihydrofolate reductase. Tetrahydrofolate and methyltetrahydrofolate are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids and generate formic acid. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in babies. Low levels in early pregnancy are believed to be the cause of more than half of babies born with NTDs (PMID: 28097362). Folic acid is also a microbial metabolite produced by Bifidobacterium and Lactobacillus (PMID: 22254078).","Is the triple Folic Acid treats anemia supported by the sentence Folic acid or folate, is a vitamin that belongs to the class of compounds known as pterins. Chemically, folate consists of three distinct chemical moieties linked together. A pterin (2-amino-4-hydroxy-pteridine) linked by a methylene bridge to a p-aminobenzoyl group that in turn is linked through an amide linkage to glutamic acid. It is a member of the vitamin B family and is primarily known as vitamin B9. Folate is required for the body to make DNA and RNA and metabolize amino acids necessary for cell division for the hematopoietic system. As humans cannot make folate, it is required in the diet, making it an essential nutrient (i.e. a vitamin). Folate occurs naturally in many foods including mushrooms, spinach, yeast, green leaves, and grasses (poaceae). Folic acid, being biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by the enzyme known as dihydrofolate reductase. Tetrahydrofolate and methyltetrahydrofolate are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids and generate formic acid. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in babies. Low levels in early pregnancy are believed to be the cause of more than half of babies born with NTDs (PMID: 28097362). Folic acid is also a microbial metabolite produced by Bifidobacterium and Lactobacillus (PMID: 22254078).",False,http://www.nhlbi.nih.gov/health/health-topics/topics/anemia/ -7700869,Methylprednisolone treats Edema,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats Edema supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-0736-9199 -19744632,Methylprednisolone disrupts Edema,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone disrupts Edema supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-0736-9199 -7414405,Methylprednisolone prevents Edema,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone prevents Edema supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-0736-9199 -7944646,Methylprednisolone related to myasthenia gravis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to myasthenia gravis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://www.ninds.nih.gov/disorders/patient-caregiver-education/fact-sheets/myasthenia-gravis-fact-sheet -45044300,Methimazole treats thyroid crisis,1650,"A thioamide inhibitor of the enzyme thyroid peroxidase (TPO), with antithyroid activity. Upon administration, methimazole inhibits the metabolism of iodide and the iodination of tyrosine residues in the thyroid hormone precursor thyroglobulin by TPO; this prevents the synthesis of the thyroid hormones triiodothyronine (T3) and thyroxine (T4).; A thioureylene antithyroid agent that inhibits the formation of thyroid hormones by interfering with the incorporation of iodine into tyrosyl residues of thyroglobulin. This is done by interfering with the oxidation of iodide ion and iodotyrosyl groups through inhibition of the peroxidase enzyme.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Methimazole treats thyroid crisis supported by the sentence A thioamide inhibitor of the enzyme thyroid peroxidase (TPO), with antithyroid activity. Upon administration, methimazole inhibits the metabolism of iodide and the iodination of tyrosine residues in the thyroid hormone precursor thyroglobulin by TPO; this prevents the synthesis of the thyroid hormones triiodothyronine (T3) and thyroxine (T4).; A thioureylene antithyroid agent that inhibits the formation of thyroid hormones by interfering with the incorporation of iodine into tyrosyl residues of thyroglobulin. This is done by interfering with the oxidation of iodide ion and iodotyrosyl groups through inhibition of the peroxidase enzyme.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-6601-2165 -8568939,Methylprednisolone treats myasthenia gravis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats myasthenia gravis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://www.ninds.nih.gov/disorders/patient-caregiver-education/fact-sheets/myasthenia-gravis-fact-sheet -10221573,Methylprednisolone treats myeloproliferative neoplasm,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats myeloproliferative neoplasm supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.cancer.gov/cancertopics/types/myeloproliferative -22175056,Methylprednisolone related to myopathy,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to myopathy supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0001-5208-3432 -8525599,Methylprednisolone causes myopathy,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone causes myopathy supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0001-5208-3432 -45039675,Furosemide treats hypertensive disorder,1652,"An anthranilic derivative and loop diuretic with antihypertensive effect. Furosemide blocks the Na-K-Cl cotransporter (NKCC) in the luminal membrane of the thick ascending limb of the loop of Henle in the kidney, by binding to the Cl-binding site located in the cotransporter's transmembrane domain, thereby inhibiting reabsorption of sodium, chloride, potassium ions and water. This agent reduces plasma and extracellular fluid volume resulting in decreased blood pressure and cardiac output. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C515"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C515"" NCI Thesaurus); A sulfamoylanthranilic acid derivative, also known as frusemide, and potent loop diuretic. Furosemide is widely used to treat hypertension and edema. This agent is highly bound to albumin and is largely excreted unchanged in the urine.; A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Furosemide treats hypertensive disorder supported by the sentence An anthranilic derivative and loop diuretic with antihypertensive effect. Furosemide blocks the Na-K-Cl cotransporter (NKCC) in the luminal membrane of the thick ascending limb of the loop of Henle in the kidney, by binding to the Cl-binding site located in the cotransporter's transmembrane domain, thereby inhibiting reabsorption of sodium, chloride, potassium ions and water. This agent reduces plasma and extracellular fluid volume resulting in decreased blood pressure and cardiac output. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C515"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C515"" NCI Thesaurus); A sulfamoylanthranilic acid derivative, also known as frusemide, and potent loop diuretic. Furosemide is widely used to treat hypertension and edema. This agent is highly bound to albumin and is largely excreted unchanged in the urine.; A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,PMID:24352797 -20879022,Methylprednisolone related to Pain,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to Pain supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0001-5208-3432 -15906641,Methylprednisolone causes Pain,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone causes Pain supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0001-5208-3432 -15906642,Methylprednisolone affects Pain,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone affects Pain supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0001-5208-3432 -10845505,Methylprednisolone affects Pain,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone affects Pain supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0001-5208-3432 -8018847,Methylprednisolone treats Pain,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats Pain supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0001-5208-3432 -30362168,Furosemide treats Dyspnea,1652,"An anthranilic derivative and loop diuretic with antihypertensive effect. Furosemide blocks the Na-K-Cl cotransporter (NKCC) in the luminal membrane of the thick ascending limb of the loop of Henle in the kidney, by binding to the Cl-binding site located in the cotransporter's transmembrane domain, thereby inhibiting reabsorption of sodium, chloride, potassium ions and water. This agent reduces plasma and extracellular fluid volume resulting in decreased blood pressure and cardiac output. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C515"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C515"" NCI Thesaurus); A sulfamoylanthranilic acid derivative, also known as frusemide, and potent loop diuretic. Furosemide is widely used to treat hypertension and edema. This agent is highly bound to albumin and is largely excreted unchanged in the urine.; A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Furosemide treats Dyspnea supported by the sentence An anthranilic derivative and loop diuretic with antihypertensive effect. Furosemide blocks the Na-K-Cl cotransporter (NKCC) in the luminal membrane of the thick ascending limb of the loop of Henle in the kidney, by binding to the Cl-binding site located in the cotransporter's transmembrane domain, thereby inhibiting reabsorption of sodium, chloride, potassium ions and water. This agent reduces plasma and extracellular fluid volume resulting in decreased blood pressure and cardiac output. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C515"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C515"" NCI Thesaurus); A sulfamoylanthranilic acid derivative, also known as frusemide, and potent loop diuretic. Furosemide is widely used to treat hypertension and edema. This agent is highly bound to albumin and is largely excreted unchanged in the urine.; A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=dyspnea -8345063,Methylprednisolone prevents Pain,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone prevents Pain supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0001-5208-3432 -26307075,Methylprednisolone treats psoriatic arthritis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats psoriatic arthritis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/psoriatic_arthropathy -14278238,"Methylprednisolone related to dermatitis, atopic",570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to dermatitis, atopic supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,PMID:27904186 -10049014,"Methylprednisolone treats dermatitis, atopic",570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats dermatitis, atopic supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,PMID:27904186 -17333962,Methylprednisolone related to Inflammation,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to Inflammation supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,ISBN:0198506732 -18534953,Methylprednisolone causes Inflammation,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone causes Inflammation supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,ISBN:0198506732 -24420470,Methylprednisolone affects Inflammation,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone affects Inflammation supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,ISBN:0198506732 -45051722,Selegiline treats Parkinson disease,1657,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; A selective, irreversible inhibitor of Type B monoamine oxidase. It is used in newly diagnosed patients with Parkinson's disease. It may slow progression of the clinical disease and delay the requirement for levodopa therapy. It also may be given with levodopa upon onset of disability. (From AMA Drug Evaluations Annual, 1994, p385) The compound without isomeric designation is Deprenyl.","Is the triple Selegiline treats Parkinson disease supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; A selective, irreversible inhibitor of Type B monoamine oxidase. It is used in newly diagnosed patients with Parkinson's disease. It may slow progression of the clinical disease and delay the requirement for levodopa therapy. It also may be given with levodopa upon onset of disability. (From AMA Drug Evaluations Annual, 1994, p385) The compound without isomeric designation is Deprenyl.",False,http://en.wikipedia.org/wiki/parkinson%27s_disease -7552935,Methylprednisolone treats Inflammation,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats Inflammation supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,ISBN:0198506732 -8640603,Methylprednisolone disrupts Inflammation,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone disrupts Inflammation supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,ISBN:0198506732 -9645180,Methylprednisolone predisposes Inflammation,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone predisposes Inflammation supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,ISBN:0198506732 -10763477,Methylprednisolone related to ulcerative colitis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to ulcerative colitis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://meshb.nlm.nih.gov/record/ui?ui=d003093 -10048898,Methylprednisolone affects ulcerative colitis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone affects ulcerative colitis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://meshb.nlm.nih.gov/record/ui?ui=d003093 -8503951,Methylprednisolone treats ulcerative colitis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats ulcerative colitis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://meshb.nlm.nih.gov/record/ui?ui=d003093 -23573980,Methylprednisolone related to pneumonia,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to pneumonia supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/pneumonia -17307095,Methylprednisolone causes pneumonia,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone causes pneumonia supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/pneumonia -30643394,Torsemide treats Edema,1660,"An anilinopyridine sulfonylurea belonging to the class of loop diuretics. Torsemide has a prolonged duration of action compared to other loop diuretics, is extensively protein bound in plasma and has a relatively long half-life.; A pyridine and sulfonamide derivative that acts as a sodium-potassium chloride symporter inhibitor (loop diuretic). It is used for the treatment of EDEMA associated with CONGESTIVE HEART FAILURE; CHRONIC RENAL INSUFFICIENCY; and LIVER DISEASES. It is also used for the management of HYPERTENSION.","Is the triple Torsemide treats Edema supported by the sentence An anilinopyridine sulfonylurea belonging to the class of loop diuretics. Torsemide has a prolonged duration of action compared to other loop diuretics, is extensively protein bound in plasma and has a relatively long half-life.; A pyridine and sulfonamide derivative that acts as a sodium-potassium chloride symporter inhibitor (loop diuretic). It is used for the treatment of EDEMA associated with CONGESTIVE HEART FAILURE; CHRONIC RENAL INSUFFICIENCY; and LIVER DISEASES. It is also used for the management of HYPERTENSION.",False,https://orcid.org/0000-0002-0736-9199 -18106042,Methylprednisolone predisposes pneumonia,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone predisposes pneumonia supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/pneumonia -30360437,Torsemide treats hypertensive disorder,1660,"An anilinopyridine sulfonylurea belonging to the class of loop diuretics. Torsemide has a prolonged duration of action compared to other loop diuretics, is extensively protein bound in plasma and has a relatively long half-life.; A pyridine and sulfonamide derivative that acts as a sodium-potassium chloride symporter inhibitor (loop diuretic). It is used for the treatment of EDEMA associated with CONGESTIVE HEART FAILURE; CHRONIC RENAL INSUFFICIENCY; and LIVER DISEASES. It is also used for the management of HYPERTENSION.","Is the triple Torsemide treats hypertensive disorder supported by the sentence An anilinopyridine sulfonylurea belonging to the class of loop diuretics. Torsemide has a prolonged duration of action compared to other loop diuretics, is extensively protein bound in plasma and has a relatively long half-life.; A pyridine and sulfonamide derivative that acts as a sodium-potassium chloride symporter inhibitor (loop diuretic). It is used for the treatment of EDEMA associated with CONGESTIVE HEART FAILURE; CHRONIC RENAL INSUFFICIENCY; and LIVER DISEASES. It is also used for the management of HYPERTENSION.",False,PMID:24352797 -7649490,Methylprednisolone treats aplastic anemia,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats aplastic anemia supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.nhlbi.nih.gov/health/health-topics/topics/aplastic/ -13166073,Methylprednisolone causes thrombocytopenia,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone causes thrombocytopenia supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-0736-9199 -8083160,Methylprednisolone treats thrombocytopenia,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats thrombocytopenia supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-0736-9199 -30351151,Sodium Bicarbonate treats acidosis disorder,1688,"The monosodium salt of carbonic acid with alkalinizing and electrolyte replacement properties. Upon dissociation, sodium bicarbonate forms sodium and bicarbonate ions. Ion formation increases plasma bicarbonate and buffers excess hydrogen ion concentration, resulting in raised blood pH.; The monosodium salt of carbonic acid with alkalinizing and electrolyte replacement properties. Upon dissociation, sodium bicarbonate forms sodium and bicarbonate ions. Ion formation increases plasma bicarbonate and buffers excess hydrogen ion concentration, resulting in raised blood pH.; A white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Sodium Bicarbonate treats acidosis disorder supported by the sentence The monosodium salt of carbonic acid with alkalinizing and electrolyte replacement properties. Upon dissociation, sodium bicarbonate forms sodium and bicarbonate ions. Ion formation increases plasma bicarbonate and buffers excess hydrogen ion concentration, resulting in raised blood pH.; The monosodium salt of carbonic acid with alkalinizing and electrolyte replacement properties. Upon dissociation, sodium bicarbonate forms sodium and bicarbonate ions. Ion formation increases plasma bicarbonate and buffers excess hydrogen ion concentration, resulting in raised blood pH.; A white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-0736-9199 -8282330,Methylprednisolone related to spinal cord injury,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to spinal cord injury supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True, -11819955,Methylprednisolone affects spinal cord injury,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone affects spinal cord injury supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True, -7980138,Methylprednisolone prevents spinal cord injury,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone prevents spinal cord injury supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True, -24691450,Methylprednisolone related to plantar fasciitis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to plantar fasciitis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True, -45052689,Telmisartan treats hypertensive disorder,1716,"A benzimidazole derivative and a non-peptide angiotensin II receptor antagonist with antihypertensive property. Telmisartan selectively antagonizes angiotensin II binding to the AT1 subtype receptor, located in vascular smooth muscle and adrenal gland. The antagonism results in vasodilation and inhibits the angiotensin II-mediated aldosterone production, which in turn leading to a decrease in sodium and water as well as an increase in potassium excretion leading to a subsequent reduction in blood pressure.; A biphenyl compound and benzimidazole derivative that acts as an angiotensin II type 1 receptor antagonist. It is used in the management of HYPERTENSION.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Telmisartan treats hypertensive disorder supported by the sentence A benzimidazole derivative and a non-peptide angiotensin II receptor antagonist with antihypertensive property. Telmisartan selectively antagonizes angiotensin II binding to the AT1 subtype receptor, located in vascular smooth muscle and adrenal gland. The antagonism results in vasodilation and inhibits the angiotensin II-mediated aldosterone production, which in turn leading to a decrease in sodium and water as well as an increase in potassium excretion leading to a subsequent reduction in blood pressure.; A biphenyl compound and benzimidazole derivative that acts as an angiotensin II type 1 receptor antagonist. It is used in the management of HYPERTENSION.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,PMID:24352797 -10812685,Methylprednisolone related to immunoglobulin a vasculitis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to immunoglobulin a vasculitis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://rarediseases.info.nih.gov/diseases/8204/henoch-schonlein-purpura -9980473,Methylprednisolone treats immunoglobulin a vasculitis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats immunoglobulin a vasculitis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://rarediseases.info.nih.gov/diseases/8204/henoch-schonlein-purpura -12672767,Methylprednisolone causes drug-induced liver injury,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone causes drug-induced liver injury supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-8169-9049 -19674675,Methylprednisolone treats microscopic polyangiitis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats microscopic polyangiitis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True, -10130342,Methylprednisolone related to adult acute respiratory distress syndrome,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to adult acute respiratory distress syndrome supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://www.ncbi.nlm.nih.gov/pmc/articles/pmc5392788/ -20254789,Methylprednisolone affects adult acute respiratory distress syndrome,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone affects adult acute respiratory distress syndrome supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://www.ncbi.nlm.nih.gov/pmc/articles/pmc5392788/ -7483648,Methylprednisolone treats adult acute respiratory distress syndrome,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats adult acute respiratory distress syndrome supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://www.ncbi.nlm.nih.gov/pmc/articles/pmc5392788/ -17478785,Methylprednisolone treats nasal cavity polyp,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats nasal cavity polyp supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,PMID:18728843 -9229208,Methylprednisolone related to vestibular neuronitis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to vestibular neuronitis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,PMID:16448876 -11313619,Methylprednisolone treats vestibular neuronitis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats vestibular neuronitis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,PMID:16448876 -8588816,Methylprednisolone treats Bell's palsy,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats Bell's palsy supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0009-0006-4530-3154 -24759961,Methylprednisolone related to non-Hodgkin lymphoma,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to non-Hodgkin lymphoma supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/non-hodgkin_lymphoma -45043292,Losartan treats hypertensive disorder,1721,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Losartan is an angiotensin II receptor blocker (ARB) used to treat hypertension.[L7423] Angiotensin-converting enzyme (ACE) inhibitors are used for a similar indication but are associated with a cough.[L7423] When patients with ACE inhibitor associated coughs are switched to ARBs like losartan, they have an incidence of cough similar to placebo or [hydrochlorothiazide].[L7423] Losartan is available as losartan potassium oral tablets as well as a combination tablet of losartan potassium and hydrochlorothiazide.[L7423,L7426] Patients taking losartan should have their renal function and potassium levels monitored.[L7423] Losartan was granted FDA approval on 14 April 1995.[L7423]","Is the triple Losartan treats hypertensive disorder supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Losartan is an angiotensin II receptor blocker (ARB) used to treat hypertension.[L7423] Angiotensin-converting enzyme (ACE) inhibitors are used for a similar indication but are associated with a cough.[L7423] When patients with ACE inhibitor associated coughs are switched to ARBs like losartan, they have an incidence of cough similar to placebo or [hydrochlorothiazide].[L7423] Losartan is available as losartan potassium oral tablets as well as a combination tablet of losartan potassium and hydrochlorothiazide.[L7423,L7426] Patients taking losartan should have their renal function and potassium levels monitored.[L7423] Losartan was granted FDA approval on 14 April 1995.[L7423]",False,PMID:24352797 -30645147,Losartan treats hypertensive disorder,1721,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Losartan is an angiotensin II receptor blocker (ARB) used to treat hypertension.[L7423] Angiotensin-converting enzyme (ACE) inhibitors are used for a similar indication but are associated with a cough.[L7423] When patients with ACE inhibitor associated coughs are switched to ARBs like losartan, they have an incidence of cough similar to placebo or [hydrochlorothiazide].[L7423] Losartan is available as losartan potassium oral tablets as well as a combination tablet of losartan potassium and hydrochlorothiazide.[L7423,L7426] Patients taking losartan should have their renal function and potassium levels monitored.[L7423] Losartan was granted FDA approval on 14 April 1995.[L7423]","Is the triple Losartan treats hypertensive disorder supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Losartan is an angiotensin II receptor blocker (ARB) used to treat hypertension.[L7423] Angiotensin-converting enzyme (ACE) inhibitors are used for a similar indication but are associated with a cough.[L7423] When patients with ACE inhibitor associated coughs are switched to ARBs like losartan, they have an incidence of cough similar to placebo or [hydrochlorothiazide].[L7423] Losartan is available as losartan potassium oral tablets as well as a combination tablet of losartan potassium and hydrochlorothiazide.[L7423,L7426] Patients taking losartan should have their renal function and potassium levels monitored.[L7423] Losartan was granted FDA approval on 14 April 1995.[L7423]",False,PMID:24352797 -24973247,Methylprednisolone causes lupus nephritis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone causes lupus nephritis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://medlineplus.gov/ency/article/000481.htm -30357401,Losartan treats proteinuria,1721,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Losartan is an angiotensin II receptor blocker (ARB) used to treat hypertension.[L7423] Angiotensin-converting enzyme (ACE) inhibitors are used for a similar indication but are associated with a cough.[L7423] When patients with ACE inhibitor associated coughs are switched to ARBs like losartan, they have an incidence of cough similar to placebo or [hydrochlorothiazide].[L7423] Losartan is available as losartan potassium oral tablets as well as a combination tablet of losartan potassium and hydrochlorothiazide.[L7423,L7426] Patients taking losartan should have their renal function and potassium levels monitored.[L7423] Losartan was granted FDA approval on 14 April 1995.[L7423]","Is the triple Losartan treats proteinuria supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Losartan is an angiotensin II receptor blocker (ARB) used to treat hypertension.[L7423] Angiotensin-converting enzyme (ACE) inhibitors are used for a similar indication but are associated with a cough.[L7423] When patients with ACE inhibitor associated coughs are switched to ARBs like losartan, they have an incidence of cough similar to placebo or [hydrochlorothiazide].[L7423] Losartan is available as losartan potassium oral tablets as well as a combination tablet of losartan potassium and hydrochlorothiazide.[L7423,L7426] Patients taking losartan should have their renal function and potassium levels monitored.[L7423] Losartan was granted FDA approval on 14 April 1995.[L7423]",False,https://en.wikipedia.org/wiki/proteinuria -8063034,Methylprednisolone treats granulomatosis with polyangiitis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats granulomatosis with polyangiitis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://en.wikipedia.org/wiki/granulomatosis_with_polyangiitis -20290784,Methylprednisolone related to membranous glomerulonephritis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to membranous glomerulonephritis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True, -14232595,Methylprednisolone treats membranous glomerulonephritis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats membranous glomerulonephritis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True, -14398237,Methylprednisolone related to IgA glomerulonephritis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to IgA glomerulonephritis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.nlm.nih.gov/medlineplus/ency/article/000466.htm -14398238,Methylprednisolone treats IgA glomerulonephritis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats IgA glomerulonephritis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.nlm.nih.gov/medlineplus/ency/article/000466.htm -25642231,Methylprednisolone treats heart disorder,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats heart disorder supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/heart_disease -9003326,Methylprednisolone related to systemic sclerosis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to systemic sclerosis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://ghr.nlm.nih.gov/condition/systemic-scleroderma -20530617,Methylprednisolone affects systemic sclerosis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone affects systemic sclerosis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://ghr.nlm.nih.gov/condition/systemic-scleroderma -30650691,Aprepitant treats Nausea,1732,"A small molecule, high-affinity substance P antagonist (SPA) with antiemetic activity. Crossing the blood brain barrier, aprepitant binds selectively to the human substance P/neurokinin 1 receptor in the central nervous system (CNS), thereby inhibiting receptor binding of endogenous substance P and substance P-induced emesis. This agent has little or no affinity for serotonin type 3 (5-HT3), dopamine, and corticosteroid receptors. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C49173"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C49173"" NCI Thesaurus); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Aprepitant treats Nausea supported by the sentence A small molecule, high-affinity substance P antagonist (SPA) with antiemetic activity. Crossing the blood brain barrier, aprepitant binds selectively to the human substance P/neurokinin 1 receptor in the central nervous system (CNS), thereby inhibiting receptor binding of endogenous substance P and substance P-induced emesis. This agent has little or no affinity for serotonin type 3 (5-HT3), dopamine, and corticosteroid receptors. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C49173"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C49173"" NCI Thesaurus); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,PMID:26770271 -8447481,Methylprednisolone related to rheumatoid arthritis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to rheumatoid arthritis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-0736-9199 -15610554,Methylprednisolone affects rheumatoid arthritis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone affects rheumatoid arthritis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-0736-9199 -7853881,Methylprednisolone treats rheumatoid arthritis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats rheumatoid arthritis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-0736-9199 -20014108,Methylprednisolone prevents rheumatoid arthritis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone prevents rheumatoid arthritis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-0736-9199 -26450412,Methylprednisolone treats leukemia,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats leukemia supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/leukemia -30353643,Sulindac treats classic familial adenomatous polyposis,1753,"A sulfinylindene derivative prodrug with potential antineoplastic activity. Converted in vivo to an active metabolite, sulindac, a nonsteroidal anti-inflammatory drug (NSAID), blocks cyclic guanosine monophosphate-phosphodiesterase (cGMP-PDE), an enzyme that inhibits the normal apoptosis signal pathway; this inhibition permits the apoptotic signal pathway to proceed unopposed, resulting in apoptotic cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C850"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C850"" NCI Thesaurus); A sulfinylindene derivative prodrug with potential antineoplastic activity. Converted in vivo to an active metabolite, sulindac, a nonsteroidal anti-inflammatory drug (NSAID), blocks cyclic guanosine monophosphate-phosphodiesterase (cGMP-PDE), an enzyme that inhibits the normal apoptosis signal pathway; this inhibition permits the apoptotic signal pathway to proceed unopposed, resulting in apoptotic cell death. (NCI04); A sulfinylindene derivative prodrug whose sulfinyl moiety is converted in vivo to an active NSAID analgesic. Specifically, the prodrug is converted by liver enzymes to a sulfide which is excreted in the bile and then reabsorbed from the intestine. This helps to maintain constant blood levels with reduced gastrointestinal side effects.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Sulindac treats classic familial adenomatous polyposis supported by the sentence A sulfinylindene derivative prodrug with potential antineoplastic activity. Converted in vivo to an active metabolite, sulindac, a nonsteroidal anti-inflammatory drug (NSAID), blocks cyclic guanosine monophosphate-phosphodiesterase (cGMP-PDE), an enzyme that inhibits the normal apoptosis signal pathway; this inhibition permits the apoptotic signal pathway to proceed unopposed, resulting in apoptotic cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C850"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C850"" NCI Thesaurus); A sulfinylindene derivative prodrug with potential antineoplastic activity. Converted in vivo to an active metabolite, sulindac, a nonsteroidal anti-inflammatory drug (NSAID), blocks cyclic guanosine monophosphate-phosphodiesterase (cGMP-PDE), an enzyme that inhibits the normal apoptosis signal pathway; this inhibition permits the apoptotic signal pathway to proceed unopposed, resulting in apoptotic cell death. (NCI04); A sulfinylindene derivative prodrug whose sulfinyl moiety is converted in vivo to an active NSAID analgesic. Specifically, the prodrug is converted by liver enzymes to a sulfide which is excreted in the bile and then reabsorbed from the intestine. This helps to maintain constant blood levels with reduced gastrointestinal side effects.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,http://www.omim.org/entry/175100?search=adenomatous%20polyposis -30372878,Ketorolac treats Miosis,1768,"A synthetic pyrrolizine carboxylic acid derivative with anti-inflammatory, analgesic, and antipyretic activities. Ketorolac non-selective inhibits the enzymes cyclooxygenase 1 (COX-1) and COX-2. The inhibition of COX-2, up-regulated at sites of inflammation, prevents conversion of arachidonic acid to pro-inflammatory prostaglandins. The inhibition of COX-1 by this agent prevents the normal steady-state production of prostaglandins that play housekeeping roles in the protection of the gastrointestinal tract, the regulation of renal blood flow, and platelet aggregation. As a result, the inhibition of COX-1 may be associated with gastrointestinal toxicity, nephrotoxicity, and the inhibition of platelet aggregation. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1219"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1219"" NCI Thesaurus); A synthetic pyrrolizine carboxylic acid derivative with anti-inflammatory, analgesic, and antipyretic activities. Ketorolac non-selective inhibits the enzymes cyclooxygenase 1 (COX-1) and COX-2. The inhibition of COX-2, up-regulated at sites of inflammation, prevents conversion of arachidonic acid to pro-inflammatory prostaglandins. The inhibition of COX-1 by this agent prevents the normal steady-state production of prostaglandins that play housekeeping roles in the protection of the gastrointestinal tract, the regulation of renal blood flow, and platelet aggregation. As a result, the inhibition of COX-1 may be associated with gastrointestinal toxicity, nephrotoxicity, and the inhibition of platelet aggregation.; A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is an NSAID and is used principally for its analgesic activity. (From Martindale The Extra Pharmacopoeia, 31st ed); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ketorolac treats Miosis supported by the sentence A synthetic pyrrolizine carboxylic acid derivative with anti-inflammatory, analgesic, and antipyretic activities. Ketorolac non-selective inhibits the enzymes cyclooxygenase 1 (COX-1) and COX-2. The inhibition of COX-2, up-regulated at sites of inflammation, prevents conversion of arachidonic acid to pro-inflammatory prostaglandins. The inhibition of COX-1 by this agent prevents the normal steady-state production of prostaglandins that play housekeeping roles in the protection of the gastrointestinal tract, the regulation of renal blood flow, and platelet aggregation. As a result, the inhibition of COX-1 may be associated with gastrointestinal toxicity, nephrotoxicity, and the inhibition of platelet aggregation. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1219"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1219"" NCI Thesaurus); A synthetic pyrrolizine carboxylic acid derivative with anti-inflammatory, analgesic, and antipyretic activities. Ketorolac non-selective inhibits the enzymes cyclooxygenase 1 (COX-1) and COX-2. The inhibition of COX-2, up-regulated at sites of inflammation, prevents conversion of arachidonic acid to pro-inflammatory prostaglandins. The inhibition of COX-1 by this agent prevents the normal steady-state production of prostaglandins that play housekeeping roles in the protection of the gastrointestinal tract, the regulation of renal blood flow, and platelet aggregation. As a result, the inhibition of COX-1 may be associated with gastrointestinal toxicity, nephrotoxicity, and the inhibition of platelet aggregation.; A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is an NSAID and is used principally for its analgesic activity. (From Martindale The Extra Pharmacopoeia, 31st ed); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0001-5889-4463 -14027935,Methylprednisolone treats diffuse large B-cell lymphoma,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats diffuse large B-cell lymphoma supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,PMID:28487884 -27228384,Methylprednisolone related to Crohn disease,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to Crohn disease supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/chron%27s_disease -30358762,Ketorolac treats Pain,1768,"A synthetic pyrrolizine carboxylic acid derivative with anti-inflammatory, analgesic, and antipyretic activities. Ketorolac non-selective inhibits the enzymes cyclooxygenase 1 (COX-1) and COX-2. The inhibition of COX-2, up-regulated at sites of inflammation, prevents conversion of arachidonic acid to pro-inflammatory prostaglandins. The inhibition of COX-1 by this agent prevents the normal steady-state production of prostaglandins that play housekeeping roles in the protection of the gastrointestinal tract, the regulation of renal blood flow, and platelet aggregation. As a result, the inhibition of COX-1 may be associated with gastrointestinal toxicity, nephrotoxicity, and the inhibition of platelet aggregation. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1219"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1219"" NCI Thesaurus); A synthetic pyrrolizine carboxylic acid derivative with anti-inflammatory, analgesic, and antipyretic activities. Ketorolac non-selective inhibits the enzymes cyclooxygenase 1 (COX-1) and COX-2. The inhibition of COX-2, up-regulated at sites of inflammation, prevents conversion of arachidonic acid to pro-inflammatory prostaglandins. The inhibition of COX-1 by this agent prevents the normal steady-state production of prostaglandins that play housekeeping roles in the protection of the gastrointestinal tract, the regulation of renal blood flow, and platelet aggregation. As a result, the inhibition of COX-1 may be associated with gastrointestinal toxicity, nephrotoxicity, and the inhibition of platelet aggregation.; A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is an NSAID and is used principally for its analgesic activity. (From Martindale The Extra Pharmacopoeia, 31st ed); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ketorolac treats Pain supported by the sentence A synthetic pyrrolizine carboxylic acid derivative with anti-inflammatory, analgesic, and antipyretic activities. Ketorolac non-selective inhibits the enzymes cyclooxygenase 1 (COX-1) and COX-2. The inhibition of COX-2, up-regulated at sites of inflammation, prevents conversion of arachidonic acid to pro-inflammatory prostaglandins. The inhibition of COX-1 by this agent prevents the normal steady-state production of prostaglandins that play housekeeping roles in the protection of the gastrointestinal tract, the regulation of renal blood flow, and platelet aggregation. As a result, the inhibition of COX-1 may be associated with gastrointestinal toxicity, nephrotoxicity, and the inhibition of platelet aggregation. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1219"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1219"" NCI Thesaurus); A synthetic pyrrolizine carboxylic acid derivative with anti-inflammatory, analgesic, and antipyretic activities. Ketorolac non-selective inhibits the enzymes cyclooxygenase 1 (COX-1) and COX-2. The inhibition of COX-2, up-regulated at sites of inflammation, prevents conversion of arachidonic acid to pro-inflammatory prostaglandins. The inhibition of COX-1 by this agent prevents the normal steady-state production of prostaglandins that play housekeeping roles in the protection of the gastrointestinal tract, the regulation of renal blood flow, and platelet aggregation. As a result, the inhibition of COX-1 may be associated with gastrointestinal toxicity, nephrotoxicity, and the inhibition of platelet aggregation.; A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is an NSAID and is used principally for its analgesic activity. (From Martindale The Extra Pharmacopoeia, 31st ed); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0001-5208-3432 -18260665,Methylprednisolone causes neoplasm,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone causes neoplasm supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-6601-2165 -27357949,Methylprednisolone affects neoplasm,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone affects neoplasm supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-6601-2165 -14636779,Methylprednisolone treats neoplasm,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats neoplasm supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0002-6601-2165 -26279366,Methylprednisolone treats angioimmunoblastic T-cell lymphoma,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats angioimmunoblastic T-cell lymphoma supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,PMID:22700722 -12183687,Methylprednisolone related to acute lymphoblastic leukemia,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to acute lymphoblastic leukemia supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.cancer.gov/dictionary?cdrid=46332 -10136260,Methylprednisolone treats acute lymphoblastic leukemia,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats acute lymphoblastic leukemia supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.cancer.gov/dictionary?cdrid=46332 -12975348,Methylprednisolone treats mature T-cell and NK-cell non-Hodgkin lymphoma,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats mature T-cell and NK-cell non-Hodgkin lymphoma supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,PMID:21919697 -7432980,Methylprednisolone treats myelodysplastic syndrome,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats myelodysplastic syndrome supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/myelodysplastic_syndrome -26513818,Methylprednisolone related to B-cell chronic lymphocytic leukemia,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to B-cell chronic lymphocytic leukemia supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.cancer.gov/dictionary?cdrid=346545 -10801960,Methylprednisolone treats B-cell chronic lymphocytic leukemia,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats B-cell chronic lymphocytic leukemia supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.cancer.gov/dictionary?cdrid=346545 -30367978,Etoposide treats neutropenia,1822,"Etoposide, also known as vepesid or VP-16, belongs to the class of organic compounds known as podophyllotoxins. These are tetralin lignans in which the benzene moiety of the tetralin skeleton is fused to a 1,3-dioxolane and the cyclohexane is fused to a butyrolactone (pyrrolidin-2-one). Etoposide is a drug. Within humans, etoposide participates in a number of enzymatic reactions. In particular, etoposide can be converted into etoposide ortho-quinone; which is mediated by the enzymes prostaglandin g/h synthase 1 and prostaglandin g/h synthase 2. In addition, etoposide and uridine diphosphate glucuronic acid can be converted into etoposide glucuronide and uridine 5'-diphosphate; which is mediated by the enzyme UDP-glucuronosyltransferase 1-1. In humans, etoposide is involved in etoposide metabolism pathway. Etoposide is formally rated as a carcinogen (by IARC 1) and is also a potentially toxic compound. Etoposide is used as a form of chemotherapy for cancers such as Kaposi's sarcoma, Ewing's sarcoma, lung cancer, testicular cancer, lymphoma, nonlymphocytic leukemia, and glioblastoma multiforme. It is given intravenously (IV) or orally in capsule or tablet form. It is believed to work by damaging DNA. Etoposide was approved for medical use in the United States in 1983. They can include low blood cell counts, vomiting, loss of appetite, diarrhea, hair loss, and fever.","Is the triple Etoposide treats neutropenia supported by the sentence Etoposide, also known as vepesid or VP-16, belongs to the class of organic compounds known as podophyllotoxins. These are tetralin lignans in which the benzene moiety of the tetralin skeleton is fused to a 1,3-dioxolane and the cyclohexane is fused to a butyrolactone (pyrrolidin-2-one). Etoposide is a drug. Within humans, etoposide participates in a number of enzymatic reactions. In particular, etoposide can be converted into etoposide ortho-quinone; which is mediated by the enzymes prostaglandin g/h synthase 1 and prostaglandin g/h synthase 2. In addition, etoposide and uridine diphosphate glucuronic acid can be converted into etoposide glucuronide and uridine 5'-diphosphate; which is mediated by the enzyme UDP-glucuronosyltransferase 1-1. In humans, etoposide is involved in etoposide metabolism pathway. Etoposide is formally rated as a carcinogen (by IARC 1) and is also a potentially toxic compound. Etoposide is used as a form of chemotherapy for cancers such as Kaposi's sarcoma, Ewing's sarcoma, lung cancer, testicular cancer, lymphoma, nonlymphocytic leukemia, and glioblastoma multiforme. It is given intravenously (IV) or orally in capsule or tablet form. It is believed to work by damaging DNA. Etoposide was approved for medical use in the United States in 1983. They can include low blood cell counts, vomiting, loss of appetite, diarrhea, hair loss, and fever.",False, -23514846,Methylprednisolone related to carpal tunnel syndrome,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to carpal tunnel syndrome supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://medlineplus.gov/ency/article/000433.htm -8095661,Methylprednisolone treats carpal tunnel syndrome,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats carpal tunnel syndrome supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://medlineplus.gov/ency/article/000433.htm -30341988,Etoposide treats leukemia,1822,"Etoposide, also known as vepesid or VP-16, belongs to the class of organic compounds known as podophyllotoxins. These are tetralin lignans in which the benzene moiety of the tetralin skeleton is fused to a 1,3-dioxolane and the cyclohexane is fused to a butyrolactone (pyrrolidin-2-one). Etoposide is a drug. Within humans, etoposide participates in a number of enzymatic reactions. In particular, etoposide can be converted into etoposide ortho-quinone; which is mediated by the enzymes prostaglandin g/h synthase 1 and prostaglandin g/h synthase 2. In addition, etoposide and uridine diphosphate glucuronic acid can be converted into etoposide glucuronide and uridine 5'-diphosphate; which is mediated by the enzyme UDP-glucuronosyltransferase 1-1. In humans, etoposide is involved in etoposide metabolism pathway. Etoposide is formally rated as a carcinogen (by IARC 1) and is also a potentially toxic compound. Etoposide is used as a form of chemotherapy for cancers such as Kaposi's sarcoma, Ewing's sarcoma, lung cancer, testicular cancer, lymphoma, nonlymphocytic leukemia, and glioblastoma multiforme. It is given intravenously (IV) or orally in capsule or tablet form. It is believed to work by damaging DNA. Etoposide was approved for medical use in the United States in 1983. They can include low blood cell counts, vomiting, loss of appetite, diarrhea, hair loss, and fever.","Is the triple Etoposide treats leukemia supported by the sentence Etoposide, also known as vepesid or VP-16, belongs to the class of organic compounds known as podophyllotoxins. These are tetralin lignans in which the benzene moiety of the tetralin skeleton is fused to a 1,3-dioxolane and the cyclohexane is fused to a butyrolactone (pyrrolidin-2-one). Etoposide is a drug. Within humans, etoposide participates in a number of enzymatic reactions. In particular, etoposide can be converted into etoposide ortho-quinone; which is mediated by the enzymes prostaglandin g/h synthase 1 and prostaglandin g/h synthase 2. In addition, etoposide and uridine diphosphate glucuronic acid can be converted into etoposide glucuronide and uridine 5'-diphosphate; which is mediated by the enzyme UDP-glucuronosyltransferase 1-1. In humans, etoposide is involved in etoposide metabolism pathway. Etoposide is formally rated as a carcinogen (by IARC 1) and is also a potentially toxic compound. Etoposide is used as a form of chemotherapy for cancers such as Kaposi's sarcoma, Ewing's sarcoma, lung cancer, testicular cancer, lymphoma, nonlymphocytic leukemia, and glioblastoma multiforme. It is given intravenously (IV) or orally in capsule or tablet form. It is believed to work by damaging DNA. Etoposide was approved for medical use in the United States in 1983. They can include low blood cell counts, vomiting, loss of appetite, diarrhea, hair loss, and fever.",False,http://en.wikipedia.org/wiki/leukemia -23209303,Methylprednisolone treats respiratory system disorder,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats respiratory system disorder supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=respiratory%20system -12755316,Methylprednisolone related to plasma cell myeloma,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to plasma cell myeloma supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.cancer.gov/dictionary?cdrid=411384 -11895116,Methylprednisolone treats plasma cell myeloma,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats plasma cell myeloma supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.cancer.gov/dictionary?cdrid=411384 -17288506,Methylprednisolone related to autoimmune thrombocytopenic purpura,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to autoimmune thrombocytopenic purpura supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://rarediseases.org/rare-diseases/immune-thrombocytopenia/ -7808987,Methylprednisolone treats autoimmune thrombocytopenic purpura,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats autoimmune thrombocytopenic purpura supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://rarediseases.org/rare-diseases/immune-thrombocytopenia/ -20286711,Methylprednisolone related to neuromyelitis optica,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to neuromyelitis optica supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/neuromyelitis_optica -16277488,Methylprednisolone affects neuromyelitis optica,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone affects neuromyelitis optica supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/neuromyelitis_optica -14897628,Methylprednisolone treats neuromyelitis optica,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats neuromyelitis optica supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/neuromyelitis_optica -30340384,Urofollitropin treats infertility disorder,1826,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T125; UMLS Semantic Type: STY:T116; Urofollitropin is a urinary-derived follicle-stimulating hormone (FSH) that is extracted and purified from human urine samples. It consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Urofollitropin is typically used injected subcutaneously in combination with human chorionic gonadotropin (hCG) to induce ovulation. Urofollitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF).","Is the triple Urofollitropin treats infertility disorder supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T125; UMLS Semantic Type: STY:T116; Urofollitropin is a urinary-derived follicle-stimulating hormone (FSH) that is extracted and purified from human urine samples. It consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Urofollitropin is typically used injected subcutaneously in combination with human chorionic gonadotropin (hCG) to induce ovulation. Urofollitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF).",False,http://en.wikipedia.org/wiki/infertility -30649189,Nitric oxide treats ischemia reperfusion injury,1829,"The biologically active molecule nitric oxide (NO) is a simple, membrane-permeable gas with unique chemistry. It is formed by the conversion of L-arginine to L-citrulline, with the release of NO. The enzymatic oxidation of L-arginine to L-citrulline takes place in the presence of oxygen and NADPH using flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), heme, thiol, and tetrahydrobiopterin as cofactors. The enzyme responsible for the generation of NO is nitric oxide synthase (E.C. 1.7.99.7; NOS). Three NOS isoforms have been described and shown to be encoded on three distinct genes: neuronal NOS (nNOS, NOS type I), inducible NOS (NOS type II), and endothelial NOS (eNOS, NOS type III). Two of them are constitutively expressed and dependent on the presence of calcium ions and calmodulin to function (nNOS and eNOS), while iNOS is considered non-constitutive and calcium-independent. However, experience has shown that constitutive expression of nNOS and eNOS is not as rigid as previously thought (i.e. either present or absent), but can be dynamically controlled during development and in response to injury. Functionally, NO may act as a hormone, neurotransmitter, paracrine messenger, mediator, cytoprotective molecule, and cytotoxic molecule. NO has multiple cellular molecular targets. It influences the activity of transcription factors, modulates upstream signaling cascades, mRNA stability and translation, and processes the primary gene products. In the brain, many processes are linked to NO. NO activates its receptor, soluble guanylate cyclase by binding to it. The stimulation of this enzyme leads to increased synthesis of the second messenger, cGMP, which in turn activates cGMP-dependent kinases in target cells. NO exerts a strong influence on glutamatergic neurotransmission by directly interacting with the N-methyl-D-aspartate (NMDA) receptor. Neuronal NOS is connected to NMDA receptors (see below) and sharply increases NO production following activation of this receptor. Thus, the level of endogenously produced NO around NMDA synapses reflects the activity of glutamate-mediated neurotransmission. However, there is recent evidence showing that non-NMDA glutamate receptors (i.e. AMPA and type I metabotropic receptors) also contribute to NO generation. Besides its influence on glutamate, NO is known to have effects on the storage, uptake and/or release of most other neurotransmitters in the CNS (acetylcholine, dopamine, noradrenaline, GABA, taurine, and glycine) as well as of certain neuropeptides. Finally, since NO is a highly diffusible molecule, it may reach extrasynaptic receptors at target cell membranes that are some distance away from the place of NO synthesis. NO is thus capable of mediating both synaptic and nonsynaptic communication processes. NO is a potent vasodilator (a major endogenous regulator of vascular tone), and an important endothelium-dependent relaxing factor. NO is synthesized by NO synthases (NOS) and NOS are inhibited by asymmetrical dimethylarginine (ADMA). ADMA is metabolized by dimethylarginine dimethylaminohydrolase (DDAH) and excreted in the kidneys. Lower ADMA levels in pregnant women compared to non-pregnant controls suggest that ADMA has a role in vascular dilatation and blood pressure changes. Several studies show an increase in ADMA levels in pregnancies complicated with preeclampsia. Elevated ADMA levels in preeclampsia are seen before clinical symptoms have developed; these findings suggest that ADMA has a role in the pathogenesis of preeclampsia. In some pulmonary hypertensive states such as ARDS, the production of endogenous NO may be impaired. Nitric oxide inhalation selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because NO is inactivated by rapidly binding to hemoglobin. In an injured lung with pulmonary hypertension, inhaled NO produces local vasodilation of well-ventilated lung units and may ""steal"" blood flow away from unventilated regions. This reduces intrapulmonary shunting and may improve systemic arterial oxygenation. Nitric oxide is a chemical mediator fundamental in the maintenance of adequate tissue perfusion and effective cardiovascular function. The use of nitrates is well established as pharmacological agents but it is only recently that it has been recognized that they act as a source of nitric oxide (PMID: 16966108, 8752507, 17181668, 16005189). Nitric oxide is used as a food additive (EAFUS: Everything Added to Food in the United States).","Is the triple Nitric oxide treats ischemia reperfusion injury supported by the sentence The biologically active molecule nitric oxide (NO) is a simple, membrane-permeable gas with unique chemistry. It is formed by the conversion of L-arginine to L-citrulline, with the release of NO. The enzymatic oxidation of L-arginine to L-citrulline takes place in the presence of oxygen and NADPH using flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), heme, thiol, and tetrahydrobiopterin as cofactors. The enzyme responsible for the generation of NO is nitric oxide synthase (E.C. 1.7.99.7; NOS). Three NOS isoforms have been described and shown to be encoded on three distinct genes: neuronal NOS (nNOS, NOS type I), inducible NOS (NOS type II), and endothelial NOS (eNOS, NOS type III). Two of them are constitutively expressed and dependent on the presence of calcium ions and calmodulin to function (nNOS and eNOS), while iNOS is considered non-constitutive and calcium-independent. However, experience has shown that constitutive expression of nNOS and eNOS is not as rigid as previously thought (i.e. either present or absent), but can be dynamically controlled during development and in response to injury. Functionally, NO may act as a hormone, neurotransmitter, paracrine messenger, mediator, cytoprotective molecule, and cytotoxic molecule. NO has multiple cellular molecular targets. It influences the activity of transcription factors, modulates upstream signaling cascades, mRNA stability and translation, and processes the primary gene products. In the brain, many processes are linked to NO. NO activates its receptor, soluble guanylate cyclase by binding to it. The stimulation of this enzyme leads to increased synthesis of the second messenger, cGMP, which in turn activates cGMP-dependent kinases in target cells. NO exerts a strong influence on glutamatergic neurotransmission by directly interacting with the N-methyl-D-aspartate (NMDA) receptor. Neuronal NOS is connected to NMDA receptors (see below) and sharply increases NO production following activation of this receptor. Thus, the level of endogenously produced NO around NMDA synapses reflects the activity of glutamate-mediated neurotransmission. However, there is recent evidence showing that non-NMDA glutamate receptors (i.e. AMPA and type I metabotropic receptors) also contribute to NO generation. Besides its influence on glutamate, NO is known to have effects on the storage, uptake and/or release of most other neurotransmitters in the CNS (acetylcholine, dopamine, noradrenaline, GABA, taurine, and glycine) as well as of certain neuropeptides. Finally, since NO is a highly diffusible molecule, it may reach extrasynaptic receptors at target cell membranes that are some distance away from the place of NO synthesis. NO is thus capable of mediating both synaptic and nonsynaptic communication processes. NO is a potent vasodilator (a major endogenous regulator of vascular tone), and an important endothelium-dependent relaxing factor. NO is synthesized by NO synthases (NOS) and NOS are inhibited by asymmetrical dimethylarginine (ADMA). ADMA is metabolized by dimethylarginine dimethylaminohydrolase (DDAH) and excreted in the kidneys. Lower ADMA levels in pregnant women compared to non-pregnant controls suggest that ADMA has a role in vascular dilatation and blood pressure changes. Several studies show an increase in ADMA levels in pregnancies complicated with preeclampsia. Elevated ADMA levels in preeclampsia are seen before clinical symptoms have developed; these findings suggest that ADMA has a role in the pathogenesis of preeclampsia. In some pulmonary hypertensive states such as ARDS, the production of endogenous NO may be impaired. Nitric oxide inhalation selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because NO is inactivated by rapidly binding to hemoglobin. In an injured lung with pulmonary hypertension, inhaled NO produces local vasodilation of well-ventilated lung units and may ""steal"" blood flow away from unventilated regions. This reduces intrapulmonary shunting and may improve systemic arterial oxygenation. Nitric oxide is a chemical mediator fundamental in the maintenance of adequate tissue perfusion and effective cardiovascular function. The use of nitrates is well established as pharmacological agents but it is only recently that it has been recognized that they act as a source of nitric oxide (PMID: 16966108, 8752507, 17181668, 16005189). Nitric oxide is used as a food additive (EAFUS: Everything Added to Food in the United States).",False, -26974005,Methylprednisolone related to hematopoietic and lymphoid system neoplasm,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to hematopoietic and lymphoid system neoplasm supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://www.ncbi.nlm.nih.gov/mesh?term=hematologic%20neoplasms -15936572,Methylprednisolone related to endocrine exophthalmos,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to endocrine exophthalmos supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,PMID:20181974 -8562694,Methylprednisolone treats endocrine exophthalmos,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats endocrine exophthalmos supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,PMID:20181974 -30648944,Nitric oxide treats fetal growth restriction,1829,"The biologically active molecule nitric oxide (NO) is a simple, membrane-permeable gas with unique chemistry. It is formed by the conversion of L-arginine to L-citrulline, with the release of NO. The enzymatic oxidation of L-arginine to L-citrulline takes place in the presence of oxygen and NADPH using flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), heme, thiol, and tetrahydrobiopterin as cofactors. The enzyme responsible for the generation of NO is nitric oxide synthase (E.C. 1.7.99.7; NOS). Three NOS isoforms have been described and shown to be encoded on three distinct genes: neuronal NOS (nNOS, NOS type I), inducible NOS (NOS type II), and endothelial NOS (eNOS, NOS type III). Two of them are constitutively expressed and dependent on the presence of calcium ions and calmodulin to function (nNOS and eNOS), while iNOS is considered non-constitutive and calcium-independent. However, experience has shown that constitutive expression of nNOS and eNOS is not as rigid as previously thought (i.e. either present or absent), but can be dynamically controlled during development and in response to injury. Functionally, NO may act as a hormone, neurotransmitter, paracrine messenger, mediator, cytoprotective molecule, and cytotoxic molecule. NO has multiple cellular molecular targets. It influences the activity of transcription factors, modulates upstream signaling cascades, mRNA stability and translation, and processes the primary gene products. In the brain, many processes are linked to NO. NO activates its receptor, soluble guanylate cyclase by binding to it. The stimulation of this enzyme leads to increased synthesis of the second messenger, cGMP, which in turn activates cGMP-dependent kinases in target cells. NO exerts a strong influence on glutamatergic neurotransmission by directly interacting with the N-methyl-D-aspartate (NMDA) receptor. Neuronal NOS is connected to NMDA receptors (see below) and sharply increases NO production following activation of this receptor. Thus, the level of endogenously produced NO around NMDA synapses reflects the activity of glutamate-mediated neurotransmission. However, there is recent evidence showing that non-NMDA glutamate receptors (i.e. AMPA and type I metabotropic receptors) also contribute to NO generation. Besides its influence on glutamate, NO is known to have effects on the storage, uptake and/or release of most other neurotransmitters in the CNS (acetylcholine, dopamine, noradrenaline, GABA, taurine, and glycine) as well as of certain neuropeptides. Finally, since NO is a highly diffusible molecule, it may reach extrasynaptic receptors at target cell membranes that are some distance away from the place of NO synthesis. NO is thus capable of mediating both synaptic and nonsynaptic communication processes. NO is a potent vasodilator (a major endogenous regulator of vascular tone), and an important endothelium-dependent relaxing factor. NO is synthesized by NO synthases (NOS) and NOS are inhibited by asymmetrical dimethylarginine (ADMA). ADMA is metabolized by dimethylarginine dimethylaminohydrolase (DDAH) and excreted in the kidneys. Lower ADMA levels in pregnant women compared to non-pregnant controls suggest that ADMA has a role in vascular dilatation and blood pressure changes. Several studies show an increase in ADMA levels in pregnancies complicated with preeclampsia. Elevated ADMA levels in preeclampsia are seen before clinical symptoms have developed; these findings suggest that ADMA has a role in the pathogenesis of preeclampsia. In some pulmonary hypertensive states such as ARDS, the production of endogenous NO may be impaired. Nitric oxide inhalation selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because NO is inactivated by rapidly binding to hemoglobin. In an injured lung with pulmonary hypertension, inhaled NO produces local vasodilation of well-ventilated lung units and may ""steal"" blood flow away from unventilated regions. This reduces intrapulmonary shunting and may improve systemic arterial oxygenation. Nitric oxide is a chemical mediator fundamental in the maintenance of adequate tissue perfusion and effective cardiovascular function. The use of nitrates is well established as pharmacological agents but it is only recently that it has been recognized that they act as a source of nitric oxide (PMID: 16966108, 8752507, 17181668, 16005189). Nitric oxide is used as a food additive (EAFUS: Everything Added to Food in the United States).","Is the triple Nitric oxide treats fetal growth restriction supported by the sentence The biologically active molecule nitric oxide (NO) is a simple, membrane-permeable gas with unique chemistry. It is formed by the conversion of L-arginine to L-citrulline, with the release of NO. The enzymatic oxidation of L-arginine to L-citrulline takes place in the presence of oxygen and NADPH using flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), heme, thiol, and tetrahydrobiopterin as cofactors. The enzyme responsible for the generation of NO is nitric oxide synthase (E.C. 1.7.99.7; NOS). Three NOS isoforms have been described and shown to be encoded on three distinct genes: neuronal NOS (nNOS, NOS type I), inducible NOS (NOS type II), and endothelial NOS (eNOS, NOS type III). Two of them are constitutively expressed and dependent on the presence of calcium ions and calmodulin to function (nNOS and eNOS), while iNOS is considered non-constitutive and calcium-independent. However, experience has shown that constitutive expression of nNOS and eNOS is not as rigid as previously thought (i.e. either present or absent), but can be dynamically controlled during development and in response to injury. Functionally, NO may act as a hormone, neurotransmitter, paracrine messenger, mediator, cytoprotective molecule, and cytotoxic molecule. NO has multiple cellular molecular targets. It influences the activity of transcription factors, modulates upstream signaling cascades, mRNA stability and translation, and processes the primary gene products. In the brain, many processes are linked to NO. NO activates its receptor, soluble guanylate cyclase by binding to it. The stimulation of this enzyme leads to increased synthesis of the second messenger, cGMP, which in turn activates cGMP-dependent kinases in target cells. NO exerts a strong influence on glutamatergic neurotransmission by directly interacting with the N-methyl-D-aspartate (NMDA) receptor. Neuronal NOS is connected to NMDA receptors (see below) and sharply increases NO production following activation of this receptor. Thus, the level of endogenously produced NO around NMDA synapses reflects the activity of glutamate-mediated neurotransmission. However, there is recent evidence showing that non-NMDA glutamate receptors (i.e. AMPA and type I metabotropic receptors) also contribute to NO generation. Besides its influence on glutamate, NO is known to have effects on the storage, uptake and/or release of most other neurotransmitters in the CNS (acetylcholine, dopamine, noradrenaline, GABA, taurine, and glycine) as well as of certain neuropeptides. Finally, since NO is a highly diffusible molecule, it may reach extrasynaptic receptors at target cell membranes that are some distance away from the place of NO synthesis. NO is thus capable of mediating both synaptic and nonsynaptic communication processes. NO is a potent vasodilator (a major endogenous regulator of vascular tone), and an important endothelium-dependent relaxing factor. NO is synthesized by NO synthases (NOS) and NOS are inhibited by asymmetrical dimethylarginine (ADMA). ADMA is metabolized by dimethylarginine dimethylaminohydrolase (DDAH) and excreted in the kidneys. Lower ADMA levels in pregnant women compared to non-pregnant controls suggest that ADMA has a role in vascular dilatation and blood pressure changes. Several studies show an increase in ADMA levels in pregnancies complicated with preeclampsia. Elevated ADMA levels in preeclampsia are seen before clinical symptoms have developed; these findings suggest that ADMA has a role in the pathogenesis of preeclampsia. In some pulmonary hypertensive states such as ARDS, the production of endogenous NO may be impaired. Nitric oxide inhalation selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because NO is inactivated by rapidly binding to hemoglobin. In an injured lung with pulmonary hypertension, inhaled NO produces local vasodilation of well-ventilated lung units and may ""steal"" blood flow away from unventilated regions. This reduces intrapulmonary shunting and may improve systemic arterial oxygenation. Nitric oxide is a chemical mediator fundamental in the maintenance of adequate tissue perfusion and effective cardiovascular function. The use of nitrates is well established as pharmacological agents but it is only recently that it has been recognized that they act as a source of nitric oxide (PMID: 16966108, 8752507, 17181668, 16005189). Nitric oxide is used as a food additive (EAFUS: Everything Added to Food in the United States).",False,https://orcid.org/0000-0002-0736-9199 -26339812,Methylprednisolone treats alcoholic hepatitis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats alcoholic hepatitis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True, -8427466,Methylprednisolone treats sinusitis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats sinusitis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0000-0001-5889-4463 -11720471,Methylprednisolone related to systemic lupus erythematosus,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to systemic lupus erythematosus supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/systemic_lupus_erythematosus -8330909,Methylprednisolone affects systemic lupus erythematosus,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone affects systemic lupus erythematosus supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/systemic_lupus_erythematosus -8330903,Methylprednisolone treats systemic lupus erythematosus,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats systemic lupus erythematosus supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/systemic_lupus_erythematosus -11882768,Methylprednisolone treats Cognitive impairment,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats Cognitive impairment supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0009-0006-4530-3154 -23934495,Methylprednisolone prevents Cognitive impairment,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone prevents Cognitive impairment supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,https://orcid.org/0009-0006-4530-3154 -20342058,Methylprednisolone related to chronic progressive multiple sclerosis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to chronic progressive multiple sclerosis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True, -7905007,Methylprednisolone treats chronic progressive multiple sclerosis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats chronic progressive multiple sclerosis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True, -26050805,Methylprednisolone related to ankylosing spondylitis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to ankylosing spondylitis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/ankylosing_spondylitis -25738014,Methylprednisolone treats ankylosing spondylitis,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats ankylosing spondylitis supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/ankylosing_spondylitis -18938435,Methylprednisolone related to graft versus host disease,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to graft versus host disease supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,PMID:31466596 -30359098,Nitric oxide treats Sepsis,1829,"The biologically active molecule nitric oxide (NO) is a simple, membrane-permeable gas with unique chemistry. It is formed by the conversion of L-arginine to L-citrulline, with the release of NO. The enzymatic oxidation of L-arginine to L-citrulline takes place in the presence of oxygen and NADPH using flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), heme, thiol, and tetrahydrobiopterin as cofactors. The enzyme responsible for the generation of NO is nitric oxide synthase (E.C. 1.7.99.7; NOS). Three NOS isoforms have been described and shown to be encoded on three distinct genes: neuronal NOS (nNOS, NOS type I), inducible NOS (NOS type II), and endothelial NOS (eNOS, NOS type III). Two of them are constitutively expressed and dependent on the presence of calcium ions and calmodulin to function (nNOS and eNOS), while iNOS is considered non-constitutive and calcium-independent. However, experience has shown that constitutive expression of nNOS and eNOS is not as rigid as previously thought (i.e. either present or absent), but can be dynamically controlled during development and in response to injury. Functionally, NO may act as a hormone, neurotransmitter, paracrine messenger, mediator, cytoprotective molecule, and cytotoxic molecule. NO has multiple cellular molecular targets. It influences the activity of transcription factors, modulates upstream signaling cascades, mRNA stability and translation, and processes the primary gene products. In the brain, many processes are linked to NO. NO activates its receptor, soluble guanylate cyclase by binding to it. The stimulation of this enzyme leads to increased synthesis of the second messenger, cGMP, which in turn activates cGMP-dependent kinases in target cells. NO exerts a strong influence on glutamatergic neurotransmission by directly interacting with the N-methyl-D-aspartate (NMDA) receptor. Neuronal NOS is connected to NMDA receptors (see below) and sharply increases NO production following activation of this receptor. Thus, the level of endogenously produced NO around NMDA synapses reflects the activity of glutamate-mediated neurotransmission. However, there is recent evidence showing that non-NMDA glutamate receptors (i.e. AMPA and type I metabotropic receptors) also contribute to NO generation. Besides its influence on glutamate, NO is known to have effects on the storage, uptake and/or release of most other neurotransmitters in the CNS (acetylcholine, dopamine, noradrenaline, GABA, taurine, and glycine) as well as of certain neuropeptides. Finally, since NO is a highly diffusible molecule, it may reach extrasynaptic receptors at target cell membranes that are some distance away from the place of NO synthesis. NO is thus capable of mediating both synaptic and nonsynaptic communication processes. NO is a potent vasodilator (a major endogenous regulator of vascular tone), and an important endothelium-dependent relaxing factor. NO is synthesized by NO synthases (NOS) and NOS are inhibited by asymmetrical dimethylarginine (ADMA). ADMA is metabolized by dimethylarginine dimethylaminohydrolase (DDAH) and excreted in the kidneys. Lower ADMA levels in pregnant women compared to non-pregnant controls suggest that ADMA has a role in vascular dilatation and blood pressure changes. Several studies show an increase in ADMA levels in pregnancies complicated with preeclampsia. Elevated ADMA levels in preeclampsia are seen before clinical symptoms have developed; these findings suggest that ADMA has a role in the pathogenesis of preeclampsia. In some pulmonary hypertensive states such as ARDS, the production of endogenous NO may be impaired. Nitric oxide inhalation selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because NO is inactivated by rapidly binding to hemoglobin. In an injured lung with pulmonary hypertension, inhaled NO produces local vasodilation of well-ventilated lung units and may ""steal"" blood flow away from unventilated regions. This reduces intrapulmonary shunting and may improve systemic arterial oxygenation. Nitric oxide is a chemical mediator fundamental in the maintenance of adequate tissue perfusion and effective cardiovascular function. The use of nitrates is well established as pharmacological agents but it is only recently that it has been recognized that they act as a source of nitric oxide (PMID: 16966108, 8752507, 17181668, 16005189). Nitric oxide is used as a food additive (EAFUS: Everything Added to Food in the United States).","Is the triple Nitric oxide treats Sepsis supported by the sentence The biologically active molecule nitric oxide (NO) is a simple, membrane-permeable gas with unique chemistry. It is formed by the conversion of L-arginine to L-citrulline, with the release of NO. The enzymatic oxidation of L-arginine to L-citrulline takes place in the presence of oxygen and NADPH using flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), heme, thiol, and tetrahydrobiopterin as cofactors. The enzyme responsible for the generation of NO is nitric oxide synthase (E.C. 1.7.99.7; NOS). Three NOS isoforms have been described and shown to be encoded on three distinct genes: neuronal NOS (nNOS, NOS type I), inducible NOS (NOS type II), and endothelial NOS (eNOS, NOS type III). Two of them are constitutively expressed and dependent on the presence of calcium ions and calmodulin to function (nNOS and eNOS), while iNOS is considered non-constitutive and calcium-independent. However, experience has shown that constitutive expression of nNOS and eNOS is not as rigid as previously thought (i.e. either present or absent), but can be dynamically controlled during development and in response to injury. Functionally, NO may act as a hormone, neurotransmitter, paracrine messenger, mediator, cytoprotective molecule, and cytotoxic molecule. NO has multiple cellular molecular targets. It influences the activity of transcription factors, modulates upstream signaling cascades, mRNA stability and translation, and processes the primary gene products. In the brain, many processes are linked to NO. NO activates its receptor, soluble guanylate cyclase by binding to it. The stimulation of this enzyme leads to increased synthesis of the second messenger, cGMP, which in turn activates cGMP-dependent kinases in target cells. NO exerts a strong influence on glutamatergic neurotransmission by directly interacting with the N-methyl-D-aspartate (NMDA) receptor. Neuronal NOS is connected to NMDA receptors (see below) and sharply increases NO production following activation of this receptor. Thus, the level of endogenously produced NO around NMDA synapses reflects the activity of glutamate-mediated neurotransmission. However, there is recent evidence showing that non-NMDA glutamate receptors (i.e. AMPA and type I metabotropic receptors) also contribute to NO generation. Besides its influence on glutamate, NO is known to have effects on the storage, uptake and/or release of most other neurotransmitters in the CNS (acetylcholine, dopamine, noradrenaline, GABA, taurine, and glycine) as well as of certain neuropeptides. Finally, since NO is a highly diffusible molecule, it may reach extrasynaptic receptors at target cell membranes that are some distance away from the place of NO synthesis. NO is thus capable of mediating both synaptic and nonsynaptic communication processes. NO is a potent vasodilator (a major endogenous regulator of vascular tone), and an important endothelium-dependent relaxing factor. NO is synthesized by NO synthases (NOS) and NOS are inhibited by asymmetrical dimethylarginine (ADMA). ADMA is metabolized by dimethylarginine dimethylaminohydrolase (DDAH) and excreted in the kidneys. Lower ADMA levels in pregnant women compared to non-pregnant controls suggest that ADMA has a role in vascular dilatation and blood pressure changes. Several studies show an increase in ADMA levels in pregnancies complicated with preeclampsia. Elevated ADMA levels in preeclampsia are seen before clinical symptoms have developed; these findings suggest that ADMA has a role in the pathogenesis of preeclampsia. In some pulmonary hypertensive states such as ARDS, the production of endogenous NO may be impaired. Nitric oxide inhalation selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because NO is inactivated by rapidly binding to hemoglobin. In an injured lung with pulmonary hypertension, inhaled NO produces local vasodilation of well-ventilated lung units and may ""steal"" blood flow away from unventilated regions. This reduces intrapulmonary shunting and may improve systemic arterial oxygenation. Nitric oxide is a chemical mediator fundamental in the maintenance of adequate tissue perfusion and effective cardiovascular function. The use of nitrates is well established as pharmacological agents but it is only recently that it has been recognized that they act as a source of nitric oxide (PMID: 16966108, 8752507, 17181668, 16005189). Nitric oxide is used as a food additive (EAFUS: Everything Added to Food in the United States).",False,https://orcid.org/0000-0002-0736-9199 -10289517,Methylprednisolone treats graft versus host disease,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone treats graft versus host disease supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,PMID:31466596 -8291272,Methylprednisolone prevents graft versus host disease,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone prevents graft versus host disease supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,PMID:31466596 -25328503,Methylprednisolone related to Meniere disease,570,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.","Is the triple Methylprednisolone related to Meniere disease supported by the sentence Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",True,http://en.wikipedia.org/wiki/m%c3%a9ni%c3%a8re%27s_disease -30347544,Nitric oxide treats acute kidney failure,1829,"The biologically active molecule nitric oxide (NO) is a simple, membrane-permeable gas with unique chemistry. It is formed by the conversion of L-arginine to L-citrulline, with the release of NO. The enzymatic oxidation of L-arginine to L-citrulline takes place in the presence of oxygen and NADPH using flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), heme, thiol, and tetrahydrobiopterin as cofactors. The enzyme responsible for the generation of NO is nitric oxide synthase (E.C. 1.7.99.7; NOS). Three NOS isoforms have been described and shown to be encoded on three distinct genes: neuronal NOS (nNOS, NOS type I), inducible NOS (NOS type II), and endothelial NOS (eNOS, NOS type III). Two of them are constitutively expressed and dependent on the presence of calcium ions and calmodulin to function (nNOS and eNOS), while iNOS is considered non-constitutive and calcium-independent. However, experience has shown that constitutive expression of nNOS and eNOS is not as rigid as previously thought (i.e. either present or absent), but can be dynamically controlled during development and in response to injury. Functionally, NO may act as a hormone, neurotransmitter, paracrine messenger, mediator, cytoprotective molecule, and cytotoxic molecule. NO has multiple cellular molecular targets. It influences the activity of transcription factors, modulates upstream signaling cascades, mRNA stability and translation, and processes the primary gene products. In the brain, many processes are linked to NO. NO activates its receptor, soluble guanylate cyclase by binding to it. The stimulation of this enzyme leads to increased synthesis of the second messenger, cGMP, which in turn activates cGMP-dependent kinases in target cells. NO exerts a strong influence on glutamatergic neurotransmission by directly interacting with the N-methyl-D-aspartate (NMDA) receptor. Neuronal NOS is connected to NMDA receptors (see below) and sharply increases NO production following activation of this receptor. Thus, the level of endogenously produced NO around NMDA synapses reflects the activity of glutamate-mediated neurotransmission. However, there is recent evidence showing that non-NMDA glutamate receptors (i.e. AMPA and type I metabotropic receptors) also contribute to NO generation. Besides its influence on glutamate, NO is known to have effects on the storage, uptake and/or release of most other neurotransmitters in the CNS (acetylcholine, dopamine, noradrenaline, GABA, taurine, and glycine) as well as of certain neuropeptides. Finally, since NO is a highly diffusible molecule, it may reach extrasynaptic receptors at target cell membranes that are some distance away from the place of NO synthesis. NO is thus capable of mediating both synaptic and nonsynaptic communication processes. NO is a potent vasodilator (a major endogenous regulator of vascular tone), and an important endothelium-dependent relaxing factor. NO is synthesized by NO synthases (NOS) and NOS are inhibited by asymmetrical dimethylarginine (ADMA). ADMA is metabolized by dimethylarginine dimethylaminohydrolase (DDAH) and excreted in the kidneys. Lower ADMA levels in pregnant women compared to non-pregnant controls suggest that ADMA has a role in vascular dilatation and blood pressure changes. Several studies show an increase in ADMA levels in pregnancies complicated with preeclampsia. Elevated ADMA levels in preeclampsia are seen before clinical symptoms have developed; these findings suggest that ADMA has a role in the pathogenesis of preeclampsia. In some pulmonary hypertensive states such as ARDS, the production of endogenous NO may be impaired. Nitric oxide inhalation selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because NO is inactivated by rapidly binding to hemoglobin. In an injured lung with pulmonary hypertension, inhaled NO produces local vasodilation of well-ventilated lung units and may ""steal"" blood flow away from unventilated regions. This reduces intrapulmonary shunting and may improve systemic arterial oxygenation. Nitric oxide is a chemical mediator fundamental in the maintenance of adequate tissue perfusion and effective cardiovascular function. The use of nitrates is well established as pharmacological agents but it is only recently that it has been recognized that they act as a source of nitric oxide (PMID: 16966108, 8752507, 17181668, 16005189). Nitric oxide is used as a food additive (EAFUS: Everything Added to Food in the United States).","Is the triple Nitric oxide treats acute kidney failure supported by the sentence The biologically active molecule nitric oxide (NO) is a simple, membrane-permeable gas with unique chemistry. It is formed by the conversion of L-arginine to L-citrulline, with the release of NO. The enzymatic oxidation of L-arginine to L-citrulline takes place in the presence of oxygen and NADPH using flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), heme, thiol, and tetrahydrobiopterin as cofactors. The enzyme responsible for the generation of NO is nitric oxide synthase (E.C. 1.7.99.7; NOS). Three NOS isoforms have been described and shown to be encoded on three distinct genes: neuronal NOS (nNOS, NOS type I), inducible NOS (NOS type II), and endothelial NOS (eNOS, NOS type III). Two of them are constitutively expressed and dependent on the presence of calcium ions and calmodulin to function (nNOS and eNOS), while iNOS is considered non-constitutive and calcium-independent. However, experience has shown that constitutive expression of nNOS and eNOS is not as rigid as previously thought (i.e. either present or absent), but can be dynamically controlled during development and in response to injury. Functionally, NO may act as a hormone, neurotransmitter, paracrine messenger, mediator, cytoprotective molecule, and cytotoxic molecule. NO has multiple cellular molecular targets. It influences the activity of transcription factors, modulates upstream signaling cascades, mRNA stability and translation, and processes the primary gene products. In the brain, many processes are linked to NO. NO activates its receptor, soluble guanylate cyclase by binding to it. The stimulation of this enzyme leads to increased synthesis of the second messenger, cGMP, which in turn activates cGMP-dependent kinases in target cells. NO exerts a strong influence on glutamatergic neurotransmission by directly interacting with the N-methyl-D-aspartate (NMDA) receptor. Neuronal NOS is connected to NMDA receptors (see below) and sharply increases NO production following activation of this receptor. Thus, the level of endogenously produced NO around NMDA synapses reflects the activity of glutamate-mediated neurotransmission. However, there is recent evidence showing that non-NMDA glutamate receptors (i.e. AMPA and type I metabotropic receptors) also contribute to NO generation. Besides its influence on glutamate, NO is known to have effects on the storage, uptake and/or release of most other neurotransmitters in the CNS (acetylcholine, dopamine, noradrenaline, GABA, taurine, and glycine) as well as of certain neuropeptides. Finally, since NO is a highly diffusible molecule, it may reach extrasynaptic receptors at target cell membranes that are some distance away from the place of NO synthesis. NO is thus capable of mediating both synaptic and nonsynaptic communication processes. NO is a potent vasodilator (a major endogenous regulator of vascular tone), and an important endothelium-dependent relaxing factor. NO is synthesized by NO synthases (NOS) and NOS are inhibited by asymmetrical dimethylarginine (ADMA). ADMA is metabolized by dimethylarginine dimethylaminohydrolase (DDAH) and excreted in the kidneys. Lower ADMA levels in pregnant women compared to non-pregnant controls suggest that ADMA has a role in vascular dilatation and blood pressure changes. Several studies show an increase in ADMA levels in pregnancies complicated with preeclampsia. Elevated ADMA levels in preeclampsia are seen before clinical symptoms have developed; these findings suggest that ADMA has a role in the pathogenesis of preeclampsia. In some pulmonary hypertensive states such as ARDS, the production of endogenous NO may be impaired. Nitric oxide inhalation selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because NO is inactivated by rapidly binding to hemoglobin. In an injured lung with pulmonary hypertension, inhaled NO produces local vasodilation of well-ventilated lung units and may ""steal"" blood flow away from unventilated regions. This reduces intrapulmonary shunting and may improve systemic arterial oxygenation. Nitric oxide is a chemical mediator fundamental in the maintenance of adequate tissue perfusion and effective cardiovascular function. The use of nitrates is well established as pharmacological agents but it is only recently that it has been recognized that they act as a source of nitric oxide (PMID: 16966108, 8752507, 17181668, 16005189). Nitric oxide is used as a food additive (EAFUS: Everything Added to Food in the United States).",False,https://orcid.org/0000-0001-5208-3432 -30347482,Nitric oxide treats Inflammation,1829,"The biologically active molecule nitric oxide (NO) is a simple, membrane-permeable gas with unique chemistry. It is formed by the conversion of L-arginine to L-citrulline, with the release of NO. The enzymatic oxidation of L-arginine to L-citrulline takes place in the presence of oxygen and NADPH using flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), heme, thiol, and tetrahydrobiopterin as cofactors. The enzyme responsible for the generation of NO is nitric oxide synthase (E.C. 1.7.99.7; NOS). Three NOS isoforms have been described and shown to be encoded on three distinct genes: neuronal NOS (nNOS, NOS type I), inducible NOS (NOS type II), and endothelial NOS (eNOS, NOS type III). Two of them are constitutively expressed and dependent on the presence of calcium ions and calmodulin to function (nNOS and eNOS), while iNOS is considered non-constitutive and calcium-independent. However, experience has shown that constitutive expression of nNOS and eNOS is not as rigid as previously thought (i.e. either present or absent), but can be dynamically controlled during development and in response to injury. Functionally, NO may act as a hormone, neurotransmitter, paracrine messenger, mediator, cytoprotective molecule, and cytotoxic molecule. NO has multiple cellular molecular targets. It influences the activity of transcription factors, modulates upstream signaling cascades, mRNA stability and translation, and processes the primary gene products. In the brain, many processes are linked to NO. NO activates its receptor, soluble guanylate cyclase by binding to it. The stimulation of this enzyme leads to increased synthesis of the second messenger, cGMP, which in turn activates cGMP-dependent kinases in target cells. NO exerts a strong influence on glutamatergic neurotransmission by directly interacting with the N-methyl-D-aspartate (NMDA) receptor. Neuronal NOS is connected to NMDA receptors (see below) and sharply increases NO production following activation of this receptor. Thus, the level of endogenously produced NO around NMDA synapses reflects the activity of glutamate-mediated neurotransmission. However, there is recent evidence showing that non-NMDA glutamate receptors (i.e. AMPA and type I metabotropic receptors) also contribute to NO generation. Besides its influence on glutamate, NO is known to have effects on the storage, uptake and/or release of most other neurotransmitters in the CNS (acetylcholine, dopamine, noradrenaline, GABA, taurine, and glycine) as well as of certain neuropeptides. Finally, since NO is a highly diffusible molecule, it may reach extrasynaptic receptors at target cell membranes that are some distance away from the place of NO synthesis. NO is thus capable of mediating both synaptic and nonsynaptic communication processes. NO is a potent vasodilator (a major endogenous regulator of vascular tone), and an important endothelium-dependent relaxing factor. NO is synthesized by NO synthases (NOS) and NOS are inhibited by asymmetrical dimethylarginine (ADMA). ADMA is metabolized by dimethylarginine dimethylaminohydrolase (DDAH) and excreted in the kidneys. Lower ADMA levels in pregnant women compared to non-pregnant controls suggest that ADMA has a role in vascular dilatation and blood pressure changes. Several studies show an increase in ADMA levels in pregnancies complicated with preeclampsia. Elevated ADMA levels in preeclampsia are seen before clinical symptoms have developed; these findings suggest that ADMA has a role in the pathogenesis of preeclampsia. In some pulmonary hypertensive states such as ARDS, the production of endogenous NO may be impaired. Nitric oxide inhalation selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because NO is inactivated by rapidly binding to hemoglobin. In an injured lung with pulmonary hypertension, inhaled NO produces local vasodilation of well-ventilated lung units and may ""steal"" blood flow away from unventilated regions. This reduces intrapulmonary shunting and may improve systemic arterial oxygenation. Nitric oxide is a chemical mediator fundamental in the maintenance of adequate tissue perfusion and effective cardiovascular function. The use of nitrates is well established as pharmacological agents but it is only recently that it has been recognized that they act as a source of nitric oxide (PMID: 16966108, 8752507, 17181668, 16005189). Nitric oxide is used as a food additive (EAFUS: Everything Added to Food in the United States).","Is the triple Nitric oxide treats Inflammation supported by the sentence The biologically active molecule nitric oxide (NO) is a simple, membrane-permeable gas with unique chemistry. It is formed by the conversion of L-arginine to L-citrulline, with the release of NO. The enzymatic oxidation of L-arginine to L-citrulline takes place in the presence of oxygen and NADPH using flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), heme, thiol, and tetrahydrobiopterin as cofactors. The enzyme responsible for the generation of NO is nitric oxide synthase (E.C. 1.7.99.7; NOS). Three NOS isoforms have been described and shown to be encoded on three distinct genes: neuronal NOS (nNOS, NOS type I), inducible NOS (NOS type II), and endothelial NOS (eNOS, NOS type III). Two of them are constitutively expressed and dependent on the presence of calcium ions and calmodulin to function (nNOS and eNOS), while iNOS is considered non-constitutive and calcium-independent. However, experience has shown that constitutive expression of nNOS and eNOS is not as rigid as previously thought (i.e. either present or absent), but can be dynamically controlled during development and in response to injury. Functionally, NO may act as a hormone, neurotransmitter, paracrine messenger, mediator, cytoprotective molecule, and cytotoxic molecule. NO has multiple cellular molecular targets. It influences the activity of transcription factors, modulates upstream signaling cascades, mRNA stability and translation, and processes the primary gene products. In the brain, many processes are linked to NO. NO activates its receptor, soluble guanylate cyclase by binding to it. The stimulation of this enzyme leads to increased synthesis of the second messenger, cGMP, which in turn activates cGMP-dependent kinases in target cells. NO exerts a strong influence on glutamatergic neurotransmission by directly interacting with the N-methyl-D-aspartate (NMDA) receptor. Neuronal NOS is connected to NMDA receptors (see below) and sharply increases NO production following activation of this receptor. Thus, the level of endogenously produced NO around NMDA synapses reflects the activity of glutamate-mediated neurotransmission. However, there is recent evidence showing that non-NMDA glutamate receptors (i.e. AMPA and type I metabotropic receptors) also contribute to NO generation. Besides its influence on glutamate, NO is known to have effects on the storage, uptake and/or release of most other neurotransmitters in the CNS (acetylcholine, dopamine, noradrenaline, GABA, taurine, and glycine) as well as of certain neuropeptides. Finally, since NO is a highly diffusible molecule, it may reach extrasynaptic receptors at target cell membranes that are some distance away from the place of NO synthesis. NO is thus capable of mediating both synaptic and nonsynaptic communication processes. NO is a potent vasodilator (a major endogenous regulator of vascular tone), and an important endothelium-dependent relaxing factor. NO is synthesized by NO synthases (NOS) and NOS are inhibited by asymmetrical dimethylarginine (ADMA). ADMA is metabolized by dimethylarginine dimethylaminohydrolase (DDAH) and excreted in the kidneys. Lower ADMA levels in pregnant women compared to non-pregnant controls suggest that ADMA has a role in vascular dilatation and blood pressure changes. Several studies show an increase in ADMA levels in pregnancies complicated with preeclampsia. Elevated ADMA levels in preeclampsia are seen before clinical symptoms have developed; these findings suggest that ADMA has a role in the pathogenesis of preeclampsia. In some pulmonary hypertensive states such as ARDS, the production of endogenous NO may be impaired. Nitric oxide inhalation selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because NO is inactivated by rapidly binding to hemoglobin. In an injured lung with pulmonary hypertension, inhaled NO produces local vasodilation of well-ventilated lung units and may ""steal"" blood flow away from unventilated regions. This reduces intrapulmonary shunting and may improve systemic arterial oxygenation. Nitric oxide is a chemical mediator fundamental in the maintenance of adequate tissue perfusion and effective cardiovascular function. The use of nitrates is well established as pharmacological agents but it is only recently that it has been recognized that they act as a source of nitric oxide (PMID: 16966108, 8752507, 17181668, 16005189). Nitric oxide is used as a food additive (EAFUS: Everything Added to Food in the United States).",False,ISBN:0198506732 -8153267,Cefotaxime treats bacterial infectious disease,576,"A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefotaxime treats bacterial infectious disease supported by the sentence A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/pathogenic_bacteria -18672205,Cefotaxime affects peritonitis,576,"A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefotaxime affects peritonitis supported by the sentence A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,http://www.merck.com/mmpe/sec02/ch011/ch011b.html#sec02-ch011-ch011b-402 -15119078,Cefotaxime treats peritonitis,576,"A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefotaxime treats peritonitis supported by the sentence A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,http://www.merck.com/mmpe/sec02/ch011/ch011b.html#sec02-ch011-ch011b-402 -12905337,Cefotaxime related to Sepsis,576,"A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefotaxime related to Sepsis supported by the sentence A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -23922029,Cefotaxime affects Sepsis,576,"A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefotaxime affects Sepsis supported by the sentence A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -11176033,Cefotaxime treats Sepsis,576,"A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefotaxime treats Sepsis supported by the sentence A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -15853591,Cefotaxime prevents Sepsis,576,"A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefotaxime prevents Sepsis supported by the sentence A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -16097513,Cefotaxime treats osteomyelitis,576,"A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Cefotaxime treats osteomyelitis supported by the sentence A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -45055281,Leurocristine treats small cell lung carcinoma,1860,"A natural alkaloid isolated from the plant Vinca rosea Linn. Vincristine binds irreversibly to microtubules and spindle proteins in S phase of the cell cycle and interferes with the formation of the mitotic spindle, thereby arresting tumor cells in metaphase. This agent also depolymerizes microtubules and may also interfere with amino acid, cyclic AMP, and glutathione metabolism; calmodulin-dependent Ca++ -transport ATPase activity; cellular respiration; and nucleic acid and lipid biosynthesis. (NCI04); An antitumor alkaloid isolated from VINCA ROSEA. (Merck, 11th ed.); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Leurocristine treats small cell lung carcinoma supported by the sentence A natural alkaloid isolated from the plant Vinca rosea Linn. Vincristine binds irreversibly to microtubules and spindle proteins in S phase of the cell cycle and interferes with the formation of the mitotic spindle, thereby arresting tumor cells in metaphase. This agent also depolymerizes microtubules and may also interfere with amino acid, cyclic AMP, and glutathione metabolism; calmodulin-dependent Ca++ -transport ATPase activity; cellular respiration; and nucleic acid and lipid biosynthesis. (NCI04); An antitumor alkaloid isolated from VINCA ROSEA. (Merck, 11th ed.); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-0736-9199 -26980543,Ceftriaxone treats Lyme disease,578,"The sodium salt form of ceftriaxone, a beta-lactam, third-generation cephalosporin antibiotic with bactericidal activity. Ceftriaxone binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to the second and first generation cephalosporins, ceftriaxone is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftriaxone also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS). Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C817"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C817"" NCI Thesaurus); The sodium salt form of ceftriaxone, a beta-lactam, third-generation cephalosporin antibiotic with bactericidal activity. Ceftriaxone binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to the second and first generation cephalosporins, ceftriaxone is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftriaxone also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS).; A broad-spectrum cephalosporin antibiotic and cefotaxime derivative with a very long half-life and high penetrability to meninges, eyes and inner ears.","Is the triple Ceftriaxone treats Lyme disease supported by the sentence The sodium salt form of ceftriaxone, a beta-lactam, third-generation cephalosporin antibiotic with bactericidal activity. Ceftriaxone binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to the second and first generation cephalosporins, ceftriaxone is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftriaxone also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS). Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C817"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C817"" NCI Thesaurus); The sodium salt form of ceftriaxone, a beta-lactam, third-generation cephalosporin antibiotic with bactericidal activity. Ceftriaxone binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to the second and first generation cephalosporins, ceftriaxone is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftriaxone also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS).; A broad-spectrum cephalosporin antibiotic and cefotaxime derivative with a very long half-life and high penetrability to meninges, eyes and inner ears.",True,http://www.cdc.gov/lyme/transmission/index.htm -26401802,Ceftriaxone treats Sepsis,578,"The sodium salt form of ceftriaxone, a beta-lactam, third-generation cephalosporin antibiotic with bactericidal activity. Ceftriaxone binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to the second and first generation cephalosporins, ceftriaxone is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftriaxone also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS). Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C817"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C817"" NCI Thesaurus); The sodium salt form of ceftriaxone, a beta-lactam, third-generation cephalosporin antibiotic with bactericidal activity. Ceftriaxone binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to the second and first generation cephalosporins, ceftriaxone is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftriaxone also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS).; A broad-spectrum cephalosporin antibiotic and cefotaxime derivative with a very long half-life and high penetrability to meninges, eyes and inner ears.","Is the triple Ceftriaxone treats Sepsis supported by the sentence The sodium salt form of ceftriaxone, a beta-lactam, third-generation cephalosporin antibiotic with bactericidal activity. Ceftriaxone binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to the second and first generation cephalosporins, ceftriaxone is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftriaxone also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS). Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C817"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C817"" NCI Thesaurus); The sodium salt form of ceftriaxone, a beta-lactam, third-generation cephalosporin antibiotic with bactericidal activity. Ceftriaxone binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to the second and first generation cephalosporins, ceftriaxone is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftriaxone also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS).; A broad-spectrum cephalosporin antibiotic and cefotaxime derivative with a very long half-life and high penetrability to meninges, eyes and inner ears.",True,https://orcid.org/0000-0002-0736-9199 -18413392,Ceftriaxone treats bacterial pneumonia,578,"The sodium salt form of ceftriaxone, a beta-lactam, third-generation cephalosporin antibiotic with bactericidal activity. Ceftriaxone binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to the second and first generation cephalosporins, ceftriaxone is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftriaxone also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS). Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C817"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C817"" NCI Thesaurus); The sodium salt form of ceftriaxone, a beta-lactam, third-generation cephalosporin antibiotic with bactericidal activity. Ceftriaxone binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to the second and first generation cephalosporins, ceftriaxone is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftriaxone also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS).; A broad-spectrum cephalosporin antibiotic and cefotaxime derivative with a very long half-life and high penetrability to meninges, eyes and inner ears.","Is the triple Ceftriaxone treats bacterial pneumonia supported by the sentence The sodium salt form of ceftriaxone, a beta-lactam, third-generation cephalosporin antibiotic with bactericidal activity. Ceftriaxone binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to the second and first generation cephalosporins, ceftriaxone is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftriaxone also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS). Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C817"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C817"" NCI Thesaurus); The sodium salt form of ceftriaxone, a beta-lactam, third-generation cephalosporin antibiotic with bactericidal activity. Ceftriaxone binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to the second and first generation cephalosporins, ceftriaxone is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftriaxone also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS).; A broad-spectrum cephalosporin antibiotic and cefotaxime derivative with a very long half-life and high penetrability to meninges, eyes and inner ears.",True,http://en.wikipedia.org/wiki/bacterial_pneumonia -45055265,Leurocristine treats acute lymphoblastic leukemia,1860,"A natural alkaloid isolated from the plant Vinca rosea Linn. Vincristine binds irreversibly to microtubules and spindle proteins in S phase of the cell cycle and interferes with the formation of the mitotic spindle, thereby arresting tumor cells in metaphase. This agent also depolymerizes microtubules and may also interfere with amino acid, cyclic AMP, and glutathione metabolism; calmodulin-dependent Ca++ -transport ATPase activity; cellular respiration; and nucleic acid and lipid biosynthesis. (NCI04); An antitumor alkaloid isolated from VINCA ROSEA. (Merck, 11th ed.); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Leurocristine treats acute lymphoblastic leukemia supported by the sentence A natural alkaloid isolated from the plant Vinca rosea Linn. Vincristine binds irreversibly to microtubules and spindle proteins in S phase of the cell cycle and interferes with the formation of the mitotic spindle, thereby arresting tumor cells in metaphase. This agent also depolymerizes microtubules and may also interfere with amino acid, cyclic AMP, and glutathione metabolism; calmodulin-dependent Ca++ -transport ATPase activity; cellular respiration; and nucleic acid and lipid biosynthesis. (NCI04); An antitumor alkaloid isolated from VINCA ROSEA. (Merck, 11th ed.); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,http://www.cancer.gov/dictionary?cdrid=46332 -25810060,Gefarnate treats gastric ulcer,589,A water insoluble terpene fatty acid used in the treatment of gastrointestinal ulcers; it facilitates the healing and function of mucosal tissue.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109,Is the triple Gefarnate treats gastric ulcer supported by the sentence A water insoluble terpene fatty acid used in the treatment of gastrointestinal ulcers; it facilitates the healing and function of mucosal tissue.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109,True,https://orcid.org/0000-0002-6601-2165 -25993651,Gefarnate disrupts gastric ulcer,589,A water insoluble terpene fatty acid used in the treatment of gastrointestinal ulcers; it facilitates the healing and function of mucosal tissue.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109,Is the triple Gefarnate disrupts gastric ulcer supported by the sentence A water insoluble terpene fatty acid used in the treatment of gastrointestinal ulcers; it facilitates the healing and function of mucosal tissue.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109,True,https://orcid.org/0000-0002-6601-2165 -24296137,Gefarnate related to duodenal ulcer,589,A water insoluble terpene fatty acid used in the treatment of gastrointestinal ulcers; it facilitates the healing and function of mucosal tissue.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109,Is the triple Gefarnate related to duodenal ulcer supported by the sentence A water insoluble terpene fatty acid used in the treatment of gastrointestinal ulcers; it facilitates the healing and function of mucosal tissue.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109,True,https://orcid.org/0000-0002-6601-2165 -25784688,Gefarnate treats duodenal ulcer,589,A water insoluble terpene fatty acid used in the treatment of gastrointestinal ulcers; it facilitates the healing and function of mucosal tissue.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109,Is the triple Gefarnate treats duodenal ulcer supported by the sentence A water insoluble terpene fatty acid used in the treatment of gastrointestinal ulcers; it facilitates the healing and function of mucosal tissue.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109,True,https://orcid.org/0000-0002-6601-2165 -19702373,Gefarnate treats peptic ulcer disease,589,A water insoluble terpene fatty acid used in the treatment of gastrointestinal ulcers; it facilitates the healing and function of mucosal tissue.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109,Is the triple Gefarnate treats peptic ulcer disease supported by the sentence A water insoluble terpene fatty acid used in the treatment of gastrointestinal ulcers; it facilitates the healing and function of mucosal tissue.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109,True,PMID:28242110 -22023951,Regadenoson treats coronary artery disorder,590,"An adenosine derivative and selective A2A adenosine receptor agonist with coronary vasodilating activity. Upon administration, regadenoson selectively binds to and activates the A2A adenosine receptor, which induces coronary vasodilation. This leads to an increase in coronary blood flow and enhances myocardial perfusion. Compared to adenosine, regadenoson has a longer half-life and shows higher selectivity towards the A2A adenosine receptor. This agent is a very weak agonist for the A1 adenosine receptor and has negligible affinity for the A2B and A3 adenosine receptors. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C74420"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C74420"" NCI Thesaurus); An adenosine derivative and selective A2A adenosine receptor agonist with coronary vasodilating activity. Upon administration, regadenoson selectively binds to and activates the A2A adenosine receptor, which induces coronary vasodilation. This leads to an increase in coronary blood flow and enhances myocardial perfusion. Compared to adenosine, regadenoson has a longer half-life and shows higher selectivity towards the A2A adenosine receptor. This agent is a very weak agonist for the A1 adenosine receptor and has negligible affinity for the A2B and A3 adenosine receptors.","Is the triple Regadenoson treats coronary artery disorder supported by the sentence An adenosine derivative and selective A2A adenosine receptor agonist with coronary vasodilating activity. Upon administration, regadenoson selectively binds to and activates the A2A adenosine receptor, which induces coronary vasodilation. This leads to an increase in coronary blood flow and enhances myocardial perfusion. Compared to adenosine, regadenoson has a longer half-life and shows higher selectivity towards the A2A adenosine receptor. This agent is a very weak agonist for the A1 adenosine receptor and has negligible affinity for the A2B and A3 adenosine receptors. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C74420"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C74420"" NCI Thesaurus); An adenosine derivative and selective A2A adenosine receptor agonist with coronary vasodilating activity. Upon administration, regadenoson selectively binds to and activates the A2A adenosine receptor, which induces coronary vasodilation. This leads to an increase in coronary blood flow and enhances myocardial perfusion. Compared to adenosine, regadenoson has a longer half-life and shows higher selectivity towards the A2A adenosine receptor. This agent is a very weak agonist for the A1 adenosine receptor and has negligible affinity for the A2B and A3 adenosine receptors.",True,PMID:31420554 -45035558,Diazoxide treats hyperinsulinism,1868,"A benzothiadiazine derivate with antihypertensive and hyperglycemic activities. Diazoxide increases membrane permeability to potassium ions in vascular smooth muscle, thereby stabilizing the membrane action potential and preventing vascular smooth muscle contraction; this results in peripheral vasodilatation and decreases in peripheral vascular resistance. This agent also inhibits insulin release by interacting with ATP-sensitive potassium channels of pancreatic islet beta-cells. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C428"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C428"" NCI Thesaurus); A benzothiadiazine derivate with antihypertensive and hyperglycemic activities. Diazoxide increases membrane permeability to potassium ions in vascular smooth muscle, thereby stabilizing the membrane action potential and preventing vascular smooth muscle contraction; this results in peripheral vasodilatation and decreases in peripheral vascular resistance. This agent also inhibits insulin release by interacting with ATP-sensitive potassium channels of pancreatic islet beta-cells.; A benzothiadiazine derivative that is a peripheral vasodilator used for hypertensive emergencies. It lacks diuretic effect, apparently because it lacks a sulfonamide group.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Diazoxide treats hyperinsulinism supported by the sentence A benzothiadiazine derivate with antihypertensive and hyperglycemic activities. Diazoxide increases membrane permeability to potassium ions in vascular smooth muscle, thereby stabilizing the membrane action potential and preventing vascular smooth muscle contraction; this results in peripheral vasodilatation and decreases in peripheral vascular resistance. This agent also inhibits insulin release by interacting with ATP-sensitive potassium channels of pancreatic islet beta-cells. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C428"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C428"" NCI Thesaurus); A benzothiadiazine derivate with antihypertensive and hyperglycemic activities. Diazoxide increases membrane permeability to potassium ions in vascular smooth muscle, thereby stabilizing the membrane action potential and preventing vascular smooth muscle contraction; this results in peripheral vasodilatation and decreases in peripheral vascular resistance. This agent also inhibits insulin release by interacting with ATP-sensitive potassium channels of pancreatic islet beta-cells.; A benzothiadiazine derivative that is a peripheral vasodilator used for hypertensive emergencies. It lacks diuretic effect, apparently because it lacks a sulfonamide group.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-6601-2165 -30646900,Diazoxide treats hyperinsulinism,1868,"A benzothiadiazine derivate with antihypertensive and hyperglycemic activities. Diazoxide increases membrane permeability to potassium ions in vascular smooth muscle, thereby stabilizing the membrane action potential and preventing vascular smooth muscle contraction; this results in peripheral vasodilatation and decreases in peripheral vascular resistance. This agent also inhibits insulin release by interacting with ATP-sensitive potassium channels of pancreatic islet beta-cells. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C428"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C428"" NCI Thesaurus); A benzothiadiazine derivate with antihypertensive and hyperglycemic activities. Diazoxide increases membrane permeability to potassium ions in vascular smooth muscle, thereby stabilizing the membrane action potential and preventing vascular smooth muscle contraction; this results in peripheral vasodilatation and decreases in peripheral vascular resistance. This agent also inhibits insulin release by interacting with ATP-sensitive potassium channels of pancreatic islet beta-cells.; A benzothiadiazine derivative that is a peripheral vasodilator used for hypertensive emergencies. It lacks diuretic effect, apparently because it lacks a sulfonamide group.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Diazoxide treats hyperinsulinism supported by the sentence A benzothiadiazine derivate with antihypertensive and hyperglycemic activities. Diazoxide increases membrane permeability to potassium ions in vascular smooth muscle, thereby stabilizing the membrane action potential and preventing vascular smooth muscle contraction; this results in peripheral vasodilatation and decreases in peripheral vascular resistance. This agent also inhibits insulin release by interacting with ATP-sensitive potassium channels of pancreatic islet beta-cells. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C428"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C428"" NCI Thesaurus); A benzothiadiazine derivate with antihypertensive and hyperglycemic activities. Diazoxide increases membrane permeability to potassium ions in vascular smooth muscle, thereby stabilizing the membrane action potential and preventing vascular smooth muscle contraction; this results in peripheral vasodilatation and decreases in peripheral vascular resistance. This agent also inhibits insulin release by interacting with ATP-sensitive potassium channels of pancreatic islet beta-cells.; A benzothiadiazine derivative that is a peripheral vasodilator used for hypertensive emergencies. It lacks diuretic effect, apparently because it lacks a sulfonamide group.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-6601-2165 -24669492,Neobiotic disrupts bacterial infectious disease,603,"A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Neobiotic disrupts bacterial infectious disease supported by the sentence A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/pathogenic_bacteria -26428369,Neobiotic prevents bacterial infectious disease,603,"A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Neobiotic prevents bacterial infectious disease supported by the sentence A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/pathogenic_bacteria -25624167,Neobiotic treats pneumonia,603,"A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Neobiotic treats pneumonia supported by the sentence A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/pneumonia -11022701,Neobiotic treats bacterial infectious disease with sepsis,603,"A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Neobiotic treats bacterial infectious disease with sepsis supported by the sentence A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,PMID:20421654 -20263460,Neobiotic affects neoplasm,603,"A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Neobiotic affects neoplasm supported by the sentence A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-6601-2165 -17119153,Neobiotic disrupts neoplasm,603,"A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Neobiotic disrupts neoplasm supported by the sentence A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-6601-2165 -17758516,Neobiotic related to Inflammation,603,"A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Neobiotic related to Inflammation supported by the sentence A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,ISBN:0198506732 -19744068,Neobiotic affects Inflammation,603,"A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Neobiotic affects Inflammation supported by the sentence A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,ISBN:0198506732 -45046945,Omeprazole treats duodenal ulcer,1894,"A benzimidazole with selective and irreversible proton pump inhibition activity. Omeprazole forms a stable disulfide bond with the sulfhydryl group of the hydrogen-potassium (H+ - K+) ATPase found on the secretory surface of parietal cells, thereby inhibiting the final transport of hydrogen ions (via exchange with potassium ions) into the gastric lumen and suppressing gastric acid secretion. This agent exhibits no anticholinergic activities and does not antagonize histamine H2 receptors. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C716"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C716"" NCI Thesaurus); A benzimidazole with selective and irreversible proton pump inhibition activity. Omeprazole forms a stable disulfide bond with the sulfhydryl group of the hydrogen-potassium (H+ - K+) ATPase found on the secretory surface of parietal cells, thereby inhibiting the final transport of hydrogen ions (via exchange with potassium ions) into the gastric lumen and suppressing gastric acid secretion. This agent exhibits no anticholinergic activities and does not antagonize histamine H2 receptors.; A 4-methoxy-3,5-dimethylpyridyl, 5-methoxybenzimidazole derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits an H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Omeprazole treats duodenal ulcer supported by the sentence A benzimidazole with selective and irreversible proton pump inhibition activity. Omeprazole forms a stable disulfide bond with the sulfhydryl group of the hydrogen-potassium (H+ - K+) ATPase found on the secretory surface of parietal cells, thereby inhibiting the final transport of hydrogen ions (via exchange with potassium ions) into the gastric lumen and suppressing gastric acid secretion. This agent exhibits no anticholinergic activities and does not antagonize histamine H2 receptors. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C716"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C716"" NCI Thesaurus); A benzimidazole with selective and irreversible proton pump inhibition activity. Omeprazole forms a stable disulfide bond with the sulfhydryl group of the hydrogen-potassium (H+ - K+) ATPase found on the secretory surface of parietal cells, thereby inhibiting the final transport of hydrogen ions (via exchange with potassium ions) into the gastric lumen and suppressing gastric acid secretion. This agent exhibits no anticholinergic activities and does not antagonize histamine H2 receptors.; A 4-methoxy-3,5-dimethylpyridyl, 5-methoxybenzimidazole derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits an H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-6601-2165 -30643846,Omeprazole treats duodenal ulcer,1894,"A benzimidazole with selective and irreversible proton pump inhibition activity. Omeprazole forms a stable disulfide bond with the sulfhydryl group of the hydrogen-potassium (H+ - K+) ATPase found on the secretory surface of parietal cells, thereby inhibiting the final transport of hydrogen ions (via exchange with potassium ions) into the gastric lumen and suppressing gastric acid secretion. This agent exhibits no anticholinergic activities and does not antagonize histamine H2 receptors. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C716"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C716"" NCI Thesaurus); A benzimidazole with selective and irreversible proton pump inhibition activity. Omeprazole forms a stable disulfide bond with the sulfhydryl group of the hydrogen-potassium (H+ - K+) ATPase found on the secretory surface of parietal cells, thereby inhibiting the final transport of hydrogen ions (via exchange with potassium ions) into the gastric lumen and suppressing gastric acid secretion. This agent exhibits no anticholinergic activities and does not antagonize histamine H2 receptors.; A 4-methoxy-3,5-dimethylpyridyl, 5-methoxybenzimidazole derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits an H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Omeprazole treats duodenal ulcer supported by the sentence A benzimidazole with selective and irreversible proton pump inhibition activity. Omeprazole forms a stable disulfide bond with the sulfhydryl group of the hydrogen-potassium (H+ - K+) ATPase found on the secretory surface of parietal cells, thereby inhibiting the final transport of hydrogen ions (via exchange with potassium ions) into the gastric lumen and suppressing gastric acid secretion. This agent exhibits no anticholinergic activities and does not antagonize histamine H2 receptors. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C716"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C716"" NCI Thesaurus); A benzimidazole with selective and irreversible proton pump inhibition activity. Omeprazole forms a stable disulfide bond with the sulfhydryl group of the hydrogen-potassium (H+ - K+) ATPase found on the secretory surface of parietal cells, thereby inhibiting the final transport of hydrogen ions (via exchange with potassium ions) into the gastric lumen and suppressing gastric acid secretion. This agent exhibits no anticholinergic activities and does not antagonize histamine H2 receptors.; A 4-methoxy-3,5-dimethylpyridyl, 5-methoxybenzimidazole derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits an H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-6601-2165 -24398401,BLINATUMOMAB treats B-cell chronic lymphocytic leukemia,612,"A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab posesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C62528"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C62528"" NCI Thesaurus); A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab possesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116","Is the triple BLINATUMOMAB treats B-cell chronic lymphocytic leukemia supported by the sentence A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab posesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C62528"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C62528"" NCI Thesaurus); A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab possesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116",True,http://www.cancer.gov/dictionary?cdrid=346545 -21947892,BLINATUMOMAB related to acute lymphoblastic leukemia,612,"A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab posesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C62528"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C62528"" NCI Thesaurus); A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab possesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116","Is the triple BLINATUMOMAB related to acute lymphoblastic leukemia supported by the sentence A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab posesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C62528"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C62528"" NCI Thesaurus); A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab possesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116",True,http://www.cancer.gov/dictionary?cdrid=46332 -21932754,BLINATUMOMAB treats acute lymphoblastic leukemia,612,"A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab posesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C62528"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C62528"" NCI Thesaurus); A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab possesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116","Is the triple BLINATUMOMAB treats acute lymphoblastic leukemia supported by the sentence A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab posesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C62528"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C62528"" NCI Thesaurus); A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab possesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116",True,http://www.cancer.gov/dictionary?cdrid=46332 -25579460,BLINATUMOMAB related to Precursor B-Cell Lymphoblastic Leukemia-Lymphoma,612,"A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab posesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C62528"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C62528"" NCI Thesaurus); A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab possesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116","Is the triple BLINATUMOMAB related to Precursor B-Cell Lymphoblastic Leukemia-Lymphoma supported by the sentence A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab posesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C62528"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C62528"" NCI Thesaurus); A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab possesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116",True, -23073290,BLINATUMOMAB treats Precursor B-Cell Lymphoblastic Leukemia-Lymphoma,612,"A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab posesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C62528"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C62528"" NCI Thesaurus); A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab possesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116","Is the triple BLINATUMOMAB treats Precursor B-Cell Lymphoblastic Leukemia-Lymphoma supported by the sentence A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab posesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C62528"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C62528"" NCI Thesaurus); A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab possesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116",True, -19572117,Ciprofloxacin related to DNA Gyrase,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin related to DNA Gyrase supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -17007621,Ciprofloxacin coexists with DNA Gyrase,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin coexists with DNA Gyrase supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -12385742,Ciprofloxacin coexists with DNA Gyrase,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin coexists with DNA Gyrase supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -8212496,Ciprofloxacin physically interacts with DNA Gyrase,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin physically interacts with DNA Gyrase supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -9387116,Ciprofloxacin physically interacts with DNA Gyrase,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin physically interacts with DNA Gyrase supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -18400322,Ciprofloxacin affects DNA Gyrase,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects DNA Gyrase supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -7781719,Ciprofloxacin affects DNA Gyrase,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects DNA Gyrase supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -19572117,Ciprofloxacin related to DNA Gyrase,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin related to DNA Gyrase supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -17007621,Ciprofloxacin coexists with DNA Gyrase,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin coexists with DNA Gyrase supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -12385742,Ciprofloxacin coexists with DNA Gyrase,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin coexists with DNA Gyrase supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -30357048,Esomeprazole treats preeclampsia,1903,"Esomeprazole is only found in individuals that have used or taken this drug. It is a highly effective inhibitor of gastric acid secretion used in the therapy of stomach ulcers and Zollinger-Ellison syndrome. The drug inhibits the H(+)-K(+)-ATPase (H(+)-K(+)-exchanging ATPase) in the proton pump of gastric parietal cells. [PubChem]Esomeprazole is a proton pump inhibitor that suppresses gastric acid secretion by specific inhibition of the H+/K+-ATPase in the gastric parietal cell. By acting specifically on the proton pump, Esomeprazole blocks the final step in acid production, thus reducing gastric acidity.","Is the triple Esomeprazole treats preeclampsia supported by the sentence Esomeprazole is only found in individuals that have used or taken this drug. It is a highly effective inhibitor of gastric acid secretion used in the therapy of stomach ulcers and Zollinger-Ellison syndrome. The drug inhibits the H(+)-K(+)-ATPase (H(+)-K(+)-exchanging ATPase) in the proton pump of gastric parietal cells. [PubChem]Esomeprazole is a proton pump inhibitor that suppresses gastric acid secretion by specific inhibition of the H+/K+-ATPase in the gastric parietal cell. By acting specifically on the proton pump, Esomeprazole blocks the final step in acid production, thus reducing gastric acidity.",False,PMID:24400024 -9387116,Ciprofloxacin physically interacts with DNA Gyrase,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin physically interacts with DNA Gyrase supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -18400322,Ciprofloxacin affects DNA Gyrase,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects DNA Gyrase supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -7781719,Ciprofloxacin affects DNA Gyrase,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects DNA Gyrase supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -30644298,Meperidine treats Pain,1922,"The hydrochloride salt of a synthetic piperidine ester with opioid analgesic activity. Meperidine mimics the actions of endogenous neuropeptides via opioid receptors such as the mu-opiiod receptor, thereby producing characteristic morphine-like effects including analgesia, euphoria, sedation, respiratory depression, miosis, bradycardia and physical dependence. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C635"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C635"" NCI Thesaurus); A synthetic piperidine ester with opioid analgesic activity. Meperidine mimics the actions of endogenous neuropeptides via opioid receptors, thereby producing the characteristic morphine-like effects on the mu-opioid receptor, including analgesia, euphoria, sedation, respiratory depression, miosis, bradycardia and physical dependence.; A narcotic analgesic that can be used for the relief of most types of moderate to severe pain, including postoperative pain and the pain of labor. Prolonged use may lead to dependence of the morphine type; withdrawal symptoms appear more rapidly than with morphine and are of shorter duration.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Meperidine treats Pain supported by the sentence The hydrochloride salt of a synthetic piperidine ester with opioid analgesic activity. Meperidine mimics the actions of endogenous neuropeptides via opioid receptors such as the mu-opiiod receptor, thereby producing characteristic morphine-like effects including analgesia, euphoria, sedation, respiratory depression, miosis, bradycardia and physical dependence. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C635"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C635"" NCI Thesaurus); A synthetic piperidine ester with opioid analgesic activity. Meperidine mimics the actions of endogenous neuropeptides via opioid receptors, thereby producing the characteristic morphine-like effects on the mu-opioid receptor, including analgesia, euphoria, sedation, respiratory depression, miosis, bradycardia and physical dependence.; A narcotic analgesic that can be used for the relief of most types of moderate to severe pain, including postoperative pain and the pain of labor. Prolonged use may lead to dependence of the morphine type; withdrawal symptoms appear more rapidly than with morphine and are of shorter duration.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0001-5208-3432 -11628762,Ciprofloxacin treats endophthalmitis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats endophthalmitis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/endophthalmitis -12292532,Ciprofloxacin prevents endophthalmitis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin prevents endophthalmitis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/endophthalmitis -8956825,Ciprofloxacin affects cystic fibrosis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects cystic fibrosis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://ghr.nlm.nih.gov/condition/cystic-fibrosis -7798648,Ciprofloxacin treats cystic fibrosis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats cystic fibrosis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://ghr.nlm.nih.gov/condition/cystic-fibrosis -30385777,Melatonin treats multiple sclerosis,1939,"Melatonin is a biogenic amine that is found in animals, plants and microbes. Aaron B. Lerner of Yale University is credited for naming the hormone and for defining its chemical structure in 1958. In mammals, melatonin is produced by the pineal gland. The pineal gland is small endocrine gland, about the size of a rice grain and shaped like a pine cone (hence the name), that is located in the center of the brain (rostro-dorsal to the superior colliculus) but outside the blood-brain barrier. The secretion of melatonin increases in darkness and decreases during exposure to light, thereby regulating the circadian rhythms of several biological functions, including the sleep-wake cycle. In particular, melatonin regulates the sleep-wake cycle by chemically causing drowsiness and. lowering the body temperature. Melatonin is also implicated in the regulation of mood,learning and memory, immune activity, dreaming, fertility and reproduction. Melatonin is also an effective antioxidant. Most of the actions of melatonin are mediated through the binding and activation of melatonin receptors. Individuals with autism spectrum disorders(ASD) may have lower than normal levels of melatonin. A 2008 study found that unaffected parents of individuals with ASD also have lower melatonin levels, and that the deficits. were associated with low activity of the ASMT gene, which encodes the last enzyme of melatonin synthesis. Reduced melatonin production has also been proposed as a likely factor in the significantly higher cancer rates in night workers.","Is the triple Melatonin treats multiple sclerosis supported by the sentence Melatonin is a biogenic amine that is found in animals, plants and microbes. Aaron B. Lerner of Yale University is credited for naming the hormone and for defining its chemical structure in 1958. In mammals, melatonin is produced by the pineal gland. The pineal gland is small endocrine gland, about the size of a rice grain and shaped like a pine cone (hence the name), that is located in the center of the brain (rostro-dorsal to the superior colliculus) but outside the blood-brain barrier. The secretion of melatonin increases in darkness and decreases during exposure to light, thereby regulating the circadian rhythms of several biological functions, including the sleep-wake cycle. In particular, melatonin regulates the sleep-wake cycle by chemically causing drowsiness and. lowering the body temperature. Melatonin is also implicated in the regulation of mood,learning and memory, immune activity, dreaming, fertility and reproduction. Melatonin is also an effective antioxidant. Most of the actions of melatonin are mediated through the binding and activation of melatonin receptors. Individuals with autism spectrum disorders(ASD) may have lower than normal levels of melatonin. A 2008 study found that unaffected parents of individuals with ASD also have lower melatonin levels, and that the deficits. were associated with low activity of the ASMT gene, which encodes the last enzyme of melatonin synthesis. Reduced melatonin production has also been proposed as a likely factor in the significantly higher cancer rates in night workers.",False,https://ghr.nlm.nih.gov/condition/multiple-sclerosis -22484062,Ciprofloxacin treats amyotrophic lateral sclerosis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats amyotrophic lateral sclerosis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www.ninds.nih.gov/disorders/amyotrophiclateralsclerosis/detail_als.htm -30385775,Melatonin treats Parkinson disease,1939,"Melatonin is a biogenic amine that is found in animals, plants and microbes. Aaron B. Lerner of Yale University is credited for naming the hormone and for defining its chemical structure in 1958. In mammals, melatonin is produced by the pineal gland. The pineal gland is small endocrine gland, about the size of a rice grain and shaped like a pine cone (hence the name), that is located in the center of the brain (rostro-dorsal to the superior colliculus) but outside the blood-brain barrier. The secretion of melatonin increases in darkness and decreases during exposure to light, thereby regulating the circadian rhythms of several biological functions, including the sleep-wake cycle. In particular, melatonin regulates the sleep-wake cycle by chemically causing drowsiness and. lowering the body temperature. Melatonin is also implicated in the regulation of mood,learning and memory, immune activity, dreaming, fertility and reproduction. Melatonin is also an effective antioxidant. Most of the actions of melatonin are mediated through the binding and activation of melatonin receptors. Individuals with autism spectrum disorders(ASD) may have lower than normal levels of melatonin. A 2008 study found that unaffected parents of individuals with ASD also have lower melatonin levels, and that the deficits. were associated with low activity of the ASMT gene, which encodes the last enzyme of melatonin synthesis. Reduced melatonin production has also been proposed as a likely factor in the significantly higher cancer rates in night workers.","Is the triple Melatonin treats Parkinson disease supported by the sentence Melatonin is a biogenic amine that is found in animals, plants and microbes. Aaron B. Lerner of Yale University is credited for naming the hormone and for defining its chemical structure in 1958. In mammals, melatonin is produced by the pineal gland. The pineal gland is small endocrine gland, about the size of a rice grain and shaped like a pine cone (hence the name), that is located in the center of the brain (rostro-dorsal to the superior colliculus) but outside the blood-brain barrier. The secretion of melatonin increases in darkness and decreases during exposure to light, thereby regulating the circadian rhythms of several biological functions, including the sleep-wake cycle. In particular, melatonin regulates the sleep-wake cycle by chemically causing drowsiness and. lowering the body temperature. Melatonin is also implicated in the regulation of mood,learning and memory, immune activity, dreaming, fertility and reproduction. Melatonin is also an effective antioxidant. Most of the actions of melatonin are mediated through the binding and activation of melatonin receptors. Individuals with autism spectrum disorders(ASD) may have lower than normal levels of melatonin. A 2008 study found that unaffected parents of individuals with ASD also have lower melatonin levels, and that the deficits. were associated with low activity of the ASMT gene, which encodes the last enzyme of melatonin synthesis. Reduced melatonin production has also been proposed as a likely factor in the significantly higher cancer rates in night workers.",False,http://en.wikipedia.org/wiki/parkinson%27s_disease -8337570,Ciprofloxacin treats bacterial infectious disease with sepsis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats bacterial infectious disease with sepsis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,PMID:20421654 -10323767,Ciprofloxacin disrupts bacterial infectious disease with sepsis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin disrupts bacterial infectious disease with sepsis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,PMID:20421654 -30380241,Melatonin treats enuresis,1939,"Melatonin is a biogenic amine that is found in animals, plants and microbes. Aaron B. Lerner of Yale University is credited for naming the hormone and for defining its chemical structure in 1958. In mammals, melatonin is produced by the pineal gland. The pineal gland is small endocrine gland, about the size of a rice grain and shaped like a pine cone (hence the name), that is located in the center of the brain (rostro-dorsal to the superior colliculus) but outside the blood-brain barrier. The secretion of melatonin increases in darkness and decreases during exposure to light, thereby regulating the circadian rhythms of several biological functions, including the sleep-wake cycle. In particular, melatonin regulates the sleep-wake cycle by chemically causing drowsiness and. lowering the body temperature. Melatonin is also implicated in the regulation of mood,learning and memory, immune activity, dreaming, fertility and reproduction. Melatonin is also an effective antioxidant. Most of the actions of melatonin are mediated through the binding and activation of melatonin receptors. Individuals with autism spectrum disorders(ASD) may have lower than normal levels of melatonin. A 2008 study found that unaffected parents of individuals with ASD also have lower melatonin levels, and that the deficits. were associated with low activity of the ASMT gene, which encodes the last enzyme of melatonin synthesis. Reduced melatonin production has also been proposed as a likely factor in the significantly higher cancer rates in night workers.","Is the triple Melatonin treats enuresis supported by the sentence Melatonin is a biogenic amine that is found in animals, plants and microbes. Aaron B. Lerner of Yale University is credited for naming the hormone and for defining its chemical structure in 1958. In mammals, melatonin is produced by the pineal gland. The pineal gland is small endocrine gland, about the size of a rice grain and shaped like a pine cone (hence the name), that is located in the center of the brain (rostro-dorsal to the superior colliculus) but outside the blood-brain barrier. The secretion of melatonin increases in darkness and decreases during exposure to light, thereby regulating the circadian rhythms of several biological functions, including the sleep-wake cycle. In particular, melatonin regulates the sleep-wake cycle by chemically causing drowsiness and. lowering the body temperature. Melatonin is also implicated in the regulation of mood,learning and memory, immune activity, dreaming, fertility and reproduction. Melatonin is also an effective antioxidant. Most of the actions of melatonin are mediated through the binding and activation of melatonin receptors. Individuals with autism spectrum disorders(ASD) may have lower than normal levels of melatonin. A 2008 study found that unaffected parents of individuals with ASD also have lower melatonin levels, and that the deficits. were associated with low activity of the ASMT gene, which encodes the last enzyme of melatonin synthesis. Reduced melatonin production has also been proposed as a likely factor in the significantly higher cancer rates in night workers.",False,https://orcid.org/0009-0006-4530-3154 -15459841,Ciprofloxacin predisposes bacterial infectious disease with sepsis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin predisposes bacterial infectious disease with sepsis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,PMID:20421654 -14398199,Ciprofloxacin treats sinusitis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats sinusitis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0001-5889-4463 -11440816,Ciprofloxacin affects typhoid fever,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects typhoid fever supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www.merriam-webster.com/medlineplus/typhoid%20feve -7423320,Ciprofloxacin treats typhoid fever,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats typhoid fever supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www.merriam-webster.com/medlineplus/typhoid%20feve -7886701,Ciprofloxacin affects chronic bronchitis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects chronic bronchitis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -24010235,Ciprofloxacin treats chronic bronchitis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats chronic bronchitis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -8758764,Ciprofloxacin predisposes gonorrhea,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin predisposes gonorrhea supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www.cdc.gov/std/gonorrhea/stdfact-gonorrhea.htm -10013051,Ciprofloxacin treats plague,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats plague supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,PMID:29628173 -14202377,Ciprofloxacin prevents plague,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin prevents plague supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,PMID:29628173 -17154464,Ciprofloxacin causes prostatitis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin causes prostatitis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-6601-2165 -9281470,Ciprofloxacin treats prostatitis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats prostatitis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-6601-2165 -30345866,Melatonin treats Cognitive impairment,1939,"Melatonin is a biogenic amine that is found in animals, plants and microbes. Aaron B. Lerner of Yale University is credited for naming the hormone and for defining its chemical structure in 1958. In mammals, melatonin is produced by the pineal gland. The pineal gland is small endocrine gland, about the size of a rice grain and shaped like a pine cone (hence the name), that is located in the center of the brain (rostro-dorsal to the superior colliculus) but outside the blood-brain barrier. The secretion of melatonin increases in darkness and decreases during exposure to light, thereby regulating the circadian rhythms of several biological functions, including the sleep-wake cycle. In particular, melatonin regulates the sleep-wake cycle by chemically causing drowsiness and. lowering the body temperature. Melatonin is also implicated in the regulation of mood,learning and memory, immune activity, dreaming, fertility and reproduction. Melatonin is also an effective antioxidant. Most of the actions of melatonin are mediated through the binding and activation of melatonin receptors. Individuals with autism spectrum disorders(ASD) may have lower than normal levels of melatonin. A 2008 study found that unaffected parents of individuals with ASD also have lower melatonin levels, and that the deficits. were associated with low activity of the ASMT gene, which encodes the last enzyme of melatonin synthesis. Reduced melatonin production has also been proposed as a likely factor in the significantly higher cancer rates in night workers.","Is the triple Melatonin treats Cognitive impairment supported by the sentence Melatonin is a biogenic amine that is found in animals, plants and microbes. Aaron B. Lerner of Yale University is credited for naming the hormone and for defining its chemical structure in 1958. In mammals, melatonin is produced by the pineal gland. The pineal gland is small endocrine gland, about the size of a rice grain and shaped like a pine cone (hence the name), that is located in the center of the brain (rostro-dorsal to the superior colliculus) but outside the blood-brain barrier. The secretion of melatonin increases in darkness and decreases during exposure to light, thereby regulating the circadian rhythms of several biological functions, including the sleep-wake cycle. In particular, melatonin regulates the sleep-wake cycle by chemically causing drowsiness and. lowering the body temperature. Melatonin is also implicated in the regulation of mood,learning and memory, immune activity, dreaming, fertility and reproduction. Melatonin is also an effective antioxidant. Most of the actions of melatonin are mediated through the binding and activation of melatonin receptors. Individuals with autism spectrum disorders(ASD) may have lower than normal levels of melatonin. A 2008 study found that unaffected parents of individuals with ASD also have lower melatonin levels, and that the deficits. were associated with low activity of the ASMT gene, which encodes the last enzyme of melatonin synthesis. Reduced melatonin production has also been proposed as a likely factor in the significantly higher cancer rates in night workers.",False,https://orcid.org/0009-0006-4530-3154 -30345038,Melatonin treats diabetes mellitus,1939,"Melatonin is a biogenic amine that is found in animals, plants and microbes. Aaron B. Lerner of Yale University is credited for naming the hormone and for defining its chemical structure in 1958. In mammals, melatonin is produced by the pineal gland. The pineal gland is small endocrine gland, about the size of a rice grain and shaped like a pine cone (hence the name), that is located in the center of the brain (rostro-dorsal to the superior colliculus) but outside the blood-brain barrier. The secretion of melatonin increases in darkness and decreases during exposure to light, thereby regulating the circadian rhythms of several biological functions, including the sleep-wake cycle. In particular, melatonin regulates the sleep-wake cycle by chemically causing drowsiness and. lowering the body temperature. Melatonin is also implicated in the regulation of mood,learning and memory, immune activity, dreaming, fertility and reproduction. Melatonin is also an effective antioxidant. Most of the actions of melatonin are mediated through the binding and activation of melatonin receptors. Individuals with autism spectrum disorders(ASD) may have lower than normal levels of melatonin. A 2008 study found that unaffected parents of individuals with ASD also have lower melatonin levels, and that the deficits. were associated with low activity of the ASMT gene, which encodes the last enzyme of melatonin synthesis. Reduced melatonin production has also been proposed as a likely factor in the significantly higher cancer rates in night workers.","Is the triple Melatonin treats diabetes mellitus supported by the sentence Melatonin is a biogenic amine that is found in animals, plants and microbes. Aaron B. Lerner of Yale University is credited for naming the hormone and for defining its chemical structure in 1958. In mammals, melatonin is produced by the pineal gland. The pineal gland is small endocrine gland, about the size of a rice grain and shaped like a pine cone (hence the name), that is located in the center of the brain (rostro-dorsal to the superior colliculus) but outside the blood-brain barrier. The secretion of melatonin increases in darkness and decreases during exposure to light, thereby regulating the circadian rhythms of several biological functions, including the sleep-wake cycle. In particular, melatonin regulates the sleep-wake cycle by chemically causing drowsiness and. lowering the body temperature. Melatonin is also implicated in the regulation of mood,learning and memory, immune activity, dreaming, fertility and reproduction. Melatonin is also an effective antioxidant. Most of the actions of melatonin are mediated through the binding and activation of melatonin receptors. Individuals with autism spectrum disorders(ASD) may have lower than normal levels of melatonin. A 2008 study found that unaffected parents of individuals with ASD also have lower melatonin levels, and that the deficits. were associated with low activity of the ASMT gene, which encodes the last enzyme of melatonin synthesis. Reduced melatonin production has also been proposed as a likely factor in the significantly higher cancer rates in night workers.",False,https://medlineplus.gov/diabetes.htm -14141218,Ciprofloxacin treats castration-resistant prostate carcinoma,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats castration-resistant prostate carcinoma supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,PMID:30324351 -14369807,Ciprofloxacin causes neutropenia,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin causes neutropenia supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -8194797,Ciprofloxacin treats neutropenia,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats neutropenia supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -9504629,Ciprofloxacin treats Sepsis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats Sepsis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -15438014,Ciprofloxacin prevents Sepsis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin prevents Sepsis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -14311974,Ciprofloxacin treats liver abscess (disease),616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats liver abscess (disease) supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-2658-1136 -16563368,Ciprofloxacin affects Fever,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects Fever supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,PMID:9759682 -8669720,Ciprofloxacin affects Fever,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects Fever supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,PMID:9759682 -8088120,Ciprofloxacin treats Fever,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats Fever supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,PMID:9759682 -26984478,Ciprofloxacin disrupts Fever,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin disrupts Fever supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,PMID:9759682 -11267024,Ciprofloxacin affects eye infectious disorder,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects eye infectious disorder supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -11304087,Ciprofloxacin treats eye infectious disorder,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats eye infectious disorder supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -8350437,Ciprofloxacin treats pyelonephritis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats pyelonephritis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -27242944,Ciprofloxacin prevents pyelonephritis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin prevents pyelonephritis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -10672042,Ciprofloxacin affects Abdominal Infection,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects Abdominal Infection supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -8956827,Ciprofloxacin treats Abdominal Infection,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats Abdominal Infection supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -30643727,Acetaminophen treats Fever,1980,"A p-aminophenol derivative with analgesic and antipyretic activities. Although the exact mechanism through which acetaminophen exert its effects has yet to be fully determined, acetaminophen may inhibit the nitric oxide (NO) pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate (NMDA) and substance P, resulting in elevation of the pain threshold. The antipyretic activity may result from inhibition of prostaglandin synthesis and release in the central nervous system (CNS) and prostaglandin-mediated effects on the heat-regulating center in the anterior hypothalamus. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C198"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C198"" NCI Thesaurus); A p-aminophenol derivative with analgesic and antipyretic activities. Although the exact mechanism through which acetaminophen exert its effects has yet to be fully determined, acetaminophen may inhibit the nitric oxide (NO) pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate (NMDA) and substance P, resulting in elevation of the pain threshold. The antipyretic activity may result from inhibition of prostaglandin synthesis and release in the central nervous system (CNS) and prostaglandin-mediated effects on the heat-regulating center in the anterior hypothalamus.; Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Acetaminophen treats Fever supported by the sentence A p-aminophenol derivative with analgesic and antipyretic activities. Although the exact mechanism through which acetaminophen exert its effects has yet to be fully determined, acetaminophen may inhibit the nitric oxide (NO) pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate (NMDA) and substance P, resulting in elevation of the pain threshold. The antipyretic activity may result from inhibition of prostaglandin synthesis and release in the central nervous system (CNS) and prostaglandin-mediated effects on the heat-regulating center in the anterior hypothalamus. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C198"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C198"" NCI Thesaurus); A p-aminophenol derivative with analgesic and antipyretic activities. Although the exact mechanism through which acetaminophen exert its effects has yet to be fully determined, acetaminophen may inhibit the nitric oxide (NO) pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate (NMDA) and substance P, resulting in elevation of the pain threshold. The antipyretic activity may result from inhibition of prostaglandin synthesis and release in the central nervous system (CNS) and prostaglandin-mediated effects on the heat-regulating center in the anterior hypothalamus.; Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,PMID:9759682 -24716241,Ciprofloxacin causes peritonitis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin causes peritonitis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www.merck.com/mmpe/sec02/ch011/ch011b.html#sec02-ch011-ch011b-402 -8190776,Ciprofloxacin treats peritonitis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats peritonitis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www.merck.com/mmpe/sec02/ch011/ch011b.html#sec02-ch011-ch011b-402 -10087799,Ciprofloxacin treats bacterial infectious disease,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats bacterial infectious disease supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/pathogenic_bacteria -9947057,Ciprofloxacin prevents bacterial infectious disease,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin prevents bacterial infectious disease supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/pathogenic_bacteria -11684450,Ciprofloxacin treats cystitis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats cystitis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://www.mayoclinic.org/diseases-conditions/cystitis/symptoms-causes/syc-20371306 -8754779,Ciprofloxacin treats rhinoscleroma,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats rhinoscleroma supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=rhinoscleroma -14572951,Ciprofloxacin treats hearing loss disorder,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats hearing loss disorder supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -13846017,Ciprofloxacin treats lung disorder,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats lung disorder supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www.nlm.nih.gov/medlineplus/ency/article/000066.htm -30361407,Acetaminophen treats delirium,1980,"A p-aminophenol derivative with analgesic and antipyretic activities. Although the exact mechanism through which acetaminophen exert its effects has yet to be fully determined, acetaminophen may inhibit the nitric oxide (NO) pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate (NMDA) and substance P, resulting in elevation of the pain threshold. The antipyretic activity may result from inhibition of prostaglandin synthesis and release in the central nervous system (CNS) and prostaglandin-mediated effects on the heat-regulating center in the anterior hypothalamus. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C198"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C198"" NCI Thesaurus); A p-aminophenol derivative with analgesic and antipyretic activities. Although the exact mechanism through which acetaminophen exert its effects has yet to be fully determined, acetaminophen may inhibit the nitric oxide (NO) pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate (NMDA) and substance P, resulting in elevation of the pain threshold. The antipyretic activity may result from inhibition of prostaglandin synthesis and release in the central nervous system (CNS) and prostaglandin-mediated effects on the heat-regulating center in the anterior hypothalamus.; Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Acetaminophen treats delirium supported by the sentence A p-aminophenol derivative with analgesic and antipyretic activities. Although the exact mechanism through which acetaminophen exert its effects has yet to be fully determined, acetaminophen may inhibit the nitric oxide (NO) pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate (NMDA) and substance P, resulting in elevation of the pain threshold. The antipyretic activity may result from inhibition of prostaglandin synthesis and release in the central nervous system (CNS) and prostaglandin-mediated effects on the heat-regulating center in the anterior hypothalamus. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C198"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C198"" NCI Thesaurus); A p-aminophenol derivative with analgesic and antipyretic activities. Although the exact mechanism through which acetaminophen exert its effects has yet to be fully determined, acetaminophen may inhibit the nitric oxide (NO) pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate (NMDA) and substance P, resulting in elevation of the pain threshold. The antipyretic activity may result from inhibition of prostaglandin synthesis and release in the central nervous system (CNS) and prostaglandin-mediated effects on the heat-regulating center in the anterior hypothalamus.; Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=delirium -9891814,Ciprofloxacin affects pneumonia,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects pneumonia supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/pneumonia -7337248,Ciprofloxacin treats pneumonia,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats pneumonia supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/pneumonia -26466958,Ciprofloxacin disrupts pneumonia,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin disrupts pneumonia supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/pneumonia -8364719,Ciprofloxacin prevents pneumonia,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin prevents pneumonia supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/pneumonia -7113733,Ciprofloxacin causes osteomyelitis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin causes osteomyelitis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -30346218,Acetaminophen treats obesity disorder,1980,"A p-aminophenol derivative with analgesic and antipyretic activities. Although the exact mechanism through which acetaminophen exert its effects has yet to be fully determined, acetaminophen may inhibit the nitric oxide (NO) pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate (NMDA) and substance P, resulting in elevation of the pain threshold. The antipyretic activity may result from inhibition of prostaglandin synthesis and release in the central nervous system (CNS) and prostaglandin-mediated effects on the heat-regulating center in the anterior hypothalamus. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C198"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C198"" NCI Thesaurus); A p-aminophenol derivative with analgesic and antipyretic activities. Although the exact mechanism through which acetaminophen exert its effects has yet to be fully determined, acetaminophen may inhibit the nitric oxide (NO) pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate (NMDA) and substance P, resulting in elevation of the pain threshold. The antipyretic activity may result from inhibition of prostaglandin synthesis and release in the central nervous system (CNS) and prostaglandin-mediated effects on the heat-regulating center in the anterior hypothalamus.; Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Acetaminophen treats obesity disorder supported by the sentence A p-aminophenol derivative with analgesic and antipyretic activities. Although the exact mechanism through which acetaminophen exert its effects has yet to be fully determined, acetaminophen may inhibit the nitric oxide (NO) pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate (NMDA) and substance P, resulting in elevation of the pain threshold. The antipyretic activity may result from inhibition of prostaglandin synthesis and release in the central nervous system (CNS) and prostaglandin-mediated effects on the heat-regulating center in the anterior hypothalamus. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C198"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C198"" NCI Thesaurus); A p-aminophenol derivative with analgesic and antipyretic activities. Although the exact mechanism through which acetaminophen exert its effects has yet to be fully determined, acetaminophen may inhibit the nitric oxide (NO) pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate (NMDA) and substance P, resulting in elevation of the pain threshold. The antipyretic activity may result from inhibition of prostaglandin synthesis and release in the central nervous system (CNS) and prostaglandin-mediated effects on the heat-regulating center in the anterior hypothalamus.; Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://en.wikipedia.org/wiki/obesity -7880629,Ciprofloxacin treats osteomyelitis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats osteomyelitis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -8956826,Ciprofloxacin affects Pseudomonas infection,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects Pseudomonas infection supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -11679354,Ciprofloxacin treats Pseudomonas infection,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats Pseudomonas infection supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -20040173,Ciprofloxacin treats lymphoma,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats lymphoma supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -14005051,Ciprofloxacin treats acute myeloid leukemia,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats acute myeloid leukemia supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www.cancer.gov/dictionary?cdrid=44363 -19067853,Ciprofloxacin treats B-cell chronic lymphocytic leukemia,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats B-cell chronic lymphocytic leukemia supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www.cancer.gov/dictionary?cdrid=346545 -10209213,Ciprofloxacin causes infectious disease,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin causes infectious disease supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://www.merriam-webster.com/medical/communicable%20disease -21996198,Ciprofloxacin affects infectious disease,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects infectious disease supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://www.merriam-webster.com/medical/communicable%20disease -9122989,Ciprofloxacin affects infectious disease,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects infectious disease supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://www.merriam-webster.com/medical/communicable%20disease -30381592,Ethanol treats essential hypertension,2016,"A volatile liquid prepared by fermentation of certain carbohydrates. Alcohol acts as a central nervous system (CNS) depressant, a diuretic, and a disinfectant. Although the exact mechanism of CNS depression is unknown, alcohol may act by inhibiting the opening of calcium channels, mediated by the binding of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) to GABA-A receptors, or through inhibitory actions at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Alcohol inhibits the production of antidiuretic hormone, thereby producing diuresis that may lead to dehydration. This agent kills organisms by denaturing their proteins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C2190"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C2190"" NCI Thesaurus); A volatile liquid prepared by fermentation of certain carbohydrates. Alcohol acts as a central nervous system (CNS) depressant, a diuretic, and a disinfectant. Although the exact mechanism of CNS depression is unknown, alcohol may act by inhibiting the opening of calcium channels, mediated by the binding of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) to GABA-A receptors, or through inhibitory actions at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Alcohol inhibits the production of antidiuretic hormone, thereby producing diuresis that may lead to dehydration. This agent kills organisms by denaturing their proteins.; A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in ALCOHOLIC BEVERAGES.; If you are like many Americans, you drink alcohol at least occasionally. For many people, moderate drinking is probably safe. But drinking less is better for your health than drinking more. And there are some people who should not drink at all. Because drinking too much can be harmful, it's important to know how alcohol affects you and how much is too much. How does alcohol affect the body? Alcohol is a central nervous system depressant. This means that it is a drug that slows down brain activity. It can change your mood, behavior, and self-control. It can cause problems with memory and thinking clearly. Alcohol can also affect your coordination and physical control. Alcohol also has effects on the other organs in your body. For example, it can raise your blood pressure and heart rate. If you drink too much at once, it could make you throw up. Why are the effects of alcohol different from person to person? Alcohol's effects vary from person to person, depending on a variety of factors, including: How much you drank How quickly you drank it The amount of food you ate before drinking Your age Your sex Your race or ethnicity Your physical condition Whether or not you have a family history of alcohol problems What is moderate drinking? For most women, moderate drinking is no more than one standard drink a day For most men, moderate drinking is no more than two standard drinks a day Even though moderate drinking may be safe for many people, there are still risks. Moderate drinking can raise the risk of death from certain cancers and heart diseases. What is a standard drink? In the United States, a standard drink is one that contains about 14 grams of pure alcohol, which is found in: 12 ounces of beer (5% alcohol content) 5 ounces of wine (12% alcohol content) 1.5 ounces or a ""shot"" of distilled spirits or liquor (40% alcohol content) Who should not drink alcohol? Some people should not drink alcohol at all, including those who: Are recovering from an alcohol use disorder (AUD) or are unable to control the amount they drink Are under age 21 Are pregnant or trying to become pregnant Are taking medicines that can interact with alcohol Have medical conditions that get can worse if you drink alcohol Are planning on driving Will be operating machinery If you have questions about whether it is safe for you to drink, talk with your health care provider. What is excessive drinking? Excessive drinking includes binge drinking and heavy alcohol use: Binge drinking is drinking so much at once that your blood alcohol concentration (BAC) level is 0.08% or more. For a man, this usually happens after having 5 or more drinks within a few hours. For a woman, it is after about 4 or more drinks within a few hours. Heavy alcohol use is having having more than 4 drinks on any day for men or more than 3 drinks for women Binge drinking raises your risk of injuries, car crashes, and alcohol poisoning. It also puts you of becoming violent or being the victim of violence. Heavy alcohol use over a long period of time may cause health problems such as: Alcohol use disorder Liver diseases, including cirrhosis and fatty liver disease Heart diseases Increased risk for certain cancers Increased risk of injuries Heavy alcohol use can also cause problems at home, at work, and with friends. But treatment can help. NIH: National Institute on Alcohol Abuse and Alcoholism; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ethanol treats essential hypertension supported by the sentence A volatile liquid prepared by fermentation of certain carbohydrates. Alcohol acts as a central nervous system (CNS) depressant, a diuretic, and a disinfectant. Although the exact mechanism of CNS depression is unknown, alcohol may act by inhibiting the opening of calcium channels, mediated by the binding of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) to GABA-A receptors, or through inhibitory actions at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Alcohol inhibits the production of antidiuretic hormone, thereby producing diuresis that may lead to dehydration. This agent kills organisms by denaturing their proteins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C2190"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C2190"" NCI Thesaurus); A volatile liquid prepared by fermentation of certain carbohydrates. Alcohol acts as a central nervous system (CNS) depressant, a diuretic, and a disinfectant. Although the exact mechanism of CNS depression is unknown, alcohol may act by inhibiting the opening of calcium channels, mediated by the binding of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) to GABA-A receptors, or through inhibitory actions at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Alcohol inhibits the production of antidiuretic hormone, thereby producing diuresis that may lead to dehydration. This agent kills organisms by denaturing their proteins.; A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in ALCOHOLIC BEVERAGES.; If you are like many Americans, you drink alcohol at least occasionally. For many people, moderate drinking is probably safe. But drinking less is better for your health than drinking more. And there are some people who should not drink at all. Because drinking too much can be harmful, it's important to know how alcohol affects you and how much is too much. How does alcohol affect the body? Alcohol is a central nervous system depressant. This means that it is a drug that slows down brain activity. It can change your mood, behavior, and self-control. It can cause problems with memory and thinking clearly. Alcohol can also affect your coordination and physical control. Alcohol also has effects on the other organs in your body. For example, it can raise your blood pressure and heart rate. If you drink too much at once, it could make you throw up. Why are the effects of alcohol different from person to person? Alcohol's effects vary from person to person, depending on a variety of factors, including: How much you drank How quickly you drank it The amount of food you ate before drinking Your age Your sex Your race or ethnicity Your physical condition Whether or not you have a family history of alcohol problems What is moderate drinking? For most women, moderate drinking is no more than one standard drink a day For most men, moderate drinking is no more than two standard drinks a day Even though moderate drinking may be safe for many people, there are still risks. Moderate drinking can raise the risk of death from certain cancers and heart diseases. What is a standard drink? In the United States, a standard drink is one that contains about 14 grams of pure alcohol, which is found in: 12 ounces of beer (5% alcohol content) 5 ounces of wine (12% alcohol content) 1.5 ounces or a ""shot"" of distilled spirits or liquor (40% alcohol content) Who should not drink alcohol? Some people should not drink alcohol at all, including those who: Are recovering from an alcohol use disorder (AUD) or are unable to control the amount they drink Are under age 21 Are pregnant or trying to become pregnant Are taking medicines that can interact with alcohol Have medical conditions that get can worse if you drink alcohol Are planning on driving Will be operating machinery If you have questions about whether it is safe for you to drink, talk with your health care provider. What is excessive drinking? Excessive drinking includes binge drinking and heavy alcohol use: Binge drinking is drinking so much at once that your blood alcohol concentration (BAC) level is 0.08% or more. For a man, this usually happens after having 5 or more drinks within a few hours. For a woman, it is after about 4 or more drinks within a few hours. Heavy alcohol use is having having more than 4 drinks on any day for men or more than 3 drinks for women Binge drinking raises your risk of injuries, car crashes, and alcohol poisoning. It also puts you of becoming violent or being the victim of violence. Heavy alcohol use over a long period of time may cause health problems such as: Alcohol use disorder Liver diseases, including cirrhosis and fatty liver disease Heart diseases Increased risk for certain cancers Increased risk of injuries Heavy alcohol use can also cause problems at home, at work, and with friends. But treatment can help. NIH: National Institute on Alcohol Abuse and Alcoholism; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,http://en.wikipedia.org/wiki/essential_hypertension -18480207,Ciprofloxacin disrupts infectious disease,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin disrupts infectious disease supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://www.merriam-webster.com/medical/communicable%20disease -8054296,Ciprofloxacin prevents infectious disease,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin prevents infectious disease supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://www.merriam-webster.com/medical/communicable%20disease -18366035,Ciprofloxacin predisposes infectious disease,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin predisposes infectious disease supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://www.merriam-webster.com/medical/communicable%20disease -13663890,Ciprofloxacin treats otitis media,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats otitis media supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/otitis_media -16836665,Ciprofloxacin related to Crohn disease,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin related to Crohn disease supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/chron%27s_disease -12942741,Ciprofloxacin affects Crohn disease,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects Crohn disease supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/chron%27s_disease -7163480,Ciprofloxacin treats Crohn disease,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats Crohn disease supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/chron%27s_disease -7592205,Ciprofloxacin affects chronic obstructive pulmonary disease,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects chronic obstructive pulmonary disease supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://www.nhlbi.nih.gov/health-topics/copd -11564697,Ciprofloxacin treats chronic obstructive pulmonary disease,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats chronic obstructive pulmonary disease supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://www.nhlbi.nih.gov/health-topics/copd -7886704,Ciprofloxacin affects bronchiectasis,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin affects bronchiectasis supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www.merck.com/mmhe/sec04/ch047/ch047a.htm -30345454,Ethanol treats obesity disorder,2016,"A volatile liquid prepared by fermentation of certain carbohydrates. Alcohol acts as a central nervous system (CNS) depressant, a diuretic, and a disinfectant. Although the exact mechanism of CNS depression is unknown, alcohol may act by inhibiting the opening of calcium channels, mediated by the binding of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) to GABA-A receptors, or through inhibitory actions at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Alcohol inhibits the production of antidiuretic hormone, thereby producing diuresis that may lead to dehydration. This agent kills organisms by denaturing their proteins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C2190"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C2190"" NCI Thesaurus); A volatile liquid prepared by fermentation of certain carbohydrates. Alcohol acts as a central nervous system (CNS) depressant, a diuretic, and a disinfectant. Although the exact mechanism of CNS depression is unknown, alcohol may act by inhibiting the opening of calcium channels, mediated by the binding of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) to GABA-A receptors, or through inhibitory actions at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Alcohol inhibits the production of antidiuretic hormone, thereby producing diuresis that may lead to dehydration. This agent kills organisms by denaturing their proteins.; A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in ALCOHOLIC BEVERAGES.; If you are like many Americans, you drink alcohol at least occasionally. For many people, moderate drinking is probably safe. But drinking less is better for your health than drinking more. And there are some people who should not drink at all. Because drinking too much can be harmful, it's important to know how alcohol affects you and how much is too much. How does alcohol affect the body? Alcohol is a central nervous system depressant. This means that it is a drug that slows down brain activity. It can change your mood, behavior, and self-control. It can cause problems with memory and thinking clearly. Alcohol can also affect your coordination and physical control. Alcohol also has effects on the other organs in your body. For example, it can raise your blood pressure and heart rate. If you drink too much at once, it could make you throw up. Why are the effects of alcohol different from person to person? Alcohol's effects vary from person to person, depending on a variety of factors, including: How much you drank How quickly you drank it The amount of food you ate before drinking Your age Your sex Your race or ethnicity Your physical condition Whether or not you have a family history of alcohol problems What is moderate drinking? For most women, moderate drinking is no more than one standard drink a day For most men, moderate drinking is no more than two standard drinks a day Even though moderate drinking may be safe for many people, there are still risks. Moderate drinking can raise the risk of death from certain cancers and heart diseases. What is a standard drink? In the United States, a standard drink is one that contains about 14 grams of pure alcohol, which is found in: 12 ounces of beer (5% alcohol content) 5 ounces of wine (12% alcohol content) 1.5 ounces or a ""shot"" of distilled spirits or liquor (40% alcohol content) Who should not drink alcohol? Some people should not drink alcohol at all, including those who: Are recovering from an alcohol use disorder (AUD) or are unable to control the amount they drink Are under age 21 Are pregnant or trying to become pregnant Are taking medicines that can interact with alcohol Have medical conditions that get can worse if you drink alcohol Are planning on driving Will be operating machinery If you have questions about whether it is safe for you to drink, talk with your health care provider. What is excessive drinking? Excessive drinking includes binge drinking and heavy alcohol use: Binge drinking is drinking so much at once that your blood alcohol concentration (BAC) level is 0.08% or more. For a man, this usually happens after having 5 or more drinks within a few hours. For a woman, it is after about 4 or more drinks within a few hours. Heavy alcohol use is having having more than 4 drinks on any day for men or more than 3 drinks for women Binge drinking raises your risk of injuries, car crashes, and alcohol poisoning. It also puts you of becoming violent or being the victim of violence. Heavy alcohol use over a long period of time may cause health problems such as: Alcohol use disorder Liver diseases, including cirrhosis and fatty liver disease Heart diseases Increased risk for certain cancers Increased risk of injuries Heavy alcohol use can also cause problems at home, at work, and with friends. But treatment can help. NIH: National Institute on Alcohol Abuse and Alcoholism; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ethanol treats obesity disorder supported by the sentence A volatile liquid prepared by fermentation of certain carbohydrates. Alcohol acts as a central nervous system (CNS) depressant, a diuretic, and a disinfectant. Although the exact mechanism of CNS depression is unknown, alcohol may act by inhibiting the opening of calcium channels, mediated by the binding of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) to GABA-A receptors, or through inhibitory actions at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Alcohol inhibits the production of antidiuretic hormone, thereby producing diuresis that may lead to dehydration. This agent kills organisms by denaturing their proteins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C2190"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C2190"" NCI Thesaurus); A volatile liquid prepared by fermentation of certain carbohydrates. Alcohol acts as a central nervous system (CNS) depressant, a diuretic, and a disinfectant. Although the exact mechanism of CNS depression is unknown, alcohol may act by inhibiting the opening of calcium channels, mediated by the binding of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) to GABA-A receptors, or through inhibitory actions at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Alcohol inhibits the production of antidiuretic hormone, thereby producing diuresis that may lead to dehydration. This agent kills organisms by denaturing their proteins.; A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in ALCOHOLIC BEVERAGES.; If you are like many Americans, you drink alcohol at least occasionally. For many people, moderate drinking is probably safe. But drinking less is better for your health than drinking more. And there are some people who should not drink at all. Because drinking too much can be harmful, it's important to know how alcohol affects you and how much is too much. How does alcohol affect the body? Alcohol is a central nervous system depressant. This means that it is a drug that slows down brain activity. It can change your mood, behavior, and self-control. It can cause problems with memory and thinking clearly. Alcohol can also affect your coordination and physical control. Alcohol also has effects on the other organs in your body. For example, it can raise your blood pressure and heart rate. If you drink too much at once, it could make you throw up. Why are the effects of alcohol different from person to person? Alcohol's effects vary from person to person, depending on a variety of factors, including: How much you drank How quickly you drank it The amount of food you ate before drinking Your age Your sex Your race or ethnicity Your physical condition Whether or not you have a family history of alcohol problems What is moderate drinking? For most women, moderate drinking is no more than one standard drink a day For most men, moderate drinking is no more than two standard drinks a day Even though moderate drinking may be safe for many people, there are still risks. Moderate drinking can raise the risk of death from certain cancers and heart diseases. What is a standard drink? In the United States, a standard drink is one that contains about 14 grams of pure alcohol, which is found in: 12 ounces of beer (5% alcohol content) 5 ounces of wine (12% alcohol content) 1.5 ounces or a ""shot"" of distilled spirits or liquor (40% alcohol content) Who should not drink alcohol? Some people should not drink alcohol at all, including those who: Are recovering from an alcohol use disorder (AUD) or are unable to control the amount they drink Are under age 21 Are pregnant or trying to become pregnant Are taking medicines that can interact with alcohol Have medical conditions that get can worse if you drink alcohol Are planning on driving Will be operating machinery If you have questions about whether it is safe for you to drink, talk with your health care provider. What is excessive drinking? Excessive drinking includes binge drinking and heavy alcohol use: Binge drinking is drinking so much at once that your blood alcohol concentration (BAC) level is 0.08% or more. For a man, this usually happens after having 5 or more drinks within a few hours. For a woman, it is after about 4 or more drinks within a few hours. Heavy alcohol use is having having more than 4 drinks on any day for men or more than 3 drinks for women Binge drinking raises your risk of injuries, car crashes, and alcohol poisoning. It also puts you of becoming violent or being the victim of violence. Heavy alcohol use over a long period of time may cause health problems such as: Alcohol use disorder Liver diseases, including cirrhosis and fatty liver disease Heart diseases Increased risk for certain cancers Increased risk of injuries Heavy alcohol use can also cause problems at home, at work, and with friends. But treatment can help. NIH: National Institute on Alcohol Abuse and Alcoholism; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://en.wikipedia.org/wiki/obesity -30344451,Ethanol treats cirrhosis of liver,2016,"A volatile liquid prepared by fermentation of certain carbohydrates. Alcohol acts as a central nervous system (CNS) depressant, a diuretic, and a disinfectant. Although the exact mechanism of CNS depression is unknown, alcohol may act by inhibiting the opening of calcium channels, mediated by the binding of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) to GABA-A receptors, or through inhibitory actions at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Alcohol inhibits the production of antidiuretic hormone, thereby producing diuresis that may lead to dehydration. This agent kills organisms by denaturing their proteins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C2190"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C2190"" NCI Thesaurus); A volatile liquid prepared by fermentation of certain carbohydrates. Alcohol acts as a central nervous system (CNS) depressant, a diuretic, and a disinfectant. Although the exact mechanism of CNS depression is unknown, alcohol may act by inhibiting the opening of calcium channels, mediated by the binding of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) to GABA-A receptors, or through inhibitory actions at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Alcohol inhibits the production of antidiuretic hormone, thereby producing diuresis that may lead to dehydration. This agent kills organisms by denaturing their proteins.; A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in ALCOHOLIC BEVERAGES.; If you are like many Americans, you drink alcohol at least occasionally. For many people, moderate drinking is probably safe. But drinking less is better for your health than drinking more. And there are some people who should not drink at all. Because drinking too much can be harmful, it's important to know how alcohol affects you and how much is too much. How does alcohol affect the body? Alcohol is a central nervous system depressant. This means that it is a drug that slows down brain activity. It can change your mood, behavior, and self-control. It can cause problems with memory and thinking clearly. Alcohol can also affect your coordination and physical control. Alcohol also has effects on the other organs in your body. For example, it can raise your blood pressure and heart rate. If you drink too much at once, it could make you throw up. Why are the effects of alcohol different from person to person? Alcohol's effects vary from person to person, depending on a variety of factors, including: How much you drank How quickly you drank it The amount of food you ate before drinking Your age Your sex Your race or ethnicity Your physical condition Whether or not you have a family history of alcohol problems What is moderate drinking? For most women, moderate drinking is no more than one standard drink a day For most men, moderate drinking is no more than two standard drinks a day Even though moderate drinking may be safe for many people, there are still risks. Moderate drinking can raise the risk of death from certain cancers and heart diseases. What is a standard drink? In the United States, a standard drink is one that contains about 14 grams of pure alcohol, which is found in: 12 ounces of beer (5% alcohol content) 5 ounces of wine (12% alcohol content) 1.5 ounces or a ""shot"" of distilled spirits or liquor (40% alcohol content) Who should not drink alcohol? Some people should not drink alcohol at all, including those who: Are recovering from an alcohol use disorder (AUD) or are unable to control the amount they drink Are under age 21 Are pregnant or trying to become pregnant Are taking medicines that can interact with alcohol Have medical conditions that get can worse if you drink alcohol Are planning on driving Will be operating machinery If you have questions about whether it is safe for you to drink, talk with your health care provider. What is excessive drinking? Excessive drinking includes binge drinking and heavy alcohol use: Binge drinking is drinking so much at once that your blood alcohol concentration (BAC) level is 0.08% or more. For a man, this usually happens after having 5 or more drinks within a few hours. For a woman, it is after about 4 or more drinks within a few hours. Heavy alcohol use is having having more than 4 drinks on any day for men or more than 3 drinks for women Binge drinking raises your risk of injuries, car crashes, and alcohol poisoning. It also puts you of becoming violent or being the victim of violence. Heavy alcohol use over a long period of time may cause health problems such as: Alcohol use disorder Liver diseases, including cirrhosis and fatty liver disease Heart diseases Increased risk for certain cancers Increased risk of injuries Heavy alcohol use can also cause problems at home, at work, and with friends. But treatment can help. NIH: National Institute on Alcohol Abuse and Alcoholism; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ethanol treats cirrhosis of liver supported by the sentence A volatile liquid prepared by fermentation of certain carbohydrates. Alcohol acts as a central nervous system (CNS) depressant, a diuretic, and a disinfectant. Although the exact mechanism of CNS depression is unknown, alcohol may act by inhibiting the opening of calcium channels, mediated by the binding of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) to GABA-A receptors, or through inhibitory actions at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Alcohol inhibits the production of antidiuretic hormone, thereby producing diuresis that may lead to dehydration. This agent kills organisms by denaturing their proteins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C2190"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C2190"" NCI Thesaurus); A volatile liquid prepared by fermentation of certain carbohydrates. Alcohol acts as a central nervous system (CNS) depressant, a diuretic, and a disinfectant. Although the exact mechanism of CNS depression is unknown, alcohol may act by inhibiting the opening of calcium channels, mediated by the binding of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) to GABA-A receptors, or through inhibitory actions at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Alcohol inhibits the production of antidiuretic hormone, thereby producing diuresis that may lead to dehydration. This agent kills organisms by denaturing their proteins.; A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in ALCOHOLIC BEVERAGES.; If you are like many Americans, you drink alcohol at least occasionally. For many people, moderate drinking is probably safe. But drinking less is better for your health than drinking more. And there are some people who should not drink at all. Because drinking too much can be harmful, it's important to know how alcohol affects you and how much is too much. How does alcohol affect the body? Alcohol is a central nervous system depressant. This means that it is a drug that slows down brain activity. It can change your mood, behavior, and self-control. It can cause problems with memory and thinking clearly. Alcohol can also affect your coordination and physical control. Alcohol also has effects on the other organs in your body. For example, it can raise your blood pressure and heart rate. If you drink too much at once, it could make you throw up. Why are the effects of alcohol different from person to person? Alcohol's effects vary from person to person, depending on a variety of factors, including: How much you drank How quickly you drank it The amount of food you ate before drinking Your age Your sex Your race or ethnicity Your physical condition Whether or not you have a family history of alcohol problems What is moderate drinking? For most women, moderate drinking is no more than one standard drink a day For most men, moderate drinking is no more than two standard drinks a day Even though moderate drinking may be safe for many people, there are still risks. Moderate drinking can raise the risk of death from certain cancers and heart diseases. What is a standard drink? In the United States, a standard drink is one that contains about 14 grams of pure alcohol, which is found in: 12 ounces of beer (5% alcohol content) 5 ounces of wine (12% alcohol content) 1.5 ounces or a ""shot"" of distilled spirits or liquor (40% alcohol content) Who should not drink alcohol? Some people should not drink alcohol at all, including those who: Are recovering from an alcohol use disorder (AUD) or are unable to control the amount they drink Are under age 21 Are pregnant or trying to become pregnant Are taking medicines that can interact with alcohol Have medical conditions that get can worse if you drink alcohol Are planning on driving Will be operating machinery If you have questions about whether it is safe for you to drink, talk with your health care provider. What is excessive drinking? Excessive drinking includes binge drinking and heavy alcohol use: Binge drinking is drinking so much at once that your blood alcohol concentration (BAC) level is 0.08% or more. For a man, this usually happens after having 5 or more drinks within a few hours. For a woman, it is after about 4 or more drinks within a few hours. Heavy alcohol use is having having more than 4 drinks on any day for men or more than 3 drinks for women Binge drinking raises your risk of injuries, car crashes, and alcohol poisoning. It also puts you of becoming violent or being the victim of violence. Heavy alcohol use over a long period of time may cause health problems such as: Alcohol use disorder Liver diseases, including cirrhosis and fatty liver disease Heart diseases Increased risk for certain cancers Increased risk of injuries Heavy alcohol use can also cause problems at home, at work, and with friends. But treatment can help. NIH: National Institute on Alcohol Abuse and Alcoholism; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-0736-9199 -16138544,Ciprofloxacin prevents diarrheal disease,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin prevents diarrheal disease supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=medical&va=diarrhea -21488232,Ciprofloxacin treats Infection,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats Infection supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -21807033,Ciprofloxacin prevents Infection,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin prevents Infection supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -10002223,Ciprofloxacin treats anthrax infection,616,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Ciprofloxacin treats anthrax infection supported by the sentence A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://en.wikipedia.org/wiki/anthrax -7351604,Chloramphenicol treats eye infectious disorder,617,"A semisynthetic, broad-spectrum antibiotic derived from Streptomyces venequelae with primarily bacteriostatic activity. Chloramphenicol diffuses through the bacterial cell wall and reversibly binds to the bacterial 50S ribosomal subunit. The binding interferes with peptidyl transferase activity, thereby prevents transfer of amino acids to the growing peptide chains and blocks peptide bond formation. As a result bacterial protein synthesis is blocked and impede bacterial cell proliferation.; An antibiotic first isolated from cultures of Streptomyces venequelae in 1947 but now produced synthetically. It has a relatively simple structure and was the first broad-spectrum antibiotic to be discovered. It acts by interfering with bacterial protein synthesis and is mainly bacteriostatic. (From Martindale, The Extra Pharmacopoeia, 29th ed, p106); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Chloramphenicol treats eye infectious disorder supported by the sentence A semisynthetic, broad-spectrum antibiotic derived from Streptomyces venequelae with primarily bacteriostatic activity. Chloramphenicol diffuses through the bacterial cell wall and reversibly binds to the bacterial 50S ribosomal subunit. The binding interferes with peptidyl transferase activity, thereby prevents transfer of amino acids to the growing peptide chains and blocks peptide bond formation. As a result bacterial protein synthesis is blocked and impede bacterial cell proliferation.; An antibiotic first isolated from cultures of Streptomyces venequelae in 1947 but now produced synthetically. It has a relatively simple structure and was the first broad-spectrum antibiotic to be discovered. It acts by interfering with bacterial protein synthesis and is mainly bacteriostatic. (From Martindale, The Extra Pharmacopoeia, 29th ed, p106); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True, -21241586,Chloramphenicol prevents eye infectious disorder,617,"A semisynthetic, broad-spectrum antibiotic derived from Streptomyces venequelae with primarily bacteriostatic activity. Chloramphenicol diffuses through the bacterial cell wall and reversibly binds to the bacterial 50S ribosomal subunit. The binding interferes with peptidyl transferase activity, thereby prevents transfer of amino acids to the growing peptide chains and blocks peptide bond formation. As a result bacterial protein synthesis is blocked and impede bacterial cell proliferation.; An antibiotic first isolated from cultures of Streptomyces venequelae in 1947 but now produced synthetically. It has a relatively simple structure and was the first broad-spectrum antibiotic to be discovered. It acts by interfering with bacterial protein synthesis and is mainly bacteriostatic. (From Martindale, The Extra Pharmacopoeia, 29th ed, p106); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Chloramphenicol prevents eye infectious disorder supported by the sentence A semisynthetic, broad-spectrum antibiotic derived from Streptomyces venequelae with primarily bacteriostatic activity. Chloramphenicol diffuses through the bacterial cell wall and reversibly binds to the bacterial 50S ribosomal subunit. The binding interferes with peptidyl transferase activity, thereby prevents transfer of amino acids to the growing peptide chains and blocks peptide bond formation. As a result bacterial protein synthesis is blocked and impede bacterial cell proliferation.; An antibiotic first isolated from cultures of Streptomyces venequelae in 1947 but now produced synthetically. It has a relatively simple structure and was the first broad-spectrum antibiotic to be discovered. It acts by interfering with bacterial protein synthesis and is mainly bacteriostatic. (From Martindale, The Extra Pharmacopoeia, 29th ed, p106); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True, -30384667,ELOSULFASE ALFA treats mucopolysaccharidosis type 4,2064,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T126; UMLS Semantic Type: STY:T116; UMLS Semantic Type: STY:T109; Elosulfase alfa is a synthetic version of the enzyme N-acetylgalactosamine-6-sulfatase. It was approved by the FDA in 2014 for the treatment of Morquio syndrome. Elosulfase alfa was developed by BioMarin Pharmaceutical Inc. and is marketed under the brand Vimizim™. The recommended dose is 2 mg per kg given intravenously over a minimum range of 3.5 to 4.5 hours, based on infusion volume, once every week.","Is the triple ELOSULFASE ALFA treats mucopolysaccharidosis type 4 supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T126; UMLS Semantic Type: STY:T116; UMLS Semantic Type: STY:T109; Elosulfase alfa is a synthetic version of the enzyme N-acetylgalactosamine-6-sulfatase. It was approved by the FDA in 2014 for the treatment of Morquio syndrome. Elosulfase alfa was developed by BioMarin Pharmaceutical Inc. and is marketed under the brand Vimizim™. The recommended dose is 2 mg per kg given intravenously over a minimum range of 3.5 to 4.5 hours, based on infusion volume, once every week.",False,http://en.wikipedia.org/wiki/morquio_syndrome -30648244,(R)-(+)-Tolvaptan treats autosomal dominant polycystic kidney disease,2065,"An orally bioavailable, selective, arginine vasopressin receptor 2 (V2, AVPR2) antagonist that can be used to treat hyponatremia. Upon oral administration, tolvaptan selectively and competitively binds to and blocks the V2 receptor located in the walls of the vasculature and luminal membranes of renal collecting ducts, thereby preventing the binding of vasopressin to the V2 receptor. This prevents water absorption in the kidneys and increases the excretion of electrolyte-free water via the kidneys. This reduces intravascular volume and increases serum sodium concentrations and osmolality.; A benzazepine derivative and selective VASOPRESSIN V2 RECEPTOR antagonist that is used to treat euvolemic and hypervolemic HYPONATREMIA. It is also used in the treatment of rapidly progressing AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE to slow the rate of cyst development and renal insufficiency.","Is the triple (R)-(+)-Tolvaptan treats autosomal dominant polycystic kidney disease supported by the sentence An orally bioavailable, selective, arginine vasopressin receptor 2 (V2, AVPR2) antagonist that can be used to treat hyponatremia. Upon oral administration, tolvaptan selectively and competitively binds to and blocks the V2 receptor located in the walls of the vasculature and luminal membranes of renal collecting ducts, thereby preventing the binding of vasopressin to the V2 receptor. This prevents water absorption in the kidneys and increases the excretion of electrolyte-free water via the kidneys. This reduces intravascular volume and increases serum sodium concentrations and osmolality.; A benzazepine derivative and selective VASOPRESSIN V2 RECEPTOR antagonist that is used to treat euvolemic and hypervolemic HYPONATREMIA. It is also used in the treatment of rapidly progressing AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE to slow the rate of cyst development and renal insufficiency.",False,https://rarediseases.info.nih.gov/diseases/10413/autosomal-dominant-polycystic-kidney-disease -9528501,Chloramphenicol treats osteomyelitis,617,"A semisynthetic, broad-spectrum antibiotic derived from Streptomyces venequelae with primarily bacteriostatic activity. Chloramphenicol diffuses through the bacterial cell wall and reversibly binds to the bacterial 50S ribosomal subunit. The binding interferes with peptidyl transferase activity, thereby prevents transfer of amino acids to the growing peptide chains and blocks peptide bond formation. As a result bacterial protein synthesis is blocked and impede bacterial cell proliferation.; An antibiotic first isolated from cultures of Streptomyces venequelae in 1947 but now produced synthetically. It has a relatively simple structure and was the first broad-spectrum antibiotic to be discovered. It acts by interfering with bacterial protein synthesis and is mainly bacteriostatic. (From Martindale, The Extra Pharmacopoeia, 29th ed, p106); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109","Is the triple Chloramphenicol treats osteomyelitis supported by the sentence A semisynthetic, broad-spectrum antibiotic derived from Streptomyces venequelae with primarily bacteriostatic activity. Chloramphenicol diffuses through the bacterial cell wall and reversibly binds to the bacterial 50S ribosomal subunit. The binding interferes with peptidyl transferase activity, thereby prevents transfer of amino acids to the growing peptide chains and blocks peptide bond formation. As a result bacterial protein synthesis is blocked and impede bacterial cell proliferation.; An antibiotic first isolated from cultures of Streptomyces venequelae in 1947 but now produced synthetically. It has a relatively simple structure and was the first broad-spectrum antibiotic to be discovered. It acts by interfering with bacterial protein synthesis and is mainly bacteriostatic. (From Martindale, The Extra Pharmacopoeia, 29th ed, p106); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0002-0736-9199 -16722213,Rebamipide causes osteoarthritis,618,"A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.","Is the triple Rebamipide causes osteoarthritis supported by the sentence A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.",True,http://www.mayoclinic.com/health/osteoarthritis/ds00019 -19949890,Rebamipide treats osteoarthritis,618,"A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.","Is the triple Rebamipide treats osteoarthritis supported by the sentence A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.",True,http://www.mayoclinic.com/health/osteoarthritis/ds00019 -10125846,Rebamipide affects gastric ulcer,618,"A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.","Is the triple Rebamipide affects gastric ulcer supported by the sentence A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.",True,https://orcid.org/0000-0002-6601-2165 -10368387,Rebamipide treats gastric ulcer,618,"A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.","Is the triple Rebamipide treats gastric ulcer supported by the sentence A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.",True,https://orcid.org/0000-0002-6601-2165 -10452606,Rebamipide prevents gastric ulcer,618,"A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.","Is the triple Rebamipide prevents gastric ulcer supported by the sentence A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.",True,https://orcid.org/0000-0002-6601-2165 -24500158,Rebamipide treats gastroesophageal reflux disease,618,"A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.","Is the triple Rebamipide treats gastroesophageal reflux disease supported by the sentence A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.",True,https://orcid.org/0000-0001-5208-3432 -8102739,Rebamipide treats gastritis,618,"A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.","Is the triple Rebamipide treats gastritis supported by the sentence A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.",True,https://orcid.org/0000-0002-0736-9199 -16923576,Rebamipide disrupts gastritis,618,"A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.","Is the triple Rebamipide disrupts gastritis supported by the sentence A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.",True,https://orcid.org/0000-0002-0736-9199 -13727344,Rebamipide prevents gastritis,618,"A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.","Is the triple Rebamipide prevents gastritis supported by the sentence A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.",True,https://orcid.org/0000-0002-0736-9199 -27679650,Rebamipide affects peptic ulcer disease,618,"A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.","Is the triple Rebamipide affects peptic ulcer disease supported by the sentence A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.",True,PMID:28242110 -12062800,Rebamipide treats peptic ulcer disease,618,"A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.","Is the triple Rebamipide treats peptic ulcer disease supported by the sentence A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.",True,PMID:28242110 -20953135,Rebamipide prevents peptic ulcer disease,618,"A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.","Is the triple Rebamipide prevents peptic ulcer disease supported by the sentence A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.",True,PMID:28242110 -13211904,Rebamipide treats ulcerative colitis,618,"A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.","Is the triple Rebamipide treats ulcerative colitis supported by the sentence A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.",True,https://meshb.nlm.nih.gov/record/ui?ui=d003093 -19364844,Rebamipide treats dry eye syndrome,618,"A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.","Is the triple Rebamipide treats dry eye syndrome supported by the sentence A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.",True,PMID:29498987 -27610972,DINUTUXIMAB treats bone osteosarcoma,619,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. It is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse.","Is the triple DINUTUXIMAB treats bone osteosarcoma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. It is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse.",True,https://orcid.org/0000-0002-6548-5200 -45055047,Vancomycin treats bacterial infectious disease with sepsis,2119,"Vancomycin is only found in individuals that have used or taken this drug. It is an antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to ristocetin that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear. [PubChem]The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Normally this is a five-point interaction. This binding of vancomycin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi.","Is the triple Vancomycin treats bacterial infectious disease with sepsis supported by the sentence Vancomycin is only found in individuals that have used or taken this drug. It is an antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to ristocetin that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear. [PubChem]The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Normally this is a five-point interaction. This binding of vancomycin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi.",False,PMID:20421654 -21740095,DINUTUXIMAB treats neoplasm,619,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. It is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse.","Is the triple DINUTUXIMAB treats neoplasm supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. It is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse.",True,https://orcid.org/0000-0002-6601-2165 -30649392,Vancomycin treats bacterial infectious disease with sepsis,2119,"Vancomycin is only found in individuals that have used or taken this drug. It is an antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to ristocetin that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear. [PubChem]The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Normally this is a five-point interaction. This binding of vancomycin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi.","Is the triple Vancomycin treats bacterial infectious disease with sepsis supported by the sentence Vancomycin is only found in individuals that have used or taken this drug. It is an antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to ristocetin that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear. [PubChem]The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Normally this is a five-point interaction. This binding of vancomycin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi.",False,PMID:20421654 -21974466,DINUTUXIMAB causes neuroblastoma,619,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. It is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse.","Is the triple DINUTUXIMAB causes neuroblastoma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. It is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse.",True,https://orcid.org/0000-0002-0736-9199 -9445080,DINUTUXIMAB treats neuroblastoma,619,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. It is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse.","Is the triple DINUTUXIMAB treats neuroblastoma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. It is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse.",True,https://orcid.org/0000-0002-0736-9199 -30644469,Vancomycin treats bacterial endocarditis,2119,"Vancomycin is only found in individuals that have used or taken this drug. It is an antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to ristocetin that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear. [PubChem]The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Normally this is a five-point interaction. This binding of vancomycin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi.","Is the triple Vancomycin treats bacterial endocarditis supported by the sentence Vancomycin is only found in individuals that have used or taken this drug. It is an antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to ristocetin that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear. [PubChem]The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Normally this is a five-point interaction. This binding of vancomycin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi.",False,https://orcid.org/0009-0006-4530-3154 -21657994,BRENTUXIMAB VEDOTIN related to mature T-cell and NK-cell non-Hodgkin lymphoma,622,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].","Is the triple BRENTUXIMAB VEDOTIN related to mature T-cell and NK-cell non-Hodgkin lymphoma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",True,PMID:21919697 -22071488,BRENTUXIMAB VEDOTIN has part mature T-cell and NK-cell non-Hodgkin lymphoma,622,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].","Is the triple BRENTUXIMAB VEDOTIN has part mature T-cell and NK-cell non-Hodgkin lymphoma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",True,PMID:21919697 -21657991,BRENTUXIMAB VEDOTIN treats mature T-cell and NK-cell non-Hodgkin lymphoma,622,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].","Is the triple BRENTUXIMAB VEDOTIN treats mature T-cell and NK-cell non-Hodgkin lymphoma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",True,PMID:21919697 -30360989,Vancomycin treats kidney failure,2119,"Vancomycin is only found in individuals that have used or taken this drug. It is an antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to ristocetin that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear. [PubChem]The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Normally this is a five-point interaction. This binding of vancomycin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi.","Is the triple Vancomycin treats kidney failure supported by the sentence Vancomycin is only found in individuals that have used or taken this drug. It is an antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to ristocetin that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear. [PubChem]The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Normally this is a five-point interaction. This binding of vancomycin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi.",False,https://orcid.org/0000-0002-0736-9199 -21472937,BRENTUXIMAB VEDOTIN treats mycosis fungoides,622,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].","Is the triple BRENTUXIMAB VEDOTIN treats mycosis fungoides supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",True, -23929422,BRENTUXIMAB VEDOTIN related to anaplastic large cell lymphoma,622,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].","Is the triple BRENTUXIMAB VEDOTIN related to anaplastic large cell lymphoma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",True,http://en.wikipedia.org/wiki/anaplastic_large-cell_lymphoma#epidemiology -22808973,BRENTUXIMAB VEDOTIN treats anaplastic large cell lymphoma,622,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].","Is the triple BRENTUXIMAB VEDOTIN treats anaplastic large cell lymphoma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",True,http://en.wikipedia.org/wiki/anaplastic_large-cell_lymphoma#epidemiology -22284390,BRENTUXIMAB VEDOTIN treats neoplasm,622,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].","Is the triple BRENTUXIMAB VEDOTIN treats neoplasm supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",True,https://orcid.org/0000-0002-6601-2165 -30343856,Vancomycin treats Infection,2119,"Vancomycin is only found in individuals that have used or taken this drug. It is an antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to ristocetin that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear. [PubChem]The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Normally this is a five-point interaction. This binding of vancomycin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi.","Is the triple Vancomycin treats Infection supported by the sentence Vancomycin is only found in individuals that have used or taken this drug. It is an antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to ristocetin that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear. [PubChem]The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Normally this is a five-point interaction. This binding of vancomycin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi.",False, -23435913,BRENTUXIMAB VEDOTIN affects lymphoma,622,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].","Is the triple BRENTUXIMAB VEDOTIN affects lymphoma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",True,https://orcid.org/0000-0002-0736-9199 -21569593,BRENTUXIMAB VEDOTIN treats lymphoma,622,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].","Is the triple BRENTUXIMAB VEDOTIN treats lymphoma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",True,https://orcid.org/0000-0002-0736-9199 -21812241,BRENTUXIMAB VEDOTIN related to Hodgkins lymphoma,622,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].","Is the triple BRENTUXIMAB VEDOTIN related to Hodgkins lymphoma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",True,https://en.wikipedia.org/wiki/hodgkin%27s_lymphoma -30341528,Filgrastim treats acute myeloid leukemia,2143,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Filgrastim is a short-acting recombinant, non-pegylated human granulocyte colony-stimulating factor (G-CSF) analog produced by recombinant DNA technology. It has an amino acid sequence identical to endogenous G-CSF, but it is non-glycosylated unlike the endogenous G-CSF and has an N-terminal methionine added in the sequence for expression in _E. Coli_.[L40714] Human G-CSF is a glycoprotein that regulates the production and release of neutrophils from the bone marrow. Filgrastim mimics the biological actions of G-CSF to increase the levels of neutrophils in the blood.[L40719] It has a number of therapeutic uses, including the management and prevention of infections and febrile neutropenia in patients receiving myelosuppressive chemotherapy or radiation therapy. It is also used to manage severe chronic neutropenia and mobilize hematopoietic progenitor cells to the peripheral blood for collection by leukapheresis in patients undergoing peripheral blood progenitor cell collection and therapy.[L40714] Filgrastim was approved in the US in 1991 and there are biosimilars available with similar therapeutic indications.[A245858] Tbo-filgrastim was approved by the FDA on August 29, 2012.[L36325] Filgrastim-sndz was approved on March 6, 2015 [L40768] and filgrastim-ayow was approved on March 2, 2022.[L40773] A long-acting, pegylated G-CSF, [pegfilgrastim], was made available to increase the duration of action of the drug.","Is the triple Filgrastim treats acute myeloid leukemia supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Filgrastim is a short-acting recombinant, non-pegylated human granulocyte colony-stimulating factor (G-CSF) analog produced by recombinant DNA technology. It has an amino acid sequence identical to endogenous G-CSF, but it is non-glycosylated unlike the endogenous G-CSF and has an N-terminal methionine added in the sequence for expression in _E. Coli_.[L40714] Human G-CSF is a glycoprotein that regulates the production and release of neutrophils from the bone marrow. Filgrastim mimics the biological actions of G-CSF to increase the levels of neutrophils in the blood.[L40719] It has a number of therapeutic uses, including the management and prevention of infections and febrile neutropenia in patients receiving myelosuppressive chemotherapy or radiation therapy. It is also used to manage severe chronic neutropenia and mobilize hematopoietic progenitor cells to the peripheral blood for collection by leukapheresis in patients undergoing peripheral blood progenitor cell collection and therapy.[L40714] Filgrastim was approved in the US in 1991 and there are biosimilars available with similar therapeutic indications.[A245858] Tbo-filgrastim was approved by the FDA on August 29, 2012.[L36325] Filgrastim-sndz was approved on March 6, 2015 [L40768] and filgrastim-ayow was approved on March 2, 2022.[L40773] A long-acting, pegylated G-CSF, [pegfilgrastim], was made available to increase the duration of action of the drug.",False,http://www.cancer.gov/dictionary?cdrid=44363 -21596847,BRENTUXIMAB VEDOTIN treats Sezary syndrome,622,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].","Is the triple BRENTUXIMAB VEDOTIN treats Sezary syndrome supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",True, -21657993,BRENTUXIMAB VEDOTIN related to primary cutaneous T-cell non-Hodgkin lymphoma,622,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].","Is the triple BRENTUXIMAB VEDOTIN related to primary cutaneous T-cell non-Hodgkin lymphoma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",True,http://en.wikipedia.org/wiki/cutaneous_t-cell_lymphoma -21657990,BRENTUXIMAB VEDOTIN treats primary cutaneous T-cell non-Hodgkin lymphoma,622,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].","Is the triple BRENTUXIMAB VEDOTIN treats primary cutaneous T-cell non-Hodgkin lymphoma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",True,http://en.wikipedia.org/wiki/cutaneous_t-cell_lymphoma -23653011,BRENTUXIMAB VEDOTIN related to diffuse large B-cell lymphoma,622,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].","Is the triple BRENTUXIMAB VEDOTIN related to diffuse large B-cell lymphoma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",True,PMID:28487884 -21553377,BRENTUXIMAB VEDOTIN has part diffuse large B-cell lymphoma,622,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].","Is the triple BRENTUXIMAB VEDOTIN has part diffuse large B-cell lymphoma supported by the sentence UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",True,PMID:28487884 -10847016,Tetracycline prevents inclusion conjunctivitis,628,UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,Is the triple Tetracycline prevents inclusion conjunctivitis supported by the sentence UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,True,https://www.visualdx.com/visualdx/diagnosis/inclusion+conjunctivitis?diagnosisid=54853&moduleid=101 -15910237,Tetracycline treats eye infectious disorder,628,UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,Is the triple Tetracycline treats eye infectious disorder supported by the sentence UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,True, -19472933,Tetracycline causes Helicobacter pylori infectious disease,628,UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,Is the triple Tetracycline causes Helicobacter pylori infectious disease supported by the sentence UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,True, -7227539,Tetracycline treats Helicobacter pylori infectious disease,628,UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,Is the triple Tetracycline treats Helicobacter pylori infectious disease supported by the sentence UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,True, -10596737,Tetracycline treats osteomyelitis,628,UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,Is the triple Tetracycline treats osteomyelitis supported by the sentence UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,True,https://orcid.org/0000-0002-0736-9199 -17969405,Tetracycline affects bacterial infectious disease,628,UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,Is the triple Tetracycline affects bacterial infectious disease supported by the sentence UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,True,http://en.wikipedia.org/wiki/pathogenic_bacteria -45031487,Calcitriol treats hypoparathyroidism,2193,"A synthetic physiologically-active analog of vitamin D, specifically the vitamin D3 form. Calcitriol regulates calcium in vivo by promoting absorption in the intestine, reabsorption in the kidneys, and, along with parathyroid hormone, regulation of bone growth. A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Calcitriol also induces cell cycle arrest at G0/G1 phase of the cell cycle, cell differentiation, and apoptosis, resulting in inhibition of proliferation of some tumor cell types. This agent may be chemopreventive for colon and prostate cancers. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C330"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C330"" NCI Thesaurus); A synthetic physiologically-active analog of vitamin D, specifically the vitamin D3 form. Calcitriol regulates calcium in vivo by promoting absorption in the intestine, reabsorption in the kidneys, and, along with parathyroid hormone, regulation of bone growth. A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Calcitriol also induces cell cycle arrest at G0/G1 phase of the cell cycle, cell differentiation, and apoptosis, resulting in inhibition of proliferation of some tumor cell types. This agent may be chemopreventive for colon and prostate cancers. (NCI04); The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (CALCIFEDIOL). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T127; UMLS Semantic Type: STY:T109","Is the triple Calcitriol treats hypoparathyroidism supported by the sentence A synthetic physiologically-active analog of vitamin D, specifically the vitamin D3 form. Calcitriol regulates calcium in vivo by promoting absorption in the intestine, reabsorption in the kidneys, and, along with parathyroid hormone, regulation of bone growth. A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Calcitriol also induces cell cycle arrest at G0/G1 phase of the cell cycle, cell differentiation, and apoptosis, resulting in inhibition of proliferation of some tumor cell types. This agent may be chemopreventive for colon and prostate cancers. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C330"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C330"" NCI Thesaurus); A synthetic physiologically-active analog of vitamin D, specifically the vitamin D3 form. Calcitriol regulates calcium in vivo by promoting absorption in the intestine, reabsorption in the kidneys, and, along with parathyroid hormone, regulation of bone growth. A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Calcitriol also induces cell cycle arrest at G0/G1 phase of the cell cycle, cell differentiation, and apoptosis, resulting in inhibition of proliferation of some tumor cell types. This agent may be chemopreventive for colon and prostate cancers. (NCI04); The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (CALCIFEDIOL). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T127; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-0736-9199 -24565223,Tetracycline prevents bacterial infectious disease,628,UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,Is the triple Tetracycline prevents bacterial infectious disease supported by the sentence UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,True,http://en.wikipedia.org/wiki/pathogenic_bacteria -20170701,Tetracycline causes periodontitis,628,UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,Is the triple Tetracycline causes periodontitis supported by the sentence UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,True,https://orcid.org/0000-0001-5889-4463 -18080767,Tetracycline affects periodontitis,628,UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,Is the triple Tetracycline affects periodontitis supported by the sentence UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,True,https://orcid.org/0000-0001-5889-4463 -10332719,Tetracycline treats periodontitis,628,UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,Is the triple Tetracycline treats periodontitis supported by the sentence UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,True,https://orcid.org/0000-0001-5889-4463 -22346012,Tetracycline treats Infection,628,UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,Is the triple Tetracycline treats Infection supported by the sentence UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,True, -11754791,(Alginate)n related to cystic fibrosis,629,"UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].","Is the triple (Alginate)n related to cystic fibrosis supported by the sentence UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].",True,http://ghr.nlm.nih.gov/condition/cystic-fibrosis -27435796,(Alginate)n affects cystic fibrosis,629,"UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].","Is the triple (Alginate)n affects cystic fibrosis supported by the sentence UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].",True,http://ghr.nlm.nih.gov/condition/cystic-fibrosis -30362374,Calcitriol treats hypoparathyroidism,2193,"A synthetic physiologically-active analog of vitamin D, specifically the vitamin D3 form. Calcitriol regulates calcium in vivo by promoting absorption in the intestine, reabsorption in the kidneys, and, along with parathyroid hormone, regulation of bone growth. A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Calcitriol also induces cell cycle arrest at G0/G1 phase of the cell cycle, cell differentiation, and apoptosis, resulting in inhibition of proliferation of some tumor cell types. This agent may be chemopreventive for colon and prostate cancers. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C330"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C330"" NCI Thesaurus); A synthetic physiologically-active analog of vitamin D, specifically the vitamin D3 form. Calcitriol regulates calcium in vivo by promoting absorption in the intestine, reabsorption in the kidneys, and, along with parathyroid hormone, regulation of bone growth. A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Calcitriol also induces cell cycle arrest at G0/G1 phase of the cell cycle, cell differentiation, and apoptosis, resulting in inhibition of proliferation of some tumor cell types. This agent may be chemopreventive for colon and prostate cancers. (NCI04); The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (CALCIFEDIOL). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T127; UMLS Semantic Type: STY:T109","Is the triple Calcitriol treats hypoparathyroidism supported by the sentence A synthetic physiologically-active analog of vitamin D, specifically the vitamin D3 form. Calcitriol regulates calcium in vivo by promoting absorption in the intestine, reabsorption in the kidneys, and, along with parathyroid hormone, regulation of bone growth. A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Calcitriol also induces cell cycle arrest at G0/G1 phase of the cell cycle, cell differentiation, and apoptosis, resulting in inhibition of proliferation of some tumor cell types. This agent may be chemopreventive for colon and prostate cancers. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C330"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C330"" NCI Thesaurus); A synthetic physiologically-active analog of vitamin D, specifically the vitamin D3 form. Calcitriol regulates calcium in vivo by promoting absorption in the intestine, reabsorption in the kidneys, and, along with parathyroid hormone, regulation of bone growth. A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Calcitriol also induces cell cycle arrest at G0/G1 phase of the cell cycle, cell differentiation, and apoptosis, resulting in inhibition of proliferation of some tumor cell types. This agent may be chemopreventive for colon and prostate cancers. (NCI04); The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (CALCIFEDIOL). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T127; UMLS Semantic Type: STY:T109",False,https://orcid.org/0000-0002-0736-9199 -10599430,(Alginate)n related to obesity disorder,629,"UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].","Is the triple (Alginate)n related to obesity disorder supported by the sentence UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].",True,https://en.wikipedia.org/wiki/obesity -23415127,(Alginate)n affects obesity disorder,629,"UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].","Is the triple (Alginate)n affects obesity disorder supported by the sentence UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].",True,https://en.wikipedia.org/wiki/obesity -23508922,(Alginate)n predisposes obesity disorder,629,"UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].","Is the triple (Alginate)n predisposes obesity disorder supported by the sentence UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].",True,https://en.wikipedia.org/wiki/obesity -12376615,(Alginate)n related to gastroesophageal reflux disease,629,"UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].","Is the triple (Alginate)n related to gastroesophageal reflux disease supported by the sentence UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].",True,https://orcid.org/0000-0001-5208-3432 -27132270,(Alginate)n affects gastroesophageal reflux disease,629,"UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].","Is the triple (Alginate)n affects gastroesophageal reflux disease supported by the sentence UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].",True,https://orcid.org/0000-0001-5208-3432 -19854419,(Alginate)n affects gastroesophageal reflux disease,629,"UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].","Is the triple (Alginate)n affects gastroesophageal reflux disease supported by the sentence UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].",True,https://orcid.org/0000-0001-5208-3432 -11016107,(Alginate)n treats gastroesophageal reflux disease,629,"UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].","Is the triple (Alginate)n treats gastroesophageal reflux disease supported by the sentence UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].",True,https://orcid.org/0000-0001-5208-3432 -8246131,(Alginate)n disrupts gastroesophageal reflux disease,629,"UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].","Is the triple (Alginate)n disrupts gastroesophageal reflux disease supported by the sentence UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].",True,https://orcid.org/0000-0001-5208-3432 -11492096,(Alginate)n prevents gastroesophageal reflux disease,629,"UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].","Is the triple (Alginate)n prevents gastroesophageal reflux disease supported by the sentence UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].",True,https://orcid.org/0000-0001-5208-3432 -11597598,Zolimidine related to peptic ulcer disease,635,ZOLIMIDINE; FULL_MW:272.33; MAX_FDA_APPROVAL_PHASE: -1.0,Is the triple Zolimidine related to peptic ulcer disease supported by the sentence ZOLIMIDINE; FULL_MW:272.33; MAX_FDA_APPROVAL_PHASE: -1.0,True,PMID:28242110 -13503760,Chlorhexidine affects periodontal disorder,638,"A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Chlorhexidine affects periodontal disorder supported by the sentence A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://www.nidcr.nih.gov/health-info/gum-disease/more-info -11792004,Chlorhexidine treats periodontal disorder,638,"A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Chlorhexidine treats periodontal disorder supported by the sentence A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://www.nidcr.nih.gov/health-info/gum-disease/more-info -19905103,Chlorhexidine prevents periodontal disorder,638,"A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Chlorhexidine prevents periodontal disorder supported by the sentence A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://www.nidcr.nih.gov/health-info/gum-disease/more-info -19942414,Chlorhexidine predisposes periodontal disorder,638,"A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Chlorhexidine predisposes periodontal disorder supported by the sentence A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://www.nidcr.nih.gov/health-info/gum-disease/more-info -16147932,Chlorhexidine causes gingivitis,638,"A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Chlorhexidine causes gingivitis supported by the sentence A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0001-5889-4463 -8506996,Chlorhexidine affects gingivitis,638,"A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Chlorhexidine affects gingivitis supported by the sentence A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0001-5889-4463 -7869752,Chlorhexidine treats gingivitis,638,"A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Chlorhexidine treats gingivitis supported by the sentence A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0001-5889-4463 -11272633,Chlorhexidine disrupts gingivitis,638,"A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Chlorhexidine disrupts gingivitis supported by the sentence A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0001-5889-4463 -7990742,Chlorhexidine prevents gingivitis,638,"A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Chlorhexidine prevents gingivitis supported by the sentence A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,https://orcid.org/0000-0001-5889-4463 -10593306,Chlorhexidine treats eye infectious disorder,638,"A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Chlorhexidine treats eye infectious disorder supported by the sentence A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True, -30643224,Ergocalciferol treats osteoporosis,2197,"A vitamin that includes both CHOLECALCIFEROLS and ERGOCALCIFEROLS, which have the common effect of preventing or curing RICKETS in animals. It can also be viewed as a hormone since it can be formed in SKIN by action of ULTRAVIOLET RAYS upon the precursors, 7-dehydrocholesterol and ERGOSTEROL, and acts on VITAMIN D RECEPTORS to regulate CALCIUM in opposition to PARATHYROID HORMONE.; Vitamins are substances that your body needs to grow and develop normally. Vitamin D helps your body absorb calcium. Calcium is one of the main building blocks of bone. A lack of vitamin D can lead to bone diseases such as osteoporosis or rickets. Vitamin D also has a role in your nerve, muscle, and immune systems. You can get vitamin D in three ways: through your skin, from your diet, and from supplements. Your body forms vitamin D naturally after exposure to sunlight. However, too much sun exposure can lead to skin aging and skin cancer. So many people try to get their vitamin D from other sources. Vitamin D-rich foods include egg yolks, saltwater fish, and liver. Some other foods, like milk and cereal, often have added vitamin D. You can also take vitamin D supplements. Check with your health care provider to see how much you should take. People who might need extra vitamin D include: Older adults Breastfed infants People with dark skin People with certain conditions, such as liver diseases, cystic fibrosis and Crohn's disease People who have obesity or have had gastric bypass surgery NIH: National Institutes of Health Office of Dietary Supplements; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T127; UMLS Semantic Type: STY:T125","Is the triple Ergocalciferol treats osteoporosis supported by the sentence A vitamin that includes both CHOLECALCIFEROLS and ERGOCALCIFEROLS, which have the common effect of preventing or curing RICKETS in animals. It can also be viewed as a hormone since it can be formed in SKIN by action of ULTRAVIOLET RAYS upon the precursors, 7-dehydrocholesterol and ERGOSTEROL, and acts on VITAMIN D RECEPTORS to regulate CALCIUM in opposition to PARATHYROID HORMONE.; Vitamins are substances that your body needs to grow and develop normally. Vitamin D helps your body absorb calcium. Calcium is one of the main building blocks of bone. A lack of vitamin D can lead to bone diseases such as osteoporosis or rickets. Vitamin D also has a role in your nerve, muscle, and immune systems. You can get vitamin D in three ways: through your skin, from your diet, and from supplements. Your body forms vitamin D naturally after exposure to sunlight. However, too much sun exposure can lead to skin aging and skin cancer. So many people try to get their vitamin D from other sources. Vitamin D-rich foods include egg yolks, saltwater fish, and liver. Some other foods, like milk and cereal, often have added vitamin D. You can also take vitamin D supplements. Check with your health care provider to see how much you should take. People who might need extra vitamin D include: Older adults Breastfed infants People with dark skin People with certain conditions, such as liver diseases, cystic fibrosis and Crohn's disease People who have obesity or have had gastric bypass surgery NIH: National Institutes of Health Office of Dietary Supplements; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T127; UMLS Semantic Type: STY:T125",False,http://www.niams.nih.gov/health_info/bone/default.asp -13955725,Chlorhexidine treats bacterial infectious disease,638,"A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Chlorhexidine treats bacterial infectious disease supported by the sentence A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/pathogenic_bacteria -19793680,Chlorhexidine disrupts bacterial infectious disease,638,"A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109","Is the triple Chlorhexidine disrupts bacterial infectious disease supported by the sentence A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",True,http://en.wikipedia.org/wiki/pathogenic_bacteria diff --git a/data/human_labeled_semmed.csv b/data/human_labeled_semmed.csv deleted file mode 100644 index 45bf5b3..0000000 --- a/data/human_labeled_semmed.csv +++ /dev/null @@ -1,101 +0,0 @@ -Predicate ID,Triple,Sentence ID,Sentence,Question,Label,Reference -10592604,Arboviruses process of Lepus capensis,16,Seroprevalence of tick-borne and mosquito-borne arboviruses in European brown hares in Northern and Western Germany.,Is the triple 'Arboviruses process of Lepus capensis' supported by the sentence: 'Seroprevalence of tick-borne and mosquito-borne arboviruses in European brown hares in Northern and Western Germany.'?,False,https://eurekamag.com/research/004/525/004525561.php -10592697,Tahyna virus is a California Group Viruses,17,"Tribec virus (Kemerovo serogroup, genus Orbivirus), Eyach virus (genus Coltivirus), and Tahyna virus (California encephalitis serogroup, genus Bunyavirus) are arthropod-borne viruses known to occur in Germany.","Is the triple 'Tahyna virus is a California Group Viruses' supported by the sentence: 'Tribec virus (Kemerovo serogroup, genus Orbivirus), Eyach virus (genus Coltivirus), and Tahyna virus (California encephalitis serogroup, genus Bunyavirus) are arthropod-borne viruses known to occur in Germany.'?",True,https://www.nature.com/articles/s41598-021-95757-2.pdf -10592728,Eyach virus is a Coltivirus,17,"Tribec virus (Kemerovo serogroup, genus Orbivirus), Eyach virus (genus Coltivirus), and Tahyna virus (California encephalitis serogroup, genus Bunyavirus) are arthropod-borne viruses known to occur in Germany.","Is the triple 'Eyach virus is a Coltivirus' supported by the sentence: 'Tribec virus (Kemerovo serogroup, genus Orbivirus), Eyach virus (genus Coltivirus), and Tahyna virus (California encephalitis serogroup, genus Bunyavirus) are arthropod-borne viruses known to occur in Germany.'?",True,https://europepmc.org/article/MED/34532065 -10592759,California Group Viruses is a Arboviruses,17,"Tribec virus (Kemerovo serogroup, genus Orbivirus), Eyach virus (genus Coltivirus), and Tahyna virus (California encephalitis serogroup, genus Bunyavirus) are arthropod-borne viruses known to occur in Germany.","Is the triple 'California Group Viruses is a Arboviruses' supported by the sentence: 'Tribec virus (Kemerovo serogroup, genus Orbivirus), Eyach virus (genus Coltivirus), and Tahyna virus (California encephalitis serogroup, genus Bunyavirus) are arthropod-borne viruses known to occur in Germany.'?",True,https://researchexperts.utmb.edu/en/publications/the-ecology-of-california-group-viruses -10592832,Disease process of Human,18,These viruses are also suspected to cause human disease.,Is the triple 'Disease process of Human' supported by the sentence: 'These viruses are also suspected to cause human disease.'?,True,https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Introductory_Biology_(CK-12)/07%3A_Prokaryotes_and_Viruses/7.12%3A_Viruses_and_Human_Disease -10592873,Virus causes Disease,18,These viruses are also suspected to cause human disease.,Is the triple 'Virus causes Disease' supported by the sentence: 'These viruses are also suspected to cause human disease.'?,True,https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Introductory_Biology_(CK-12)/07%3A_Prokaryotes_and_Viruses/7.12%3A_Viruses_and_Human_Disease -10593057,Lepus capensis location of Antibodies,23,"For the first time, antibodies against Tribec virus could be found in a European brown hare in Germany.","Is the triple 'Lepus capensis location of Antibodies' supported by the sentence: 'For the first time, antibodies against Tribec virus could be found in a European brown hare in Germany.'?",True,https://europepmc.org/article/PMC/3853023 -10593208,Binding Protein part of FHL1,26,"Structure-function mapping of BbCRASP-1, the key complement factor H and FHL-1 binding protein of Borrelia burgdorferi.","Is the triple 'Binding Protein part of FHL1' supported by the sentence: 'Structure-function mapping of BbCRASP-1, the key complement factor H and FHL-1 binding protein of Borrelia burgdorferi.'?",True,https://www.academia.edu/26303972/Structure_function_mapping_of_BbCRASP_1_the_key_complement_factor_H_and_FHL_1_binding_protein_of_Borrelia_burgdorferi -10593243,COMPLEMENT FACTOR H|CFH part of Borrelia burgdorferi,26,"Structure-function mapping of BbCRASP-1, the key complement factor H and FHL-1 binding protein of Borrelia burgdorferi.","Is the triple 'COMPLEMENT FACTOR H|CFH part of Borrelia burgdorferi' supported by the sentence: 'Structure-function mapping of BbCRASP-1, the key complement factor H and FHL-1 binding protein of Borrelia burgdorferi.'?",True,https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0013519 -10593287,Binding Protein part of Borrelia burgdorferi,26,"Structure-function mapping of BbCRASP-1, the key complement factor H and FHL-1 binding protein of Borrelia burgdorferi.","Is the triple 'Binding Protein part of Borrelia burgdorferi' supported by the sentence: 'Structure-function mapping of BbCRASP-1, the key complement factor H and FHL-1 binding protein of Borrelia burgdorferi.'?",True,https://www.rcsb.org/structure/1W33 -10593621,XS part of Borrelia burgdorferi,34,Functionality of Borrelia burgdorferi LuxS: the Lyme disease spirochete produces and responds to the pheromone autoinducer-2 and lacks a complete activated-methyl cycle.,Is the triple 'XS part of Borrelia burgdorferi' supported by the sentence: 'Functionality of Borrelia burgdorferi LuxS: the Lyme disease spirochete produces and responds to the pheromone autoinducer-2 and lacks a complete activated-methyl cycle.'?,True,https://europepmc.org/article/PMC/128172 -10593815,XS produces homocysteine,39,"While a large number of bacteria utilize homocysteine, the other LuxS product, for synthesis of methionine as part of the activated-methyl cycle, B. burgdorferi was found to lack that ability.","Is the triple 'XS produces homocysteine' supported by the sentence: 'While a large number of bacteria utilize homocysteine, the other LuxS product, for synthesis of methionine as part of the activated-methyl cycle, B. burgdorferi was found to lack that ability.'?",True,https://link.springer.com/article/10.1007/s00253-018-9170-7 -10593856,Bacteria interacts with Methionine,39,"While a large number of bacteria utilize homocysteine, the other LuxS product, for synthesis of methionine as part of the activated-methyl cycle, B. burgdorferi was found to lack that ability.","Is the triple 'Bacteria interacts with Methionine' supported by the sentence: 'While a large number of bacteria utilize homocysteine, the other LuxS product, for synthesis of methionine as part of the activated-methyl cycle, B. burgdorferi was found to lack that ability.'?",True,https://europepmc.org/article/MED/31383657 -10593932,Pheromone affects Gene Expression,40,We propose that the main function of B. burgdorferi LuxS is to synthesize DPD and that the Lyme disease spirochete utilizes a form of DPD as a pheromone to control gene expression.,Is the triple 'Pheromone affects Gene Expression' supported by the sentence: 'We propose that the main function of B. burgdorferi LuxS is to synthesize DPD and that the Lyme disease spirochete utilizes a form of DPD as a pheromone to control gene expression.'?,True,https://www.biorxiv.org/content/10.1101/2021.06.18.449021v1.full.pdf -10594285,B.S.S. treats Adult,50,"I. ricinus nymphs harbored almost exclusively B. burgdorferi s.s. and B. garinii OspA type 4, while in adults a broad variety of B. burgdorferi s.l. types was found.","Is the triple 'B.S.S. treats Adult' supported by the sentence: 'I. ricinus nymphs harbored almost exclusively B. burgdorferi s.s. and B. garinii OspA type 4, while in adults a broad variety of B. burgdorferi s.l. types was found.'?",False,https://pdfs.semanticscholar.org/3ce5/013aeaacc164655507d251cc167997d94ec4.pdf -10594435,host part of Vertebrates,53,These data strongly suggest that B. burgdorferi s.s. and B. garinii OspA type 4 are maintained in these areas by specific transmission cycles involving a so far undetermined vertebrate host which is frequently fed on by I. ricinus larvae.,Is the triple 'host part of Vertebrates' supported by the sentence: 'These data strongly suggest that B. burgdorferi s.s. and B. garinii OspA type 4 are maintained in these areas by specific transmission cycles involving a so far undetermined vertebrate host which is frequently fed on by I. ricinus larvae.'?,False,https://zoo.sav.sk/data/people_publictions_106_Lencakova_et_al.2006.IJMM.pdf -10594472,B.S.S. affects host,53,These data strongly suggest that B. burgdorferi s.s. and B. garinii OspA type 4 are maintained in these areas by specific transmission cycles involving a so far undetermined vertebrate host which is frequently fed on by I. ricinus larvae.,Is the triple 'B.S.S. affects host' supported by the sentence: 'These data strongly suggest that B. burgdorferi s.s. and B. garinii OspA type 4 are maintained in these areas by specific transmission cycles involving a so far undetermined vertebrate host which is frequently fed on by I. ricinus larvae.'?,True,https://iopscience.iop.org/article/10.1088/1748-9326/11/4/043001/pdf -10594584,Farm Animals is a Animals,55,Monitoring of antimicrobial resistance in pathogenic bacteria from livestock animals.,Is the triple 'Farm Animals is a Animals' supported by the sentence: 'Monitoring of antimicrobial resistance in pathogenic bacteria from livestock animals.'?,True,https://itsmyschoollibrary.com/2023/04/28/farm-animals-definition-types-classification-agricultural-science-lesson-note/ -10594689,Disease process of Farm Animals,57,The establishment of corresponding management options relies on scientifically defensible efforts to obtain objective data on the prevalence of bacterial resistance in healthy and diseased livestock.,Is the triple 'Disease process of Farm Animals' supported by the sentence: 'The establishment of corresponding management options relies on scientifically defensible efforts to obtain objective data on the prevalence of bacterial resistance in healthy and diseased livestock.'?,True,https://www.rvc.ac.uk/Media/Default/UoLW%20Distance%20Learning/Modules/Animal%20Disease%20%28Current%20Concepts%29.pdf -10594898,Therapeutic procedure uses Microbicides,62,"This incorporates regional differences in animal population density, (2) the avoidance of \""copy strains\","Is the triple 'Therapeutic procedure uses Microbicides' supported by the sentence: 'This incorporates regional differences in animal population density, (2) the avoidance of \""copy strains\'?",False,https://www.hiv.gov/hiv-basics/hiv-prevention/potential-future-options/microbicides/ -10595006,Therapeutic procedure uses Microbicides,64,"In applied antimicrobial therapy, the data can serve as a decision guidance in choosing the antimicrobial agent most adapted to the prevailing epidemiological situation.","Is the triple 'Therapeutic procedure uses Microbicides' supported by the sentence: 'In applied antimicrobial therapy, the data can serve as a decision guidance in choosing the antimicrobial agent most adapted to the prevailing epidemiological situation.'?",False,https://www.hiv.gov/hiv-basics/hiv-prevention/potential-future-options/microbicides/ -10595160,enrofloxacin is a Fluoroquinolones,67,"Only rare cases of resistance to enrofloxacin (fluoroquinolone) could be detected, and only 3% of bacterial strains tested proved resistant to 3rd and 4th generation cephalosporins, including substances prescribed in human medicine.","Is the triple 'enrofloxacin is a Fluoroquinolones' supported by the sentence: 'Only rare cases of resistance to enrofloxacin (fluoroquinolone) could be detected, and only 3% of bacterial strains tested proved resistant to 3rd and 4th generation cephalosporins, including substances prescribed in human medicine.'?",True,https://www.drugs.com/drug-class/quinolones.html -10595193,enrofloxacin coexists with Pharmaceutical Preparations,67,"Only rare cases of resistance to enrofloxacin (fluoroquinolone) could be detected, and only 3% of bacterial strains tested proved resistant to 3rd and 4th generation cephalosporins, including substances prescribed in human medicine.","Is the triple 'enrofloxacin coexists with Pharmaceutical Preparations' supported by the sentence: 'Only rare cases of resistance to enrofloxacin (fluoroquinolone) could be detected, and only 3% of bacterial strains tested proved resistant to 3rd and 4th generation cephalosporins, including substances prescribed in human medicine.'?",False,https://www.mdpi.com/2076-2615/11/8/2312 -10595361,Covers treats Tick-Borne Encephalitis,70,Spatial analysis revealed that the land cover and precise seasonal patterns of climatic indices (temperature and normalized difference vegetation index) can explain 55% of the observed spatial variation in TBE incidence over the period 1993-98 across all the Baltic States.,Is the triple 'Covers treats Tick-Borne Encephalitis' supported by the sentence: 'Spatial analysis revealed that the land cover and precise seasonal patterns of climatic indices (temperature and normalized difference vegetation index) can explain 55% of the observed spatial variation in TBE incidence over the period 1993-98 across all the Baltic States.'?,False,https://www.cdc.gov/tick-borne-encephalitis/symptoms-diagnosis-treatment/index.html -10595474,Behavior process of Human,72,"Further time series analysis of climate, together with analysis of biotic factors, socio-economic conditions, and human behaviour is being undertaken to explain the epidemiological patterns more fully.","Is the triple 'Behavior process of Human' supported by the sentence: 'Further time series analysis of climate, together with analysis of biotic factors, socio-economic conditions, and human behaviour is being undertaken to explain the epidemiological patterns more fully.'?",True,https://exploringyourmind.com/8-basic-psychological-processes/ -10595632,Infection process of Adult,75,"The study objective was to prospectively determine the etiology of infection among adults exposed to tick bite and to detect acute human granulocytic anaplasmosis (HGA), a recently emerging infection, in north-eastern Poland.","Is the triple 'Infection process of Adult' supported by the sentence: 'The study objective was to prospectively determine the etiology of infection among adults exposed to tick bite and to detect acute human granulocytic anaplasmosis (HGA), a recently emerging infection, in north-eastern Poland.'?",True,https://www.cdc.gov/infectioncontrol/spread/index.html -10595725,Fever process of Patients,76,"We evaluated 68 patients (34 males and 34 females, mean age 44.2+/-15 years) who had fever within 4 weeks after a tick bite.","Is the triple 'Fever process of Patients' supported by the sentence: 'We evaluated 68 patients (34 males and 34 females, mean age 44.2+/-15 years) who had fever within 4 weeks after a tick bite.'?",True,https://www.uptodate.com/contents/pathophysiology-and-treatment-of-fever-in-adults -10595759,Fever process of Females,76,"We evaluated 68 patients (34 males and 34 females, mean age 44.2+/-15 years) who had fever within 4 weeks after a tick bite.","Is the triple 'Fever process of Females' supported by the sentence: 'We evaluated 68 patients (34 males and 34 females, mean age 44.2+/-15 years) who had fever within 4 weeks after a tick bite.'?",True,https://www.clinicbarcelona.org/en/assistance/be-healthy/fever/causes -10595794,Fever process of Males,76,"We evaluated 68 patients (34 males and 34 females, mean age 44.2+/-15 years) who had fever within 4 weeks after a tick bite.","Is the triple 'Fever process of Males' supported by the sentence: 'We evaluated 68 patients (34 males and 34 females, mean age 44.2+/-15 years) who had fever within 4 weeks after a tick bite.'?",True,https://www.clinicbarcelona.org/en/assistance/be-healthy/fever/causes -10595906,Recombinant DNA part of 16s,78,Microscopic examination of EDTA whole blood and nested PCR targeting A. phagocytophilum 16S rDNA gene fragment were carried out at enrolment.,Is the triple 'Recombinant DNA part of 16s' supported by the sentence: 'Microscopic examination of EDTA whole blood and nested PCR targeting A. phagocytophilum 16S rDNA gene fragment were carried out at enrolment.'?,False,https://pubs.rsc.org/en/content/articlelanding/2022/ra/d2ra03069a -10595985,Tick-Borne Infections process of Individual,79,Tick-borne infections were diagnosed in 57 individuals (84%).,Is the triple 'Tick-Borne Infections process of Individual' supported by the sentence: 'Tick-borne infections were diagnosed in 57 individuals (84%).'?,False,https://www.cdc.gov/ticks/diseases/index.html -10596143,"Glossitis, Benign Migratory process of Patients",81,"Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.","Is the triple 'Glossitis, Benign Migratory process of Patients' supported by the sentence: 'Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.'?",False,https://dermnetnz.org/topics/geographic-tongue -10596167,"Glossitis, Benign Migratory is a Symptoms",81,"Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.","Is the triple 'Glossitis, Benign Migratory is a Symptoms' supported by the sentence: 'Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.'?",False,https://dermnetnz.org/topics/geographic-tongue -10596199,"Glossitis, Benign Migratory process of Patients",81,"Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.","Is the triple 'Glossitis, Benign Migratory process of Patients' supported by the sentence: 'Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.'?",False,https://dermnetnz.org/topics/geographic-tongue -10596244,Symptoms process of Patients,81,"Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.","Is the triple 'Symptoms process of Patients' supported by the sentence: 'Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.'?",True,https://bmcpalliatcare.biomedcentral.com/articles/10.1186/s12904-018-0314-4 -10596294,Lyme Disease process of Patients,81,"Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.","Is the triple 'Lyme Disease process of Patients' supported by the sentence: 'Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.'?",True,https://www.cdc.gov/lyme/index.html -10596383,Diagnosis treats Patients,82,Diagnosis of HGA was confirmed in one patient by PCR and in another one by seroconversion.,Is the triple 'Diagnosis treats Patients' supported by the sentence: 'Diagnosis of HGA was confirmed in one patient by PCR and in another one by seroconversion.'?,False,https://www.mayoclinic.org/diseases-conditions/cancer/diagnosis-treatment/drc-20370594 -10596492,Immunofluorescence diagnoses Infection,83,"In two further individuals, A. phagocytophilum infection was confirmed by immunofluorescence (antibody titers > or = 1:128), which, however, does not fulfil the ESCAR (European Society of Clinical Microbiology and Infectious Diseases Study Group on Coxiella, Anaplasma, Rickettsia, and Bartonella) criteria for HGA case definition.","Is the triple 'Immunofluorescence diagnoses Infection' supported by the sentence: 'In two further individuals, A. phagocytophilum infection was confirmed by immunofluorescence (antibody titers > or = 1:128), which, however, does not fulfil the ESCAR (European Society of Clinical Microbiology and Infectious Diseases Study Group on Coxiella, Anaplasma, Rickettsia, and Bartonella) criteria for HGA case definition.'?",True,https://link.springer.com/chapter/10.1007/978-3-319-77694-1_16 -10596565,Lyme Disease process of Patients,84,Lyme borreliosis was diagnosed in 16 patients in six of them as a single infection.,Is the triple 'Lyme Disease process of Patients' supported by the sentence: 'Lyme borreliosis was diagnosed in 16 patients,True,https://www.mayoclinic.org/diseases-conditions/lyme-disease/symptoms-causes/syc-20374651 -10596660,Lyme Disease process of Individual,85,Both confirmed HGA cases and seropositive individuals had A. phagocytophilum infection concurrent either with Lyme borreliosis (two cases) or with TBE (two cases).,Is the triple 'Lyme Disease process of Individual' supported by the sentence: 'Both confirmed HGA cases and seropositive individuals had A. phagocytophilum infection concurrent either with Lyme borreliosis (two cases) or with TBE (two cases).'?,True,https://www.mayoclinic.org/diseases-conditions/lyme-disease/symptoms-causes/syc-20374651 -10596772,Disease process of Adult,87,TBE was found the most prevalent disease among adults with febrile illnesses occurring after a tick bite in north-eastern Poland.,Is the triple 'Disease process of Adult' supported by the sentence: 'TBE was found the most prevalent disease among adults with febrile illnesses occurring after a tick bite in north-eastern Poland.'?,True,https://www.ecdc.europa.eu/en/tick-borne-encephalitis/facts/factsheet -10596805,Disorder characterized by fever process of Adult,87,TBE was found the most prevalent disease among adults with febrile illnesses occurring after a tick bite in north-eastern Poland.,Is the triple 'Disorder characterized by fever process of Adult' supported by the sentence: 'TBE was found the most prevalent disease among adults with febrile illnesses occurring after a tick bite in north-eastern Poland.'?,True,https://www.ecdc.europa.eu/en/tick-borne-encephalitis/facts/factsheet -10597199,"4,5-dibromo-2-pyrrolic acid compared with 1-oleoyl-2-stearoylphosphatidylcholine",97,Comparison of dbpA sequences with ospC sequences from a subset of 59 strains revealed all kinds of cross-connections indicating processes of lateral gene transfer among strains.,"Is the triple '4,5-dibromo-2-pyrrolic acid compared with 1-oleoyl-2-stearoylphosphatidylcholine' supported by the sentence: 'Comparison of dbpA sequences with ospC sequences from a subset of 59 strains revealed all kinds of cross-connections indicating processes of lateral gene transfer among strains.'?",False,https://www.sigmaaldrich.com/UA/en/product/aldrich/656291 -10597287,"4,5-dibromo-2-pyrrolic acid inhibits DNA",98,"The extent of sequence identity within the dbpA genes decreases from the DNA (67%) to the amino acid (AA) level (44%) by about 23%, in contrast ospC sequence identities differed only by about 10%.","Is the triple '4,5-dibromo-2-pyrrolic acid inhibits DNA' supported by the sentence: 'The extent of sequence identity within the dbpA genes decreases from the DNA (67%) to the amino acid (AA) level (44%) by about 23%, in contrast ospC sequence identities differed only by about 10%.'?",False,https://researchportal.helsinki.fi/en/publications/n-phenyl-45-dibromopyrrolamides-and-n-phenylindolamides-as-atp-co -10597421,"4,5-dibromo-2-pyrrolic acid interacts with Specific antigen",100,Immunoblots using four recombinant DbpAs representing groups I-IV show that DbpA proteins are sensitive and specific antigens and complement one another in their reactivity.,"Is the triple '4,5-dibromo-2-pyrrolic acid interacts with Specific antigen' supported by the sentence: 'Immunoblots using four recombinant DbpAs representing groups I-IV show that DbpA proteins are sensitive and specific antigens and complement one another in their reactivity.'?",True,https://link.springer.com/article/10.1007/s11094-022-02723-x -10597542,Neuropeptides affects Inflammation,102,"A neuropeptide in immune-mediated inflammation, Y?","Is the triple 'Neuropeptides affects Inflammation' supported by the sentence: 'A neuropeptide in immune-mediated inflammation, Y?'?",False,https://link.springer.com/chapter/10.1007/978-94-011-2996-1_9 -10597633,Crosstalk causes Autoimmunity,103,Disturbances in crosstalk between the immune system and the sympathetic nervous system (SNS) can contribute to the pathogenesis of Th1-mediated autoimmunity.,Is the triple 'Crosstalk causes Autoimmunity' supported by the sentence: 'Disturbances in crosstalk between the immune system and the sympathetic nervous system (SNS) can contribute to the pathogenesis of Th1-mediated autoimmunity.'?,False,https://www.frontiersin.org/articles/10.3389/fimmu.2021.747143/full -10597756,neuropeptide Y|NPY interacts with T-Lymphocyte,105,"The precise role of NPY has been an enigma, but a recent study provides a breakthrough, demonstrating that NPY has a bimodal role as a negative regulator of T cells and an activator of antigen-presenting cell function.","Is the triple 'neuropeptide Y|NPY interacts with T-Lymphocyte' supported by the sentence: 'The precise role of NPY has been an enigma, but a recent study provides a breakthrough, demonstrating that NPY has a bimodal role as a negative regulator of T cells and an activator of antigen-presenting cell function.'?",True,https://www.frontiersin.org/articles/10.3389/fimmu.2020.580378/full -10597803,neuropeptide Y|NPY stimulates Antigen-Presenting Cells,105,"The precise role of NPY has been an enigma, but a recent study provides a breakthrough, demonstrating that NPY has a bimodal role as a negative regulator of T cells and an activator of antigen-presenting cell function.","Is the triple 'neuropeptide Y|NPY stimulates Antigen-Presenting Cells' supported by the sentence: 'The precise role of NPY has been an enigma, but a recent study provides a breakthrough, demonstrating that NPY has a bimodal role as a negative regulator of T cells and an activator of antigen-presenting cell function.'?",True,https://www.frontiersin.org/articles/10.3389/fimmu.2020.580378/full -10597925,Mammals location of Toll-like receptors,107,Toll-like receptors (TLRs) have an important role in innate immunity in mammals by recognizing conserved microbial components that are known as pathogen-associated molecular patterns (PAMPs).,Is the triple 'Mammals location of Toll-like receptors' supported by the sentence: 'Toll-like receptors (TLRs) have an important role in innate immunity in mammals by recognizing conserved microbial components that are known as pathogen-associated molecular patterns (PAMPs).'?,True,https://www.hindawi.com/journals/bmri/2021/1157023/ -10598015,Endosomes location of Compartments,108,"Although the majority of these receptors sense pathogen components on the cell surface, a subset of them (TLR3, TLR7, TLR8 and TLR9) senses viral and bacterial nucleic acids in endosomal compartments.","Is the triple 'Endosomes location of Compartments' supported by the sentence: 'Although the majority of these receptors sense pathogen components on the cell surface, a subset of them (TLR3, TLR7, TLR8 and TLR9) senses viral and bacterial nucleic acids in endosomal compartments.'?",False,https://link.springer.com/referenceworkentry/10.1007/978-3-642-16483-5_1892 -10598051,Cell surface location of receptor,108,"Although the majority of these receptors sense pathogen components on the cell surface, a subset of them (TLR3, TLR7, TLR8 and TLR9) senses viral and bacterial nucleic acids in endosomal compartments.","Is the triple 'Cell surface location of receptor' supported by the sentence: 'Although the majority of these receptors sense pathogen components on the cell surface, a subset of them (TLR3, TLR7, TLR8 and TLR9) senses viral and bacterial nucleic acids in endosomal compartments.'?",True,https://en.wikipedia.org/wiki/Cell_surface_receptor -10598148,"RNA, Small Interfering interacts with Ribose",110,This immune activation by siRNAs can be abrogated by the 2'-ribose modification of uridines.,"Is the triple 'RNA, Small Interfering interacts with Ribose' supported by the sentence: 'This immune activation by siRNAs can be abrogated by the 2'-ribose modification of uridines.'?",False,https://jbiomedsci.biomedcentral.com/articles/10.1186/s12929-023-00981-9 -10598263,E2F1 gene|E2F1|UBE2L3 causes Apoptosis,112,E2F1-induced apoptosis: turning killers into therapeutics.,Is the triple 'E2F1 gene|E2F1|UBE2L3 causes Apoptosis' supported by the sentence: 'E2F1-induced apoptosis: turning killers into therapeutics.'?,True,https://www.omim.org/entry/189971 -10598476,E2F1 gene|E2F1|UBE2L3 interacts with Pharmaceutical Preparations,116,"Here, these findings are highlighted in the context of the most recent follow-up studies that have used apoptotic E2F1 genes as new therapeutics or drug targets, thereby providing insight into the basic mechanisms of E2F1-induced apoptosis and its possible clinical implications.","Is the triple 'E2F1 gene|E2F1|UBE2L3 interacts with Pharmaceutical Preparations' supported by the sentence: 'Here, these findings are highlighted in the context of the most recent follow-up studies that have used apoptotic E2F1 genes as new therapeutics or drug targets, thereby providing insight into the basic mechanisms of E2F1-induced apoptosis and its possible clinical implications.'?",False,https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2021.723137/full -10598517,E2F1 gene|E2F1|UBE2L3 causes Apoptosis,116,"Here, these findings are highlighted in the context of the most recent follow-up studies that have used apoptotic E2F1 genes as new therapeutics or drug targets, thereby providing insight into the basic mechanisms of E2F1-induced apoptosis and its possible clinical implications.","Is the triple 'E2F1 gene|E2F1|UBE2L3 causes Apoptosis' supported by the sentence: 'Here, these findings are highlighted in the context of the most recent follow-up studies that have used apoptotic E2F1 genes as new therapeutics or drug targets, thereby providing insight into the basic mechanisms of E2F1-induced apoptosis and its possible clinical implications.'?",True,https://www.frontiersin.org/articles/10.3389/fmolb.2020.599332/full -10599076,Gene Expression process of Scorpaenidae,123,Protein and gene expression of VTG in response to 4-nonylphenol in rockfish (Sebastes schlegeli).,Is the triple 'Gene Expression process of Scorpaenidae' supported by the sentence: 'Protein and gene expression of VTG in response to 4-nonylphenol in rockfish (Sebastes schlegeli).'?,True,https://en.wikipedia.org/wiki/Scorpaenidae -10599190,Vitellogenins part of Scorpaenidae,124,"To investigate the in vivo estrogenic activity of 4-nonylphenol (4-NP) on reproductive function, we have measured the expression level of rockfish vitellogenin (rVTG) mRNA, concentration of plasma VTG and levels of plasma estradiol-17beta(E(2)) and testosterone (T) by radioimmunoassay (RIA).","Is the triple 'Vitellogenins part of Scorpaenidae' supported by the sentence: 'To investigate the in vivo estrogenic activity of 4-nonylphenol (4-NP) on reproductive function, we have measured the expression level of rockfish vitellogenin (rVTG) mRNA, concentration of plasma VTG and levels of plasma estradiol-17beta(E(2)) and testosterone (T) by radioimmunoassay (RIA).'?",False,https://en.wikipedia.org/wiki/Scorpaenidae -10599329,Vitellogenins part of Scorpaenidae,125,"An rVTG mRNA transcript of approximately 4.0 kb was extracted from hepatic tissue for Northern blot analysis, and the effects of 4-NP on rVTG mRNA expression in vivo with both male and female juvenile rockfish were examined.","Is the triple 'Vitellogenins part of Scorpaenidae' supported by the sentence: 'An rVTG mRNA transcript of approximately 4.0 kb was extracted from hepatic tissue for Northern blot analysis, and the effects of 4-NP on rVTG mRNA expression in vivo with both male and female juvenile rockfish were examined.'?",False,https://en.wikipedia.org/wiki/Scorpaenidae -10599368,Vitellogenins part of Scorpaenidae,125,"An rVTG mRNA transcript of approximately 4.0 kb was extracted from hepatic tissue for Northern blot analysis, and the effects of 4-NP on rVTG mRNA expression in vivo with both male and female juvenile rockfish were examined.","Is the triple 'Vitellogenins part of Scorpaenidae' supported by the sentence: 'An rVTG mRNA transcript of approximately 4.0 kb was extracted from hepatic tissue for Northern blot analysis, and the effects of 4-NP on rVTG mRNA expression in vivo with both male and female juvenile rockfish were examined.'?",False,https://en.wikipedia.org/wiki/Scorpaenidae -10599395,Vitellogenins affects No past history,125,"An rVTG mRNA transcript of approximately 4.0 kb was extracted from hepatic tissue for Northern blot analysis, and the effects of 4-NP on rVTG mRNA expression in vivo with both male and female juvenile rockfish were examined.","Is the triple 'Vitellogenins affects No past history' supported by the sentence: 'An rVTG mRNA transcript of approximately 4.0 kb was extracted from hepatic tissue for Northern blot analysis, and the effects of 4-NP on rVTG mRNA expression in vivo with both male and female juvenile rockfish were examined.'?",False,https://academic.oup.com/gbe/article/10/10/2709/5101341 -10599484,Vitellogenins part of Scorpaenidae,126,The level of rVTG mRNA expression was increased 48 h after injection with 4-NP of 10 mg/kg body mass and after injection in both male and female rockfish.,Is the triple 'Vitellogenins part of Scorpaenidae' supported by the sentence: 'The level of rVTG mRNA expression was increased 48 h after injection with 4-NP of 10 mg/kg body mass and after injection in both male and female rockfish.'?,False,https://en.wikipedia.org/wiki/Vitellogenin -10599560,Vitellogenins part of Scorpaenidae,127,"The level of rVTG mRNA expression was increased 24 h after injection in male rockfish injected with 4-NP of 25 mg/kg body mass, while the level of rVTG mRNA expression was increased 12h after injection in female injected with same dosage.","Is the triple 'Vitellogenins part of Scorpaenidae' supported by the sentence: 'The level of rVTG mRNA expression was increased 24 h after injection in male rockfish injected with 4-NP of 25 mg/kg body mass, while the level of rVTG mRNA expression was increased 12h after injection in female injected with same dosage.'?",False,https://en.wikipedia.org/wiki/Vitellogenin -10599602,Vitellogenins part of Scorpaenidae,127,"The level of rVTG mRNA expression was increased 24 h after injection in male rockfish injected with 4-NP of 25 mg/kg body mass, while the level of rVTG mRNA expression was increased 12h after injection in female injected with same dosage.","Is the triple 'Vitellogenins part of Scorpaenidae' supported by the sentence: 'The level of rVTG mRNA expression was increased 24 h after injection in male rockfish injected with 4-NP of 25 mg/kg body mass, while the level of rVTG mRNA expression was increased 12h after injection in female injected with same dosage.'?",False,https://en.wikipedia.org/wiki/Vitellogenin -10599653,Injection procedure treats Female,127,"The level of rVTG mRNA expression was increased 24 h after injection in male rockfish injected with 4-NP of 25 mg/kg body mass, while the level of rVTG mRNA expression was increased 12h after injection in female injected with same dosage.","Is the triple 'Injection procedure treats Female' supported by the sentence: 'The level of rVTG mRNA expression was increased 24 h after injection in male rockfish injected with 4-NP of 25 mg/kg body mass, while the level of rVTG mRNA expression was increased 12h after injection in female injected with same dosage.'?",True,https://www.mercy.com/health-care-services/urology/treatments/urethral-bulking-injection -10599747,Vitellogenins part of Scorpaenidae,128,"Concentrations of plasma rVTG in female injected with 4-NP of 10 and 25 mg/kg b.w. were increased 72 h after injection and reached 35 and 66 mg/mL, respectively.","Is the triple 'Vitellogenins part of Scorpaenidae' supported by the sentence: 'Concentrations of plasma rVTG in female injected with 4-NP of 10 and 25 mg/kg b.w. were increased 72 h after injection and reached 35 and 66 mg/mL, respectively.'?",False,https://www.frontiersin.org/articles/10.3389/fphys.2019.01067/full -10599840,Vitellogenins part of Scorpaenidae,129,"In male, rVTG concentrations with the dosage of 25 mg/kg body mass were increased 72 h after injection and reached to 14 and 65 mg/mL at 168 h, respectively.","Is the triple 'Vitellogenins part of Scorpaenidae' supported by the sentence: 'In male, rVTG concentrations with the dosage of 25 mg/kg body mass were increased 72 h after injection and reached to 14 and 65 mg/mL at 168 h, respectively.'?",False,https://www.frontiersin.org/articles/10.3389/fphys.2019.01067/full -10600338,Homologous Gene part of Hemicentrotus pulcherrimus,141,"Developmental expression of HpNanos, the Hemicentrotus pulcherrimus homologue of nanos.","Is the triple 'Homologous Gene part of Hemicentrotus pulcherrimus' supported by the sentence: 'Developmental expression of HpNanos, the Hemicentrotus pulcherrimus homologue of nanos.'?",False,https://europepmc.org/article/MED/16530490 -10600422,cDNA Library part of Gastrula,142,"The Hemicentrotus pulcherrimus homologue of nanos (HpNanos), that encodes a protein containing two CCHC zinc finger motifs, was isolated from a gastrula cDNA library.","Is the triple 'cDNA Library part of Gastrula' supported by the sentence: 'The Hemicentrotus pulcherrimus homologue of nanos (HpNanos), that encodes a protein containing two CCHC zinc finger motifs, was isolated from a gastrula cDNA library.'?",False,https://europepmc.org/article/PMC/540274 -10600456,Homologous Gene part of Hemicentrotus pulcherrimus,142,"The Hemicentrotus pulcherrimus homologue of nanos (HpNanos), that encodes a protein containing two CCHC zinc finger motifs, was isolated from a gastrula cDNA library.","Is the triple 'Homologous Gene part of Hemicentrotus pulcherrimus' supported by the sentence: 'The Hemicentrotus pulcherrimus homologue of nanos (HpNanos), that encodes a protein containing two CCHC zinc finger motifs, was isolated from a gastrula cDNA library.'?",False,https://db.cngb.org/stomics/publications/16530490 -10600542,Blastocyst structure part of Mesenchyma,144,"Developmental northern blot analysis revealed that HpNanos mRNA markedly accumulated during the blastula stages, and then decreased in abundance at the mesenchyme blastula stage.","Is the triple 'Blastocyst structure part of Mesenchyma' supported by the sentence: 'Developmental northern blot analysis revealed that HpNanos mRNA markedly accumulated during the blastula stages, and then decreased in abundance at the mesenchyme blastula stage.'?",False,https://en.wikipedia.org/wiki/Blastocyst -10600645,In Situ Hybridization uses Mounts,146,Whole-mount in situ hybridization showed that the HpNanos was exclusively expressed in four to six small micromere-descendant cells at the blastula stage.,Is the triple 'In Situ Hybridization uses Mounts' supported by the sentence: 'Whole-mount in situ hybridization showed that the HpNanos was exclusively expressed in four to six small micromere-descendant cells at the blastula stage.'?,False,https://www.jove.com/v/5330/whole-mount-in-situ-hybridization -10600813,Embryo location of PPY,151,"PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.","Is the triple 'Embryo location of PPY' supported by the sentence: 'PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.'?",True,https://www.proteinatlas.org/ENSG00000204174-NPY4R -10600845,Inferior Colliculus part of Males,151,"PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.","Is the triple 'Inferior Colliculus part of Males' supported by the sentence: 'PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.'?",False,https://www.healthline.com/human-body-maps/inferior-colliculus -10600962,PPY part of Mothers,153,The maternal PPYR1 is localized in the cytoplasm of the follicular and nurse cells and is deposited as a ribonucleoprotein complex in the oocyte.,Is the triple 'PPY part of Mothers' supported by the sentence: 'The maternal PPYR1 is localized in the cytoplasm of the follicular and nurse cells and is deposited as a ribonucleoprotein complex in the oocyte.'?,True,https://www.frontiersin.org/articles/10.3389/fcell.2023.1240481/full -10600997,Cells part of Nurses,153,The maternal PPYR1 is localized in the cytoplasm of the follicular and nurse cells and is deposited as a ribonucleoprotein complex in the oocyte.,Is the triple 'Cells part of Nurses' supported by the sentence: 'The maternal PPYR1 is localized in the cytoplasm of the follicular and nurse cells and is deposited as a ribonucleoprotein complex in the oocyte.'?,False,https://en.wikipedia.org/wiki/Nurse_cell -10601037,Cytoplasm location of PPY,153,The maternal PPYR1 is localized in the cytoplasm of the follicular and nurse cells and is deposited as a ribonucleoprotein complex in the oocyte.,Is the triple 'Cytoplasm location of PPY' supported by the sentence: 'The maternal PPYR1 is localized in the cytoplasm of the follicular and nurse cells and is deposited as a ribonucleoprotein complex in the oocyte.'?,True,https://www.uniprot.org/uniprotkb/P01298/entry -10601150,Cytoplasm part of Spermatocytes,155,"Zygotic PPYR1 is expressed exclusively in the testes, predominantly in the cytoplasm of the spermatocytes.","Is the triple 'Cytoplasm part of Spermatocytes' supported by the sentence: 'Zygotic PPYR1 is expressed exclusively in the testes, predominantly in the cytoplasm of the spermatocytes.'?",True,https://www.frontiersin.org/articles/10.3389/fvets.2023.1188479/full -10601184,Inferior Colliculus location of PPY,155,"Zygotic PPYR1 is expressed exclusively in the testes, predominantly in the cytoplasm of the spermatocytes.","Is the triple 'Inferior Colliculus location of PPY' supported by the sentence: 'Zygotic PPYR1 is expressed exclusively in the testes, predominantly in the cytoplasm of the spermatocytes.'?",False,https://www.healthline.com/human-body-maps/inferior-colliculus#1 -10601265,Cell Nucleus part of Cells,156,PPY is localized in the nuclei of the same cells.,Is the triple 'Cell Nucleus part of Cells' supported by the sentence: 'PPY is localized in the nuclei of the same cells.'?,True,https://biologydictionary.net/cell-parts-and-functions/ -10601441,Column location of Diastasis,160,"Phenacetin was chosen as the internal standard, and the separation was achieved on a C18 column with methanol and 0.02 M phosphate buffer (pH 3.2) as mobile phase.","Is the triple 'Column location of Diastasis' supported by the sentence: 'Phenacetin was chosen as the internal standard, and the separation was achieved on a C18 column with methanol and 0.02 M phosphate buffer (pH 3.2) as mobile phase.'?",False,https://radiopaedia.org/articles/diastasis-recti -10601592,Drug Kinetics process of Rattus norvegicus,163,This method can be used to study the pharmacokinetics of AKF-PD in rat.,Is the triple 'Drug Kinetics process of Rattus norvegicus' supported by the sentence: 'This method can be used to study the pharmacokinetics of AKF-PD in rat.'?,True,https://www.journal-imab-bg.org/issues-2022/issue3/vol28issue3p4525-4531.html -10601714,Glycosaminoglycans is a Polysaccharides,165,"Complex polysaccharides, glycosaminoglycans (GAGs), are a class of ubiquitous macromolecules exhibiting a wide range of biological functions.","Is the triple 'Glycosaminoglycans is a Polysaccharides' supported by the sentence: 'Complex polysaccharides, glycosaminoglycans (GAGs), are a class of ubiquitous macromolecules exhibiting a wide range of biological functions.'?",True,https://www.frontiersin.org/articles/10.3389/fmolb.2021.639666/full -10601803,Extracellular Matrix location of Proteoglycan,166,They are widely distributed as sidechains of proteoglycans (PGs) in the extracellular matrix and at cellular level.,Is the triple 'Extracellular Matrix location of Proteoglycan' supported by the sentence: 'They are widely distributed as sidechains of proteoglycans (PGs) in the extracellular matrix and at cellular level.'?,True,https://www.frontiersin.org/articles/10.3389/fcell.2021.760532/full -10601941,GAG Gene converts to Glycosaminoglycans,168,"Analytical electrophoretic separation techniques, including agarose-gel, capillary electrophoresis (HPCE) and fluorophore-assisted carbohydrate electrophoresis (FACE), of GAGs and GAG-derived oligosaccharides have been employed for the structural analysis and quantification of hyaluronic acid (HA), chondroitin sulfate (CS), dermatan sulfate (DS), keratan sulfate (KS), heparan sulfate (HS), heparin (Hep) and acidic bacterial polysaccharides.","Is the triple 'GAG Gene converts to Glycosaminoglycans' supported by the sentence: 'Analytical electrophoretic separation techniques, including agarose-gel, capillary electrophoresis (HPCE) and fluorophore-assisted carbohydrate electrophoresis (FACE), of GAGs and GAG-derived oligosaccharides have been employed for the structural analysis and quantification of hyaluronic acid (HA), chondroitin sulfate (CS), dermatan sulfate (DS), keratan sulfate (KS), heparan sulfate (HS), heparin (Hep) and acidic bacterial polysaccharides.'?",False,https://www.frontiersin.org/articles/10.3389/fcell.2021.709018/full -10601994,GAG Gene converts to Oligosaccharides,168,"Analytical electrophoretic separation techniques, including agarose-gel, capillary electrophoresis (HPCE) and fluorophore-assisted carbohydrate electrophoresis (FACE), of GAGs and GAG-derived oligosaccharides have been employed for the structural analysis and quantification of hyaluronic acid (HA), chondroitin sulfate (CS), dermatan sulfate (DS), keratan sulfate (KS), heparan sulfate (HS), heparin (Hep) and acidic bacterial polysaccharides.","Is the triple 'GAG Gene converts to Oligosaccharides' supported by the sentence: 'Analytical electrophoretic separation techniques, including agarose-gel, capillary electrophoresis (HPCE) and fluorophore-assisted carbohydrate electrophoresis (FACE), of GAGs and GAG-derived oligosaccharides have been employed for the structural analysis and quantification of hyaluronic acid (HA), chondroitin sulfate (CS), dermatan sulfate (DS), keratan sulfate (KS), heparan sulfate (HS), heparin (Hep) and acidic bacterial polysaccharides.'?",False,https://link.springer.com/chapter/10.1007/978-3-662-63123-2_41 -10602026,Electrophoresis uses Structural analysis,168,"Analytical electrophoretic separation techniques, including agarose-gel, capillary electrophoresis (HPCE) and fluorophore-assisted carbohydrate electrophoresis (FACE), of GAGs and GAG-derived oligosaccharides have been employed for the structural analysis and quantification of hyaluronic acid (HA), chondroitin sulfate (CS), dermatan sulfate (DS), keratan sulfate (KS), heparan sulfate (HS), heparin (Hep) and acidic bacterial polysaccharides.","Is the triple 'Electrophoresis uses Structural analysis' supported by the sentence: 'Analytical electrophoretic separation techniques, including agarose-gel, capillary electrophoresis (HPCE) and fluorophore-assisted carbohydrate electrophoresis (FACE), of GAGs and GAG-derived oligosaccharides have been employed for the structural analysis and quantification of hyaluronic acid (HA), chondroitin sulfate (CS), dermatan sulfate (DS), keratan sulfate (KS), heparan sulfate (HS), heparin (Hep) and acidic bacterial polysaccharides.'?",False,https://sciencing.com/list-applications-electrophoresis-5606215.html -10602109,Enzymes interacts with Glycosaminoglycans,169,"Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.","Is the triple 'Enzymes interacts with Glycosaminoglycans' supported by the sentence: 'Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.'?",True,https://www.frontiersin.org/articles/10.3389/fmolb.2021.639666/full -10602147,Chemicals interacts with Glycosaminoglycans,169,"Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.","Is the triple 'Chemicals interacts with Glycosaminoglycans' supported by the sentence: 'Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.'?",True,https://www.frontiersin.org/articles/10.3389/fmolb.2021.639666/full -10602185,Glycosaminoglycans converts to Disaccharides,169,"Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.","Is the triple 'Glycosaminoglycans converts to Disaccharides' supported by the sentence: 'Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.'?",True,https://europepmc.org/article/MED/23234263 -10602215,Glycosaminoglycans converts to Oligosaccharides,169,"Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.","Is the triple 'Glycosaminoglycans converts to Oligosaccharides' supported by the sentence: 'Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.'?",True,https://link.springer.com/chapter/10.1007/978-3-662-63123-2_41 -10602419,Diabetes process of Patients,173,"Aim of this study was to set up a method by capillary electrophoresis to detect lactulose and mannitol in urine after an oral load, and to estimate the intestinal permeability in controls and in type I diabetes patients.","Is the triple 'Diabetes process of Patients' supported by the sentence: 'Aim of this study was to set up a method by capillary electrophoresis to detect lactulose and mannitol in urine after an oral load, and to estimate the intestinal permeability in controls and in type I diabetes patients.'?",True,https://www.cdc.gov/diabetes/basics/type2.html -10602491,Detection uses Sorbate,174,"The underivatized carbohydrates were monitored by indirect UV detection using sorbate, cetyltrimethylammonium bromide and LiOH as background electrolyte.","Is the triple 'Detection uses Sorbate' supported by the sentence: 'The underivatized carbohydrates were monitored by indirect UV detection using sorbate, cetyltrimethylammonium bromide and LiOH as background electrolyte.'?",False,https://www.pharmatutor.org/articles/review-on-determination-preservatives-food-stuffs-different-analytical-methods -10602733,Atrial Flutter is a Tachycardia,182,"It should be distinguished from other types of tachycardia - such as atrial flutter, atrial ectopic tachycardia, permanent junctional re-entry tachycardia, and ventricular tachycardia.","Is the triple 'Atrial Flutter is a Tachycardia' supported by the sentence: 'It should be distinguished from other types of tachycardia - such as atrial flutter, atrial ectopic tachycardia, permanent junctional re-entry tachycardia, and ventricular tachycardia.'?",True,https://www.lecturio.com/concepts/atrial-flutter/ -10602764,"Tachycardia, Ectopic Atrial is a Tachycardia",182,"It should be distinguished from other types of tachycardia - such as atrial flutter, atrial ectopic tachycardia, permanent junctional re-entry tachycardia, and ventricular tachycardia.","Is the triple 'Tachycardia, Ectopic Atrial is a Tachycardia' supported by the sentence: 'It should be distinguished from other types of tachycardia - such as atrial flutter, atrial ectopic tachycardia, permanent junctional re-entry tachycardia, and ventricular tachycardia.'?",True,https://litfl.com/atrial-tachycardia-ecg-library/ -10602804,"Tachycardia, Ectopic Junctional is a Tachycardia",182,"It should be distinguished from other types of tachycardia - such as atrial flutter, atrial ectopic tachycardia, permanent junctional re-entry tachycardia, and ventricular tachycardia.","Is the triple 'Tachycardia, Ectopic Junctional is a Tachycardia' supported by the sentence: 'It should be distinguished from other types of tachycardia - such as atrial flutter, atrial ectopic tachycardia, permanent junctional re-entry tachycardia, and ventricular tachycardia.'?",True,https://academic.oup.com/eurheartj/article/19/6/936/406303 -10602837,"Tachycardia, Ventricular is a Tachycardia",182,"It should be distinguished from other types of tachycardia - such as atrial flutter, atrial ectopic tachycardia, permanent junctional re-entry tachycardia, and ventricular tachycardia.","Is the triple 'Tachycardia, Ventricular is a Tachycardia' supported by the sentence: 'It should be distinguished from other types of tachycardia - such as atrial flutter, atrial ectopic tachycardia, permanent junctional re-entry tachycardia, and ventricular tachycardia.'?",True,https://www.mayoclinic.org/diseases-conditions/ventricular-tachycardia/symptoms-causes/syc-20355138 -10603013,"PTH protein, human|PTH associated with osteosarcoma",187,"The American Food and Drug Administration approval of parathyroid hormone (PTH) administration for osteoporosis as well as the possibility for its future therapeutic applications requires an examination of the suggested association between PTH and cancer, particularly osteosarcomas.","Is the triple 'PTH protein, human|PTH associated with osteosarcoma' supported by the sentence: 'The American Food and Drug Administration approval of parathyroid hormone (PTH) administration for osteoporosis as well as the possibility for its future therapeutic applications requires an examination of the suggested association between PTH and cancer, particularly osteosarcomas.'?",True,https://www.frontiersin.org/articles/10.3389/fvets.2021.637614/full -10603029,osteosarcoma is a Malignant Neoplasms,187,"The American Food and Drug Administration approval of parathyroid hormone (PTH) administration for osteoporosis as well as the possibility for its future therapeutic applications requires an examination of the suggested association between PTH and cancer, particularly osteosarcomas.","Is the triple 'osteosarcoma is a Malignant Neoplasms' supported by the sentence: 'The American Food and Drug Administration approval of parathyroid hormone (PTH) administration for osteoporosis as well as the possibility for its future therapeutic applications requires an examination of the suggested association between PTH and cancer, particularly osteosarcomas.'?",True,https://www.mayoclinic.org/diseases-conditions/osteosarcoma/symptoms-causes/syc-20351052 -10603069,"PTH protein, human|PTH associated with Malignant Neoplasms",187,"The American Food and Drug Administration approval of parathyroid hormone (PTH) administration for osteoporosis as well as the possibility for its future therapeutic applications requires an examination of the suggested association between PTH and cancer, particularly osteosarcomas.","Is the triple 'PTH protein, human|PTH associated with Malignant Neoplasms' supported by the sentence: 'The American Food and Drug Administration approval of parathyroid hormone (PTH) administration for osteoporosis as well as the possibility for its future therapeutic applications requires an examination of the suggested association between PTH and cancer, particularly osteosarcomas.'?",True,https://www.frontiersin.org/articles/10.3389/fvets.2021.637614/full diff --git a/data/predicate-remap.yaml b/data/predicate-remap.yaml deleted file mode 100644 index 0a6030e..0000000 --- a/data/predicate-remap.yaml +++ /dev/null @@ -1,5034 +0,0 @@ -ATC:has_member: - operation: keep - core_predicate: biolink:has_member -ATC:inverse_isa: - operation: invert - core_predicate: biolink:subclass_of -ATC:isa: - operation: keep - core_predicate: biolink:subclass_of -ATC:member_of: - operation: invert - core_predicate: biolink:has_member -BFO:0000050: - operation: invert - core_predicate: biolink:has_part -BFO:0000051: - operation: keep - core_predicate: biolink:has_part -BFO:0000054: - operation: keep - core_predicate: biolink:related_to -BFO:0000055: - operation: keep - core_predicate: biolink:has_part -# BFO:0000056: -# operation: invert -# core_predicate: biolink:has_participant -BFO:0000062: - operation: invert - core_predicate: biolink:precedes -BFO:0000063: - operation: keep - core_predicate: biolink:precedes -BFO:0000066: - operation: keep - core_predicate: biolink:occurs_in -BFO:0000067: - operation: keep - core_predicate: biolink:occurs_in -BFO:0000068: - operation: keep - core_predicate: biolink:related_to -BFO:0000069: - operation: keep - core_predicate: biolink:related_to -BFO:0000117: - operation: keep - core_predicate: biolink:has_part -BFO:0000167: - operation: keep - core_predicate: biolink:has_participant -BSPO:0000096: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0000097: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0000098: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0000099: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0000100: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0000102: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0000104: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0000107: - operation: keep - core_predicate: biolink:located_in -BSPO:0000108: - operation: keep - core_predicate: biolink:located_in -BSPO:0000110: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0000113: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0000120: - operation: keep - core_predicate: biolink:located_in -BSPO:0000121: - operation: keep - core_predicate: biolink:located_in -BSPO:0000122: - operation: keep - core_predicate: biolink:located_in -BSPO:0000123: - operation: keep - core_predicate: biolink:located_in -BSPO:0000124: - operation: keep - core_predicate: biolink:located_in -BSPO:0000125: - operation: keep - core_predicate: biolink:located_in -BSPO:0000126: - operation: keep - core_predicate: biolink:located_in -BSPO:0001100: - operation: keep - core_predicate: biolink:located_in -BSPO:0001101: - operation: keep - core_predicate: biolink:located_in -BSPO:0001102: - operation: delete -BSPO:0001106: - operation: invert - core_predicate: biolink:has_part -BSPO:0001107: - operation: keep - core_predicate: biolink:located_in -BSPO:0001108: - operation: invert - core_predicate: biolink:has_part -BSPO:0001113: - operation: invert - core_predicate: biolink:has_part -BSPO:0001115: - operation: invert - core_predicate: biolink:has_part -BSPO:0005001: - operation: keep - core_predicate: biolink:overlaps -BSPO:0015001: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0015002: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0015003: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0015005: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0015006: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0015007: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0015008: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0015009: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0015012: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0015014: - operation: keep - core_predicate: biolink:coexists_with -BSPO:0015101: - operation: keep - core_predicate: biolink:located_in -BSPO:0015102: - operation: keep - core_predicate: biolink:located_in -BSPO:0015202: - operation: keep - core_predicate: biolink:located_in -BSPO:0020001: - operation: invert - core_predicate: biolink:has_part -# BSPO:parallel_to: -# operation: keep -# core_predicate: biolink:coexists_with -BTO:develops_from: - operation: keep - core_predicate: biolink:develops_from -BTO:related_to: - operation: keep - core_predicate: biolink:related_to -# CHEBI:25212: -# operation: invert -# core_predicate: biolink:has_metabolite -CHEBI:has_functional_parent: - operation: keep - core_predicate: biolink:chemically_similar_to -CHEBI:has_parent_hydride: - operation: keep - core_predicate: biolink:subclass_of -CHEBI:is_conjugate_acid_of: - operation: keep - core_predicate: biolink:related_to -CHEBI:is_conjugate_base_of: - operation: keep - core_predicate: biolink:related_to -CHEBI:is_enantiomer_of: - operation: keep - core_predicate: biolink:close_match -CHEBI:is_substituent_group_from: - operation: invert - core_predicate: biolink:has_part -CHEBI:is_tautomer_of: - operation: keep - core_predicate: biolink:close_match -CHEMBL.MECHANISM:activator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -CHEMBL.MECHANISM:agonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -CHEMBL.MECHANISM:allosteric_antagonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -CHEMBL.MECHANISM:antagonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -CHEMBL.MECHANISM:antisense_inhibitor: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: degradation - object_direction: increased -CHEMBL.MECHANISM:binding_agent: - operation: keep - core_predicate: biolink:physically_interacts_with -CHEMBL.MECHANISM:blocker: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -CHEMBL.MECHANISM:chelating_agent: - operation: keep - core_predicate: biolink:physically_interacts_with -CHEMBL.MECHANISM:cross-linking_agent: - operation: keep - core_predicate: biolink:physically_interacts_with -CHEMBL.MECHANISM:degrader: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: degradation - object_direction: increased -CHEMBL.MECHANISM:disrupting_agent: - operation: keep - core_predicate: biolink:disrupts -CHEMBL.MECHANISM:equivalent_to: - operation: keep - core_predicate: biolink:same_as -CHEMBL.MECHANISM:hydrolytic_enzyme: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: degradation - object_direction: increased -CHEMBL.MECHANISM:inhibitor: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -CHEMBL.MECHANISM:inverse_agonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -CHEMBL.MECHANISM:modulator: - operation: keep - core_predicate: biolink:regulates -CHEMBL.MECHANISM:negative_allosteric_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -CHEMBL.MECHANISM:negative_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -CHEMBL.MECHANISM:opener: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -CHEMBL.MECHANISM:other: - operation: delete -CHEMBL.MECHANISM:overlaps_with: - operation: keep - core_predicate: biolink:overlaps -CHEMBL.MECHANISM:oxidative_enzyme: - operation: keep - core_predicate: biolink:physically_interacts_with -CHEMBL.MECHANISM:partial_agonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -CHEMBL.MECHANISM:positive_allosteric_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -CHEMBL.MECHANISM:positive_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -CHEMBL.MECHANISM:proteolytic_enzyme: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: degradation - object_direction: increased -CHEMBL.MECHANISM:reducing_agent: - operation: keep - core_predicate: biolink:physically_interacts_with -CHEMBL.MECHANISM:releasing_agent: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -CHEMBL.MECHANISM:rnai_inhibitor: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: abundance - object_direction: decreased -CHEMBL.MECHANISM:vaccine_antigen: - operation: keep - core_predicate: biolink:related_to -CHEMBL.MECHANISM:sequestering_agent: - operation: keep - core_predicate: biolink:physically_interacts_with -CHEMBL.MECHANISM:stabiliser: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: stability - object_direction: increased -CHEMBL.MECHANISM:subset_of: - operation: keep - core_predicate: biolink:subclass_of -CHEMBL.MECHANISM:substrate: - operation: keep - core_predicate: biolink:physically_interacts_with -CHEMBL.MECHANISM:superset_of: - operation: keep - core_predicate: biolink:superclass_of -CL:4030044: # has not completed - operation: keep - core_predicate: biolink:has_not_completed -CL:4030045: # lacks part - operation: keep - core_predicate: biolink:lacks_part -CL:4030046: # lacks plasma membrane part - operation: keep - core_predicate: biolink:lacks_part -CL:has_completed: - operation: keep - core_predicate: biolink:has_completed -CL:has_high_plasma_membrane_amount: - operation: keep - core_predicate: biolink:has_increased_amount -CL:has_low_plasma_membrane_amount: - operation: keep - core_predicate: biolink:has_decreased_amount -CL:has_not_completed: - operation: keep - core_predicate: biolink:has_not_completed -CL:lacks_part: - operation: keep - core_predicate: biolink:lacks_part -CL:lacks_plasma_membrane_part: - operation: keep - core_predicate: biolink:lacks_part -CTD:increases_expression_of: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: expression - object_direction: increased -DDANAT:develops_from: - operation: keep - core_predicate: biolink:develops_from -DGIdb:activator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -# DGIdb:adduct: -# operation: keep -# core_predicate: biolink:directly_physically_interacts_with -DGIdb:affects: - operation: keep - core_predicate: biolink:affects -DGIdb:agonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -DGIdb:allosteric_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity -DGIdb:antagonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DGIdb:antibody: - operation: keep - core_predicate: biolink:physically_interacts_with -DGIdb:antisense_oligonucleotide: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: expression - object_direction: decreased -# DGIdb:binder: -# operation: keep -# core_predicate: biolink:interacts_with -DGIdb:blocker: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -# DGIdb:channel_blocker: -# operation: keep -# core_predicate: biolink:affects -# qualified_predicate: biolink:causes -# qualifiers: -# object_aspect: activity -# object_direction: decreased -# DGIdb:chaperone: -# operation: keep -# core_predicate: biolink:directly_physically_interacts_with -# DGIdb:cleavage: -# operation: keep -# core_predicate: biolink:affects -# qualifiers: -# object_aspect: degradation -DGIdb:cofactor: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -# DGIdb:gating_inhibitor: -# operation: keep -# core_predicate: biolink:affects -# qualified_predicate: biolink:causes -# qualifiers: -# object_aspect: activity -# object_direction: decreased -DGIdb:inducer: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -DGIdb:inhibitor: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DGIdb:inhibitory_allosteric_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DGIdb:inverse_agonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -# DGIdb:ligand: -# operation: keep -# core_predicate: biolink:directly_physically_interacts_with -DGIdb:modulator: - operation: keep - core_predicate: biolink:affects -# DGIdb:multitarget: -# operation: keep -# core_predicate: biolink:directly_physically_interacts_with -DGIdb:negative_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DGIdb:partial_agonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -# DGIdb:partial_antagonist: -# operation: keep -# core_predicate: biolink:affects -# qualified_predicate: biolink:causes -# qualifiers: -# object_aspect: activity -# object_direction: decreased -DGIdb:positive_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -# DGIdb:potentiator: -# operation: keep -# core_predicate: biolink:affects -# qualified_predicate: biolink:causes -# qualifiers: -# object_aspect: activity -# object_direction: increased -# DGIdb:product_of: -# operation: keep -# core_predicate: biolink:derives_from -# DGIdb:stimulator: -# operation: keep -# core_predicate: biolink:affects -# qualified_predicate: biolink:causes -# qualifiers: -# object_aspect: activity -# object_direction: increased -# DGIdb:substrate: -# operation: keep -# core_predicate: biolink:affects -# qualified_predicate: biolink:causes -# qualifiers: -# object_aspect: degradation -# object_direction: increased -DGIdb:suppressor: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DGIdb:vaccine: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -#DOID-PROPERTY:derives_from: -# operation: keep -# core_predicate: biolink:related_to_at_instance_level -# DOID-PROPERTY:has_symptom: -# operation: keep -# core_predicate: biolink:has_phenotype -DRUGBANK:activator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -# DRUGBANK:adduct: -# operation: keep -# core_predicate: biolink:directly_physically_interacts_with -# DRUGBANK:aggregation_inhibitor: -# operation: keep -# core_predicate: biolink:affects -# qualified_predicate: biolink:causes -# qualifiers: -# object_aspect: activity -# object_direction: decreased -DRUGBANK:agonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -DRUGBANK:allosteric_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity -DRUGBANK:antagonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DRUGBANK:antibody: - operation: keep - core_predicate: biolink:physically_interacts_with -DRUGBANK:antisense_oligonucleotide: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: expression - object_direction: decreased -DRUGBANK:atc-code: - operation: keep - core_predicate: biolink:close_match -DRUGBANK:atc-code-level: - operation: keep - core_predicate: biolink:related_to -DRUGBANK:binder: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -DRUGBANK:binding: - operation: keep - core_predicate: biolink:physically_interacts_with -DRUGBANK:blocker: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity_or_abundance - object_direction: decreased -DRUGBANK:carrier: - operation: keep - core_predicate: biolink:related_to -DRUGBANK:category: - operation: keep - core_predicate: biolink:subclass_of -DRUGBANK:chaperone: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -DRUGBANK:chelator: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -DRUGBANK:cleavage: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: degradation -DRUGBANK:cofactor: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -DRUGBANK:component_of: - operation: invert - core_predicate: biolink:has_part -DRUGBANK:degradation: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: degradation -# DRUGBANK:deoxidizer: -# operation: keep -# core_predicate: biolink:affects -# qualified_predicate: biolink:causes -# qualifiers: -# object_aspect: molecular_modification -# object_direction: decreased -# DRUGBANK:desensitize_the_target: -# operation: keep -# core_predicate: biolink:decreases_response_to -DRUGBANK:downregulator: - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: downregulated -DRUGBANK:drug-interaction: - operation: keep - core_predicate: biolink:physically_interacts_with -DRUGBANK:external-identifier: - operation: keep - core_predicate: biolink:same_as -DRUGBANK:external-identifier-protein: - operation: keep - core_predicate: biolink:derives_from -DRUGBANK:gene_replacement: - operation: keep - core_predicate: biolink:close_match -DRUGBANK:group: - operation: keep - core_predicate: biolink:related_to -DRUGBANK:inactivator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DRUGBANK:incorporation_into_and_destabilization: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: degradation -DRUGBANK:inducer: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -DRUGBANK:inhibition_of_synthesis: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: synthesis - object_direction: decreased -DRUGBANK:inhibitor: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DRUGBANK:inhibitory_allosteric_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DRUGBANK:intercalation: - operation: keep - core_predicate: biolink:physically_interacts_with -DRUGBANK:inverse_agonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DRUGBANK:ligand: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -DRUGBANK:modulator: - operation: keep - core_predicate: biolink:affects -DRUGBANK:multitarget: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -DRUGBANK:negative_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DRUGBANK:neutralizer: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DRUGBANK:nucleotide_exchange_blocker: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DRUGBANK:oxidizer: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: molecular_modification - object_direction: increased -DRUGBANK:partial_agonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -DRUGBANK:partial_antagonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DRUGBANK:pathway: - operation: invert - core_predicate: biolink:has_participant -DRUGBANK:positive_allosteric_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -# DRUGBANK:positive_modulator: -# operation: keep -# core_predicate: biolink:regulates -# qualified_predicate: biolink:causes -# qualifiers: -# object_direction: increased -DRUGBANK:potentiator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -DRUGBANK:product_of: - operation: keep - core_predicate: biolink:derives_from -DRUGBANK:regulator: - operation: keep - core_predicate: biolink:regulates -DRUGBANK:stabilization: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: stability - object_direction: increased -DRUGBANK:stimulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -DRUGBANK:substrate: - operation: keep - core_predicate: biolink:physically_interacts_with -DRUGBANK:suppressor: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DRUGBANK:target: - operation: keep - core_predicate: biolink:physically_interacts_with -DRUGBANK:translocation_inhibitor: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -# DRUGBANK:treats: -# operation: keep -# core_predicate: biolink:treats -DRUGBANK:weak_inhibitor: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -# DrugCentral:5271: -# operation: keep -# core_predicate: biolink:diagnoses -DrugCentral:other: - operation: delete -DrugCentral:PA: - operation: keep - core_predicate: biolink:subclass_of -DrugCentral:activator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -DrugCentral:agonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -DrugCentral:allosteric_antagonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DrugCentral:allosteric_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity -DrugCentral:antagonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DrugCentral:antibody_binding: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -DrugCentral:antisense_inhibitor: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: expression - object_direction: decreased -DrugCentral:binding_agent: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -DrugCentral:blocker: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity_or_abundance - object_direction: decreased -DrugCentral:contraindication: - operation: keep - core_predicate: biolink:contraindicated_for -DrugCentral:gating_inhibitor: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DrugCentral:has_role: - operation: keep - core_predicate: biolink:related_to -DrugCentral:indication: - operation: keep - core_predicate: biolink:treats -DrugCentral:inhibitor: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity_or_abundance - object_direction: decreased -DrugCentral:inverse_agonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -DrugCentral:modulator: - operation: keep - core_predicate: biolink:affects -DrugCentral:negative_allosteric_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_direction: decreased -DrugCentral:negative_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_direction: decreased -DrugCentral:off-label_use: - operation: keep - core_predicate: biolink:treats -DrugCentral:opener: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -DrugCentral:partial_agonist: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -DrugCentral:pharmacological_chaperone: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -DrugCentral:positive_allosteric_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -DrugCentral:positive_modulator: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -DrugCentral:reduce_risk: - operation: keep - core_predicate: biolink:affects_risk_for - qualifiers: - object_direction: decreased -DrugCentral:releasing_agent: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: expression - object_direction: increased -DrugCentral:struct2atc: - operation: keep - core_predicate: biolink:close_match -DrugCentral:substrate: - operation: keep - core_predicate: biolink:physically_interacts_with -DrugCentral:symptomatic_treatment: - operation: keep - core_predicate: biolink:treats -EFO:0000784: - operation: keep - core_predicate: biolink:located_in -EFO:0001697: - operation: invert - core_predicate: biolink:related_to -EFO:0006351: - operation: keep - core_predicate: biolink:related_to -EFO:is_executed_in: - operation: keep - core_predicate: biolink:related_to -ENVO:01001307: - operation: keep - core_predicate: biolink:coexists_with -# FMA:SIB: -# operation: delete -FMA:adheres_to: - operation: keep - core_predicate: biolink:physically_interacts_with -FMA:adjacent_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:afferent_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:anatomical_entity_observed_in: - operation: delete -FMA:anterior_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:anteroinferior_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:anterolateral_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:anteromedial_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:anterosuperior_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:arterial_supply_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:articulates_with: - operation: keep - core_predicate: biolink:coexists_with -FMA:attaches_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:bounded_by: - operation: keep - core_predicate: biolink:coexists_with -FMA:bounds: - operation: keep - core_predicate: biolink:coexists_with -FMA:branch_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:connected_to: - operation: keep - core_predicate: biolink:related_to -FMA:connection_type_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:constitutional_part_of: - operation: invert - core_predicate: biolink:has_part -FMA:contained_in: - operation: invert - core_predicate: biolink:has_part -FMA:contains: - operation: keep - core_predicate: biolink:has_part -FMA:continuation_branch_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:continuous_distally_with: - operation: keep - core_predicate: biolink:coexists_with -FMA:continuous_proximally_with: - operation: keep - core_predicate: biolink:coexists_with -FMA:continuous_with: - operation: keep - core_predicate: biolink:related_to -FMA:corresponds_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:derives: - operation: invert - core_predicate: biolink:derives_from -FMA:derives_from: - operation: keep - core_predicate: biolink:derives_from -FMA:development_type_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:developmental_stage_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:develops_from: - operation: keep - core_predicate: biolink:develops_from -FMA:develops_into: - operation: keep - core_predicate: biolink:develops_from -FMA:direct_cell_shape_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:direct_left_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:direct_right_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:distal_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:drains_into: - operation: keep - core_predicate: biolink:coexists_with -FMA:efferent_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:external_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:formed_by: - operation: keep - core_predicate: biolink:coexists_with -FMA:forms: - operation: keep - core_predicate: biolink:coexists_with -FMA:full_grown_phenotype_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:fuses_with: - operation: keep - core_predicate: biolink:coexists_with -FMA:fusion_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:germ_origin_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_adherent: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_arterial_supply: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_branch: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_connection_type: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_constitutional_part: - operation: keep - core_predicate: biolink:has_part -FMA:has_continuation_branch: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_development_type: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_developmental_stage: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_direct_cell_shape: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_full_grown_phenotype: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_fusion: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_germ_origin: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_inherent_3d_shape: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_insertion: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_location: - operation: keep - core_predicate: biolink:located_in -FMA:has_lymphatic_drainage: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_member: - operation: keep - core_predicate: biolink:has_part -FMA:has_nerve_supply: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_observed_anatomical_entity: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_origin: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_part: - operation: keep - core_predicate: biolink:has_part -FMA:has_primary_segmental_supply: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_projection: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_regional_part: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_related_developmental_entity: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_secondary_segmental_supply: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_segmental_composition: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_segmental_supply: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_tributary: - operation: keep - core_predicate: biolink:coexists_with -FMA:has_venous_drainage: - operation: keep - core_predicate: biolink:coexists_with -FMA:homonym_for: - operation: delete -FMA:homonym_of: - operation: keep - core_predicate: biolink:related_to -FMA:inferior_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:inferolateral_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:inferomedial_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:inherent_3d_shape_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:insertion_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:internal_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:inverse_isa: - operation: invert - core_predicate: biolink:subclass_of -FMA:isa: - operation: keep - core_predicate: biolink:subclass_of -FMA:lateral_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:left_lateral_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:left_medial_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:location_of: - operation: invert - core_predicate: biolink:located_in -FMA:lymphatic_drainage_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:matures_from: - operation: keep - core_predicate: biolink:coexists_with -FMA:matures_into: - operation: keep - core_predicate: biolink:coexists_with -FMA:medial_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:member_of: - operation: invert - core_predicate: biolink:has_part -FMA:merges_with: - operation: keep - core_predicate: biolink:coexists_with -FMA:nerve_supply_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:origin_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:part_of: - operation: invert - core_predicate: biolink:has_part -FMA:posterior_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:posteroinferior_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:posterolateral_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:posteromedial_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:posterosuperior_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:primary_segmental_supply_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:projects_from: - operation: keep - core_predicate: biolink:coexists_with -FMA:projects_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:proximal_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:receives_attachment_from: - operation: keep - core_predicate: biolink:coexists_with -FMA:receives_drainage_from: - operation: keep - core_predicate: biolink:coexists_with -FMA:receives_input_from: - operation: keep - core_predicate: biolink:coexists_with -FMA:receives_projection: - operation: keep - core_predicate: biolink:coexists_with -FMA:regional_part_of: - operation: invert - core_predicate: biolink:has_part -FMA:related_developmental_entity_of: - operation: keep - core_predicate: biolink:related_to -FMA:related_object: - operation: keep - core_predicate: biolink:related_to -FMA:related_part: - operation: keep - core_predicate: biolink:coexists_with -FMA:right_lateral_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:right_medial_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:secondary_segmental_supply_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:segmental_composition_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:segmental_supply_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:sends_output_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:superior_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:superolateral_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:superomedial_to: - operation: keep - core_predicate: biolink:coexists_with -FMA:surrounded_by: - operation: keep - core_predicate: biolink:coexists_with -FMA:surrounds: - operation: keep - core_predicate: biolink:coexists_with -FMA:transforms_from: - operation: invert - core_predicate: biolink:precedes -FMA:transforms_into: - operation: keep - core_predicate: biolink:precedes -FMA:tributary_of: - operation: keep - core_predicate: biolink:coexists_with -FMA:venous_drainage_of: - operation: keep - core_predicate: biolink:coexists_with -FOODON:00001301: - operation: keep - core_predicate: biolink:model_of -FOODON:00001563: - operation: keep - core_predicate: biolink:has_part -FOODON:00002420: - operation: keep - core_predicate: biolink:has_part -GENEPIO:0001739: - operation: invert - core_predicate: biolink:precedes -# GENO:0000382: -# operation: keep -# core_predicate: biolink:has_variant_part -# GENO:0000790: -# operation: keep -# core_predicate: biolink:related_condition -# GENO:0000840: -# operation: keep -# core_predicate: biolink:gene_associated_with_condition -# GENO:0000841: -# operation: keep -# core_predicate: biolink:gene_associated_with_condition -# GO:SIB: -# operation: delete -GO:RB: - operation: invert - core_predicate: biolink:subclass_of -GO:RN: - operation: keep - core_predicate: biolink:subclass_of -GO:RO: - operation: keep - core_predicate: biolink:related_to -GO:SY: - operation: keep - core_predicate: biolink:close_match -GO:acts_upstream_of: - operation: keep - core_predicate: biolink:affects -GO:acts_upstream_of_negative_effect: - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: downregulated -GO:acts_upstream_of_or_within: - operation: keep - core_predicate: biolink:affects -GO:acts_upstream_of_or_within_negative_effect: - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: decreased -GO:acts_upstream_of_or_within_positive_effect: - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -GO:acts_upstream_of_positive_effect: - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -GO:colocalizes_with: - operation: keep - core_predicate: biolink:colocalizes_with -GO:contributes_to: - operation: keep - core_predicate: biolink:contributes_to -GO:enables: - operation: keep - core_predicate: biolink:enables -GO:ends_during: - operation: keep - core_predicate: biolink:related_to -GO:happens_during: - operation: keep - core_predicate: biolink:related_to -GO:has_occurrence: - operation: keep - core_predicate: biolink:capable_of -GO:has_part: - operation: keep - core_predicate: biolink:has_part -GO:inverse_ends_during: - operation: keep - core_predicate: biolink:related_to -GO:inverse_happens_during: - operation: delete -GO:inverse_isa: - operation: keep - core_predicate: biolink:superclass_of -GO:involved_in: - operation: invert - core_predicate: biolink:has_participant -GO:is_active_in: - operation: keep - core_predicate: biolink:actively_involved_in -GO:isa: - operation: keep - core_predicate: biolink:subclass_of -GO:located_in: - operation: keep - core_predicate: biolink:located_in -GO:mth_expanded_form_of: - operation: keep - core_predicate: biolink:close_match -GO:mth_has_expanded_form: - operation: keep - core_predicate: biolink:close_match -GO:negatively_regulated_by: - operation: invert - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: downregulated -GO:negatively_regulates: - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: downregulated -GO:occurs_in: - operation: keep - core_predicate: biolink:occurs_in -GO:part_of: - operation: invert - core_predicate: biolink:has_part -GO:positively_regulated_by: - operation: invert - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: upregulated -GO:positively_regulates: - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: upregulated -GO:regulated_by: - operation: invert - core_predicate: biolink:regulates -GO:regulates: - operation: keep - core_predicate: biolink:regulates -GOREL:0000040: - operation: keep - core_predicate: biolink:causes -# GOREL:0001004: -# operation: keep -# core_predicate: biolink:located_in -# GOREL:0001006: -# operation: keep -# core_predicate: biolink:affects -GOREL:0002003: - operation: keep - core_predicate: biolink:affects - qualifiers: - object_aspect: localization -GOREL:0002004: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: degradation - object_direction: increased -# GOREL:0002005: -# operation: keep -# core_predicate: biolink:related_to -GOREL:0012006: - operation: keep - core_predicate: biolink:related_to -# GTEx:affects_expression_in: -# operation: keep -# core_predicate: biolink:affects -# qualified_predicate: biolink:affects -# qualifiers: -# object_aspect: expression -HANCESTRO:0301: - operation: keep - core_predicate: biolink:related_to -HANCESTRO:0308: - operation: keep - core_predicate: biolink:related_to -HANCESTRO:0330: - operation: keep - core_predicate: biolink:related_to -HCPCS:CHD: - operation: keep - core_predicate: biolink:subclass_of -HCPCS:PAR: - operation: invert - core_predicate: biolink:subclass_of -HCPCS:mapped_from: - operation: delete -HCPCS:mapped_to: - operation: keep - core_predicate: biolink:related_to -HGNC:alias_of: - operation: keep - core_predicate: biolink:close_match -HGNC:expanded_form_of: - operation: keep - core_predicate: biolink:close_match -HGNC:has_alias: - operation: keep - core_predicate: biolink:close_match -HGNC:has_expanded_form: - operation: keep - core_predicate: biolink:close_match -HGNC:has_prev_name: - operation: keep - core_predicate: biolink:close_match -HGNC:has_prev_symbol: - operation: keep - core_predicate: biolink:close_match -HGNC:prev_name_of: - operation: keep - core_predicate: biolink:close_match -HGNC:prev_symbol_of: - operation: keep - core_predicate: biolink:close_match -HMDB:at_cellular_location: - operation: keep - core_predicate: biolink:located_in -HMDB:at_tissue: - operation: keep - core_predicate: biolink:located_in -HMDB:disease: - operation: keep - core_predicate: biolink:related_to -HMDB:has_protein_association: - operation: keep - core_predicate: biolink:related_to -HMDB:in_biospecimen: - operation: keep - core_predicate: biolink:located_in -HMDB:in_pathway: - operation: invert - core_predicate: biolink:has_participant -HP:RB: - operation: invert - core_predicate: biolink:subclass_of -HP:RN: - operation: keep - core_predicate: biolink:subclass_of -HP:RO: - operation: keep - core_predicate: biolink:related_to -HP:SY: - operation: keep - core_predicate: biolink:close_match -HP:inverse_isa: - operation: invert - core_predicate: biolink:subclass_of -HP:isa: - operation: keep - core_predicate: biolink:subclass_of -IAO:0000039: - operation: keep - core_predicate: biolink:related_to -IAO:0000136: - operation: keep - core_predicate: biolink:related_to -IAO:0000142: - operation: keep - core_predicate: biolink:mentions -IAO:0000219: - operation: keep - core_predicate: biolink:related_to -ICD10PCS:CHD: - operation: keep - core_predicate: biolink:subclass_of -ICD10PCS:PAR: - operation: invert - core_predicate: biolink:subclass_of -ICD10PCS:expanded_form_of: - operation: keep - core_predicate: biolink:close_match -ICD10PCS:has_expanded_form: - operation: keep - core_predicate: biolink:close_match -ICD9:CHD: - operation: keep - core_predicate: biolink:subclass_of -ICD9:PAR: - operation: invert - core_predicate: biolink:subclass_of -IDO:0000664: - operation: invert - core_predicate: biolink:contributes_to -JensenLab:associated_with: - operation: keep - core_predicate: biolink:gene_associated_with_condition -KEGG:compound_to_enzyme: - operation: keep - core_predicate: biolink:physically_interacts_with -KEGG:compound_to_pathway: - operation: invert - core_predicate: biolink:has_participant -KEGG:compound_to_reaction: - operation: invert - core_predicate: biolink:has_participant -KEGG:enzyme_to_pathway: - operation: invert - core_predicate: biolink:has_participant -KEGG:enzyme_to_reaction: - operation: keep - core_predicate: biolink:catalyzes -KEGG:glycan_to_enzyme: - operation: keep - core_predicate: biolink:physically_interacts_with -KEGG:glycan_to_pathway: - operation: invert - core_predicate: biolink:has_participant -KEGG:glycan_to_reaction: - operation: invert - core_predicate: biolink:has_participant -KEGG:pathway_to_compound: - operation: keep - core_predicate: biolink:has_participant -KEGG:pathway_to_drug: - operation: keep - core_predicate: biolink:has_participant -KEGG:pathway_to_glycan: - operation: keep - core_predicate: biolink:has_participant -KEGG:reaction_to_enzyme: - operation: invert - core_predicate: biolink:catalyzes -KEGG:reaction_to_pathway: - operation: invert - core_predicate: biolink:has_participant -linkml:examples: - operation: delete -linkml:local_names: - operation: delete -LOINC:adjustment_of: - operation: delete -LOINC:analyzed_by: - operation: delete -LOINC:analyzes: - operation: keep - core_predicate: biolink:related_to -LOINC:answer_to: - operation: delete -LOINC:archetype_of: - operation: delete -LOINC:associated_with: - operation: keep - core_predicate: biolink:correlated_with -LOINC:challenge_of: - operation: delete -LOINC:class_of: - operation: keep - core_predicate: biolink:subclass_of -LOINC:component_of: - operation: invert - core_predicate: biolink:has_part -LOINC:count_of: - operation: delete -LOINC:divisor_of: - operation: delete -LOINC:evaluation_of: - operation: delete -# LOINC:fragments_for_synonyms_of: -# operation: delete -LOINC:has_action_guidance: - operation: keep - core_predicate: biolink:related_to -LOINC:has_adjustment: - operation: keep - core_predicate: biolink:related_to -LOINC:has_aggregation_view: - operation: keep - core_predicate: biolink:related_to -LOINC:has_answer: - operation: keep - core_predicate: biolink:related_to -LOINC:has_approach_guidance: - operation: keep - core_predicate: biolink:related_to -LOINC:has_archetype: - operation: keep - core_predicate: biolink:subclass_of -LOINC:has_challenge: - operation: keep - core_predicate: biolink:related_to -LOINC:has_class: - operation: invert - core_predicate: biolink:subclass_of -LOINC:has_component: - operation: keep - core_predicate: biolink:has_part -LOINC:has_count: - operation: keep - core_predicate: biolink:related_to -LOINC:has_divisor: - operation: keep - core_predicate: biolink:related_to -LOINC:has_evaluation: - operation: keep - core_predicate: biolink:related_to -LOINC:has_exam: - operation: keep - core_predicate: biolink:related_to -# LOINC:has_fragments_for_synonyms: -# operation: keep -# core_predicate: biolink:has_input -LOINC:has_given_pharmaceutical_substance: - operation: delete -LOINC:has_imaged_location: - operation: keep - core_predicate: biolink:occurs_in -LOINC:has_imaging_focus: - operation: keep - core_predicate: biolink:located_in -LOINC:has_lateral_anatomic_location: - operation: keep - core_predicate: biolink:coexists_with -LOINC:has_lateral_location_presence: - operation: keep - core_predicate: biolink:coexists_with -LOINC:has_loinc_number: - operation: delete -LOINC:has_maneuver_type: - operation: delete -LOINC:has_member: - operation: keep - core_predicate: biolink:has_part -LOINC:has_method: - operation: keep - core_predicate: biolink:related_to -LOINC:has_modality_subtype: - operation: keep - core_predicate: biolink:related_to -LOINC:has_modality_type: - operation: keep - core_predicate: biolink:related_to -# LOINC:has_multipart: -# operation: delete -LOINC:has_object_guidance: - operation: keep - core_predicate: biolink:related_to -LOINC:has_parent_group: - operation: keep - core_predicate: biolink:subclass_of -LOINC:has_pharmaceutical_route: - operation: keep - core_predicate: biolink:related_to -LOINC:has_presence_guidance: - operation: delete -LOINC:has_property: - operation: delete -LOINC:has_scale: - operation: keep - core_predicate: biolink:related_to -LOINC:has_subject: - operation: keep - core_predicate: biolink:has_participant -LOINC:has_suffix: - operation: keep - core_predicate: biolink:related_to -LOINC:has_supersystem: - operation: invert - core_predicate: biolink:has_part -LOINC:has_system: - operation: keep - core_predicate: biolink:has_input -LOINC:has_time_aspect: - operation: keep - core_predicate: biolink:related_to -LOINC:has_time_modifier: - operation: keep - core_predicate: biolink:related_to -LOINC:has_timing_of: - operation: keep - core_predicate: biolink:related_to -LOINC:has_view_type: - operation: keep - core_predicate: biolink:related_to -LOINC:is_action_guidance_for: - operation: delete -LOINC:is_aggregation_view_of: - operation: delete -LOINC:is_approach_guidance_for: - operation: delete -LOINC:is_exam_for: - operation: delete -LOINC:is_given_pharmaceutical_substance_for: - operation: invert - core_predicate: biolink:has_participant -LOINC:is_imaged_location_for: - operation: delete -LOINC:is_imaging_focus_of: - operation: delete -LOINC:is_lateral_anatomic_location_of: - operation: delete -LOINC:is_maneuver_type_for: - operation: delete -LOINC:is_modality_subtype_for: - operation: delete -LOINC:is_modality_type_for: - operation: delete -LOINC:is_object_guidance_for: - operation: delete -LOINC:is_pharmaceutical_route_for: - operation: delete -LOINC:is_presence_guidance_for: - operation: keep - core_predicate: biolink:subclass_of -LOINC:is_presence_of_lateral_location: - operation: delete -LOINC:is_subject_of: - operation: delete -LOINC:is_timing_for: - operation: delete -LOINC:is_view_type_for: - operation: delete -LOINC:loinc_number_of: - operation: delete -LOINC:mapped_from: - operation: delete -LOINC:mapped_to: - operation: keep - core_predicate: biolink:related_to -LOINC:measured_by: - operation: keep - core_predicate: biolink:related_to -LOINC:measures: - operation: delete -LOINC:member_of: - operation: invert - core_predicate: biolink:has_part -LOINC:method_of: - operation: delete -LOINC:mth_expanded_form_of: - operation: delete -LOINC:mth_has_expanded_form: - operation: keep - core_predicate: biolink:related_to -# LOINC:multipart_of: -# operation: invert -# core_predicate: biolink:has_part -LOINC:parent_group_of: - operation: delete -LOINC:property_of: - operation: keep - core_predicate: biolink:related_to -LOINC:scale_of: - operation: delete -LOINC:suffix_of: - operation: delete -LOINC:supersystem_of: - operation: delete -LOINC:system_of: - operation: delete -LOINC:time_aspect_of: - operation: delete -LOINC:time_modifier_of: - operation: delete -# MEDDRA:classified_as: -# operation: keep -# core_predicate: biolink:close_match -# MEDDRA:has_member: -# operation: keep -# core_predicate: biolink:has_part -# MEDDRA:member_of: -# operation: invert -# core_predicate: biolink:has_part -MESH:AQ: - operation: delete -MESH:CHD: - operation: keep - core_predicate: biolink:subclass_of -MESH:PAR: - operation: invert - core_predicate: biolink:subclass_of -MESH:QB: - operation: delete -MESH:RB: - operation: invert - core_predicate: biolink:subclass_of -MESH:RN: - operation: keep - core_predicate: biolink:subclass_of -MESH:RO: - operation: keep - core_predicate: biolink:related_to -# MESH:SIB: -# operation: delete -MESH:has_mapping_qualifier: - operation: keep - core_predicate: biolink:related_to -MESH:has_permuted_term: - operation: keep - core_predicate: biolink:close_match -MESH:inverse_isa: - operation: keep - core_predicate: biolink:superclass_of -MESH:isa: - operation: keep - core_predicate: biolink:subclass_of -MESH:mapped_from: - operation: delete -MESH:mapped_to: - operation: keep - core_predicate: biolink:related_to -MESH:mapping_qualifier_of: - operation: delete -MESH:permuted_term_of: - operation: keep - core_predicate: biolink:close_match -MI:0192: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0194: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0195: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0197: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0203: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0204: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0210: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0211: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0212: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0213: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0214: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0216: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0217: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0220: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0403: - operation: keep - core_predicate: biolink:colocalizes_with -MI:0407: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0408: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0414: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0556: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0557: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0559: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0566: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0567: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0569: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0570: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0572: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0844: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0871: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0882: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0883: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0902: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:0914: - operation: keep - core_predicate: biolink:physically_interacts_with -MI:0915: - operation: keep - core_predicate: biolink:physically_interacts_with -MI:0945: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:1126: - operation: keep - core_predicate: biolink:physically_interacts_with -MI:1127: - operation: keep - core_predicate: biolink:physically_interacts_with -MI:1148: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:1237: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:1310: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:2252: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -MI:2364: - operation: keep - core_predicate: biolink:colocalizes_with -MONDO:0100332: - operation: invert - core_predicate: biolink:causes -MONDO:0100333: - operation: invert - core_predicate: biolink:causes -MONDO:0700097: - operation: delete -MONDO:disease_causes_feature: - operation: keep - core_predicate: biolink:causes -MONDO:disease_has_basis_in_accumulation_of: - operation: keep - core_predicate: biolink:disease_has_basis_in -MONDO:disease_has_basis_in_development_of: - operation: keep - core_predicate: biolink:disease_has_basis_in -# MONDO:disease_has_location: -# operation: keep -# core_predicate: biolink:disease_has_location -MONDO:disease_has_major_feature: - operation: keep - core_predicate: biolink:has_part -MONDO:disease_responds_to: - operation: invert - core_predicate: biolink:treats -MONDO:disease_shares_features_of: - operation: keep - core_predicate: biolink:related_to -MONDO:disease_triggers: - operation: keep - core_predicate: biolink:causes -MONDO:equivalentTo: - operation: keep - core_predicate: biolink:same_as -MONDO:has_onset: - operation: keep - core_predicate: biolink:related_to -MONDO:has_onset_before: - operation: keep - core_predicate: biolink:related_to -MONDO:has_onset_during_or_after: - operation: keep - core_predicate: biolink:related_to -MONDO:part_of_progression_of_disease: - operation: invert - core_predicate: biolink:has_part -MONDO:predisposes_towards: - operation: keep - core_predicate: biolink:contributes_to -NCBITaxon:CHD: - operation: keep - core_predicate: biolink:subclass_of -NCBITaxon:PAR: - operation: invert - core_predicate: biolink:subclass_of -NCBITaxon:expanded_form_of: - operation: keep - core_predicate: biolink:close_match -NCBITaxon:has_expanded_form: - operation: keep - core_predicate: biolink:close_match -NCIT:C2861: - operation: keep - core_predicate: biolink:has_side_effect -NCIT:R163: - operation: keep - core_predicate: biolink:related_to -NCIT:R81: - operation: keep - core_predicate: biolink:related_to -NCIT:R82: - operation: invert - core_predicate: biolink:has_part -NCIT:abnormal_cell_affected_by_chemical_or_drug: - operation: delete -NCIT:abnormality_associated_with_allele: - operation: delete -NCIT:activity_of_allele: - operation: delete -NCIT:allele_absent_from_wild-type_chromosomal_location: - operation: keep - core_predicate: biolink:located_in -NCIT:allele_has_abnormality: - operation: keep - core_predicate: biolink:causes -NCIT:allele_has_activity: - operation: keep - core_predicate: biolink:has_molecular_consequence -NCIT:allele_in_chromosomal_location: - operation: keep - core_predicate: biolink:located_in -NCIT:allele_plays_altered_role_in_process: - operation: keep - core_predicate: biolink:affects -NCIT:allele_plays_role_in_metabolism_of_chemical_or_drug: - operation: keep - core_predicate: biolink:affects -NCIT:anatomic_structure_has_location: - operation: delete -NCIT:anatomic_structure_is_physical_part_of: - operation: invert - core_predicate: biolink:has_part -NCIT:anatomy_originated_from_biological_process: - operation: delete -NCIT:associated_with_malfunction_of_gene_product: - operation: delete -NCIT:biological_process_has_associated_location: - operation: keep - core_predicate: biolink:affects -NCIT:biological_process_has_initiator_chemical_or_drug: - operation: delete -NCIT:biological_process_has_initiator_process: - operation: delete -NCIT:biological_process_has_result_anatomy: - operation: keep - core_predicate: biolink:has_output -NCIT:biological_process_has_result_biological_process: - operation: keep - core_predicate: biolink:causes -NCIT:biological_process_has_result_chemical_or_drug: - operation: keep - core_predicate: biolink:produces -NCIT:biological_process_involves_chemical_or_drug: - operation: invert - core_predicate: biolink:actively_involved_in -NCIT:biological_process_involves_gene_product: - operation: delete -NCIT:biological_process_is_part_of_process: - operation: delete -NCIT:biological_process_results_from_biological_process: - operation: delete -NCIT:biomarker_type_includes_gene: - operation: delete -NCIT:biomarker_type_includes_gene_product: - operation: delete -# NCIT:cdrh_parent_of: -# operation: invert -# core_predicate: biolink:subclass_of -NCIT:cell_type_is_associated_with_eo_disease: - operation: delete -NCIT:cell_type_or_tissue_affected_by_chemical_or_drug: - operation: delete -NCIT:chemical_or_drug_affects_abnormal_cell: - operation: keep - core_predicate: biolink:affects -NCIT:chemical_or_drug_affects_cell_type_or_tissue: - operation: keep - core_predicate: biolink:affects -NCIT:chemical_or_drug_affects_gene_product: - operation: keep - core_predicate: biolink:affects -NCIT:chemical_or_drug_has_mechanism_of_action: - operation: keep - core_predicate: biolink:affects -NCIT:chemical_or_drug_has_physiologic_effect: - operation: keep - core_predicate: biolink:causes -NCIT:chemical_or_drug_initiates_biological_process: - operation: keep - core_predicate: biolink:causes -NCIT:chemical_or_drug_is_metabolized_by_enzyme: - operation: delete -NCIT:chemical_or_drug_is_product_of_biological_process: - operation: delete -NCIT:chemical_or_drug_metabolism_is_associated_with_allele: - operation: delete -NCIT:chemical_or_drug_plays_role_in_biological_process: - operation: delete -NCIT:chemotherapy_regimen_has_component: - operation: delete -NCIT:chromosomal_location_of_allele: - operation: delete -NCIT:chromosomal_location_of_wild-type_gene: - operation: delete -NCIT:chromosome_involved_in_cytogenetic_abnormality: - operation: delete -NCIT:chromosome_mapped_to_disease: - operation: keep - core_predicate: biolink:causes -NCIT:completely_excised_anatomy_has_procedure: - operation: delete -NCIT:completely_excised_anatomy_may_have_procedure: - operation: delete -NCIT:complex_has_physical_part: - operation: keep - core_predicate: biolink:has_part -NCIT:concept_in_subset: - operation: delete -NCIT:conceptual_part_of: - operation: invert - core_predicate: biolink:has_part -NCIT:ctcae_5_parent_of: - operation: keep - core_predicate: biolink:superclass_of -NCIT:is_ctdc_value_of: - operation: delete -NCIT:cytogenetic_abnormality_involves_chromosome: - operation: keep - core_predicate: biolink:affects -NCIT:data_element_of: - operation: delete -NCIT:disease_excludes_abnormal_cell: - operation: delete -NCIT:disease_excludes_cytogenetic_abnormality: - operation: delete -NCIT:disease_excludes_finding: - operation: delete -NCIT:disease_excludes_metastatic_anatomic_site: - operation: delete -NCIT:disease_excludes_molecular_abnormality: - operation: delete -NCIT:disease_excludes_normal_cell_origin: - operation: delete -NCIT:disease_excludes_normal_tissue_origin: - operation: delete -NCIT:disease_excludes_primary_anatomic_site: - operation: delete -NCIT:disease_has_abnormal_cell: - operation: delete -NCIT:disease_has_accepted_treatment_with_regimen: - operation: delete -NCIT:disease_has_associated_anatomic_site: - operation: keep - core_predicate: biolink:affects -NCIT:disease_has_associated_disease: - operation: keep - core_predicate: biolink:associated_with -NCIT:disease_has_associated_gene: - operation: delete -NCIT:disease_has_cytogenetic_abnormality: - operation: delete -NCIT:disease_has_finding: - operation: invert - core_predicate: biolink:biomarker_for -NCIT:disease_has_metastatic_anatomic_site: - operation: keep - core_predicate: biolink:affects -NCIT:disease_has_molecular_abnormality: - operation: invert - core_predicate: biolink:biomarker_for -NCIT:disease_has_normal_cell_origin: - operation: delete -NCIT:disease_has_normal_tissue_origin: - operation: keep - core_predicate: biolink:causes -NCIT:disease_has_primary_anatomic_site: - operation: keep - core_predicate: biolink:affects -NCIT:disease_is_grade: - operation: keep - core_predicate: biolink:related_to -NCIT:disease_is_marked_by_gene: - operation: invert - core_predicate: biolink:biomarker_for -NCIT:disease_is_stage: - operation: keep - core_predicate: biolink:related_to -NCIT:disease_mapped_to_chromosome: - operation: delete -NCIT:disease_mapped_to_gene: - operation: delete -NCIT:disease_may_have_abnormal_cell: - operation: keep - core_predicate: biolink:affects -NCIT:disease_may_have_associated_disease: - operation: keep - core_predicate: biolink:related_to -NCIT:disease_may_have_cytogenetic_abnormality: - operation: delete -NCIT:disease_may_have_finding: - operation: keep - core_predicate: biolink:has_phenotype -NCIT:disease_may_have_molecular_abnormality: - operation: keep - core_predicate: biolink:has_phenotype -NCIT:disease_may_have_normal_cell_origin: - operation: invert - core_predicate: biolink:derives_from -NCIT:disease_may_have_normal_tissue_origin: - operation: invert - core_predicate: biolink:derives_from -NCIT:endogenous_product_related_to: - operation: delete -NCIT:enzyme_metabolizes_chemical_or_drug: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: localization - object_direction: increased -NCIT:eo_anatomy_is_associated_with_eo_disease: - operation: delete -NCIT:eo_disease_has_associated_cell_type: - operation: keep - core_predicate: biolink:affects -NCIT:eo_disease_has_associated_eo_anatomy: - operation: keep - core_predicate: biolink:affects -NCIT:eo_disease_has_property_or_attribute: - operation: keep - core_predicate: biolink:related_to -NCIT:eo_disease_maps_to_human_disease: - operation: delete -NCIT:excised_anatomy_has_procedure: - operation: delete -NCIT:excised_anatomy_may_have_procedure: - operation: delete -NCIT:gene_associated_with_disease: - operation: keep - core_predicate: biolink:gene_associated_with_condition -NCIT:gene_encodes_gene_product: - operation: invert - core_predicate: biolink:gene_product_of -NCIT:gene_found_in_organism: - operation: keep - core_predicate: biolink:in_taxon -NCIT:gene_has_abnormality: - operation: delete -NCIT:gene_has_physical_location: - operation: keep - core_predicate: biolink:located_in -NCIT:gene_in_chromosomal_location: - operation: keep - core_predicate: biolink:located_in -NCIT:gene_involved_in_molecular_abnormality: - operation: keep - core_predicate: biolink:actively_involved_in -NCIT:gene_involved_in_pathogenesis_of_disease: - operation: keep - core_predicate: biolink:gene_associated_with_condition -NCIT:gene_is_biomarker_of: - operation: keep - core_predicate: biolink:biomarker_for -NCIT:gene_is_biomarker_type: - operation: keep - core_predicate: biolink:subclass_of -NCIT:gene_is_element_in_pathway: - operation: invert - core_predicate: biolink:has_participant -NCIT:gene_mapped_to_disease: - operation: keep - core_predicate: biolink:affects -NCIT:gene_mutant_encodes_gene_product_sequence_variation: - operation: invert - core_predicate: biolink:gene_product_of -NCIT:gene_plays_role_in_process: - operation: invert - core_predicate: biolink:has_participant -NCIT:gene_product_affected_by_chemical_or_drug: - operation: delete -NCIT:gene_product_encoded_by_gene: - operation: delete -NCIT:gene_product_expressed_in_tissue: - operation: keep - core_predicate: biolink:expressed_in -NCIT:gene_product_has_abnormality: - operation: keep - core_predicate: biolink:affects -NCIT:gene_product_has_associated_anatomy: - operation: keep - core_predicate: biolink:expressed_in -NCIT:gene_product_has_biochemical_function: - operation: keep - core_predicate: biolink:capable_of -NCIT:gene_product_has_chemical_classification: - operation: keep - core_predicate: biolink:subclass_of -NCIT:gene_product_has_gene_product_variant: - operation: delete -NCIT:gene_product_has_organism_source: - operation: keep - core_predicate: biolink:in_taxon -NCIT:gene_product_has_structural_domain_or_motif: - operation: keep - core_predicate: biolink:has_part -NCIT:gene_product_is_biomarker_of: - operation: keep - core_predicate: biolink:biomarker_for -NCIT:gene_product_is_biomarker_type: - operation: keep - core_predicate: biolink:subclass_of -NCIT:gene_product_is_element_in_pathway: - operation: invert - core_predicate: biolink:has_participant -NCIT:gene_product_is_physical_part_of: - operation: invert - core_predicate: biolink:has_participant -NCIT:gene_product_malfunction_associated_with_disease: - operation: keep - core_predicate: biolink:gene_associated_with_condition -NCIT:gene_product_plays_role_in_biological_process: - operation: invert - core_predicate: biolink:has_participant -NCIT:gene_product_sequence_variation_encoded_by_gene_mutant: - operation: keep - core_predicate: biolink:is_sequence_variant_of -NCIT:gene_product_variant_of_gene_product: - operation: keep - core_predicate: biolink:is_sequence_variant_of -NCIT:genetic_biomarker_related_to: - operation: keep - core_predicate: biolink:biomarker_for -# NCIT:has_cdrh_parent: -# operation: delete -NCIT:has_conceptual_part: - operation: delete -NCIT:has_ctcae_5_parent: - operation: delete -NCIT:has_ctdc_value: - operation: delete -NCIT:has_data_element: - operation: keep - core_predicate: biolink:related_to -NCIT:has_dipg_dmg_permissible_value: - operation: delete -NCIT:has_free_acid_or_base_form: - operation: delete -NCIT:has_gdc_value: - operation: delete -NCIT:has_gene_product_element: - operation: delete -NCIT:has_icdc_value: - operation: delete -NCIT:has_inc_parent: - operation: keep - core_predicate: biolink:subclass_of -# NCIT:has_nichd_parent: -# operation: keep -# core_predicate: biolink:related_to -NCIT:has_pcdc_all_permissible_value: - operation: delete -NCIT:has_pcdc_aml_permissible_value: - operation: delete -NCIT:has_pcdc_ews_permissible_value: - operation: delete -NCIT:has_pcdc_data_type: - operation: delete -NCIT:has_pcdc_gct_permissible_value: - operation: delete -NCIT:has_pcdc_hl_permissible_value: - operation: delete -NCIT:has_pcdc_os_permissible_value: - operation: delete -NCIT:has_pharmaceutical_administration_method: - operation: keep - core_predicate: biolink:related_to -NCIT:has_pharmaceutical_basic_dose_form: - operation: keep - core_predicate: biolink:related_to -NCIT:has_pharmaceutical_intended_site: - operation: keep - core_predicate: biolink:related_to -NCIT:has_pharmaceutical_release_characteristics: - operation: keep - core_predicate: biolink:related_to -NCIT:has_pharmaceutical_state_of_matter: - operation: keep - core_predicate: biolink:related_to -NCIT:has_pharmaceutical_transformation: - operation: keep - core_predicate: biolink:related_to -NCIT:has_physical_part_of_anatomic_structure: - operation: delete -NCIT:has_salt_form: - operation: keep - core_predicate: biolink:chemically_similar_to -NCIT:has_seronet_permissible_value: - operation: delete -NCIT:has_target: - operation: keep - core_predicate: biolink:physically_interacts_with -NCIT:has_tradename: - operation: keep - core_predicate: biolink:close_match -NCIT:human_disease_maps_to_eo_disease: - operation: keep - core_predicate: biolink:related_to -NCIT:icdc_value_of: - operation: delete -NCIT:imaged_anatomy_has_procedure: - operation: delete -NCIT:inc_parent_of: - operation: delete -NCIT:inverse_isa: - operation: invert - core_predicate: biolink:subclass_of -NCIT:isa: - operation: keep - core_predicate: biolink:subclass_of -NCIT:is_abnormal_cell_of_disease: - operation: keep - core_predicate: biolink:related_to -NCIT:is_abnormality_of_gene: - operation: delete -NCIT:is_abnormality_of_gene_product: - operation: delete -NCIT:is_associated_anatomic_site_of: - operation: delete -NCIT:is_associated_anatomy_of_gene_product: - operation: delete -NCIT:is_associated_disease_of: - operation: keep - core_predicate: biolink:correlated_with -NCIT:is_biochemical_function_of_gene_product: - operation: delete -NCIT:is_chemical_classification_of_gene_product: - operation: delete -NCIT:is_chromosomal_location_of_gene: - operation: delete -NCIT:is_component_of_chemotherapy_regimen: - operation: invert - core_predicate: biolink:has_part -NCIT:is_cytogenetic_abnormality_of_disease: - operation: invert - core_predicate: biolink:correlated_with -NCIT:is_dipg_dmg_permissible_value_for_variable: - operation: delete -NCIT:is_finding_of_disease: - operation: delete -NCIT:is_grade_of_disease: - operation: delete -NCIT:is_location_of_anatomic_structure: - operation: keep - core_predicate: biolink:located_in -NCIT:is_location_of_biological_process: - operation: delete -NCIT:is_marked_by_gene_product: - operation: delete -NCIT:is_mechanism_of_action_of_chemical_or_drug: - operation: delete -NCIT:is_metastatic_anatomic_site_of_disease: - operation: delete -NCIT:is_molecular_abnormality_of_disease: - operation: keep - core_predicate: biolink:biomarker_for -NCIT:is_normal_cell_origin_of_disease: - operation: invert - core_predicate: biolink:derives_from -NCIT:is_normal_tissue_origin_of_disease: - operation: delete -NCIT:is_not_abnormal_cell_of_disease: - operation: delete -NCIT:is_not_cytogenetic_abnormality_of_disease: - operation: delete -NCIT:is_not_finding_of_disease: - operation: delete -NCIT:is_not_metastatic_anatomic_site_of_disease: - operation: delete -NCIT:is_not_molecular_abnormality_of_disease: - operation: delete -NCIT:is_not_normal_cell_origin_of_disease: - operation: delete -NCIT:is_not_normal_tissue_origin_of_disease: - operation: delete -NCIT:is_not_primary_anatomic_site_of_disease: - operation: delete -NCIT:is_organism_source_of_gene_product: - operation: invert - core_predicate: biolink:in_taxon -NCIT:is_paired_with_value_set: - operation: delete -NCIT:is_pcdc_all_permissible_value_for_variable: - operation: delete -NCIT:is_pcdc_aml_permissible_value_for_variable: - operation: delete -NCIT:is_pcdc_ews_permissible_value_for_variable: - operation: delete -NCIT:is_pcdc_gct_permissible_value_for_variable: - operation: delete -NCIT:is_pcdc_hl_permissible_value_for_variable: - operation: delete -NCIT:is_pcdc_os_permissible_value_for_variable: - operation: delete -NCIT:is_physical_location_of_gene: - operation: delete -NCIT:is_physiologic_effect_of_chemical_or_drug: - operation: delete -NCIT:is_primary_anatomic_site_of_disease: - operation: delete -NCIT:is_property_or_attribute_of_eo_disease: - operation: delete -NCIT:is_qualified_by: - operation: keep - core_predicate: biolink:related_to -NCIT:is_related_to_endogenous_product: - operation: keep - core_predicate: biolink:related_to -NCIT:is_seronet_permissible_value_for_variable: - operation: delete -NCIT:is_stage_of_disease: - operation: delete -NCIT:is_structural_domain_or_motif_of_gene_product: - operation: delete -NCIT:is_target: - operation: delete -NCIT:is_value_for_gdc_property: - operation: delete -NCIT:kind_is_domain_of: - operation: delete -NCIT:kind_is_range_of: - operation: delete -NCIT:may_be_abnormal_cell_of_disease: - operation: delete -NCIT:may_be_associated_disease_of_disease: - operation: delete -NCIT:may_be_cytogenetic_abnormality_of_disease: - operation: delete -NCIT:may_be_finding_of_disease: - operation: delete -NCIT:may_be_molecular_abnormality_of_disease: - operation: delete -NCIT:may_be_normal_cell_origin_of_disease: - operation: invert - core_predicate: biolink:derives_from -NCIT:may_be_normal_tissue_origin_of_disease: - operation: invert - core_predicate: biolink:derives_from -NCIT:molecular_abnormality_involves_gene: - operation: delete -NCIT:neoplasm_has_special_category: - operation: keep - core_predicate: biolink:subclass_of -# NCIT:nichd_parent_of: -# operation: delete -NCIT:organism_has_gene: - operation: invert - core_predicate: biolink:in_taxon -NCIT:partially_excised_anatomy_has_procedure: - operation: delete -NCIT:partially_excised_anatomy_may_have_procedure: - operation: delete -NCIT:pathogenesis_of_disease_involves_gene: - operation: delete -NCIT:pathway_has_gene_element: - operation: keep - core_predicate: biolink:has_participant -NCIT:pcdc_data_type_of: - operation: delete -NCIT:pharmaceutical_administration_method_of: - operation: delete -NCIT:pharmaceutical_basic_dose_form_of: - operation: delete -NCIT:pharmaceutical_intended_site_of: - operation: delete -NCIT:pharmaceutical_release_characteristics_of: - operation: delete -NCIT:pharmaceutical_state_of_matter_of: - operation: delete -NCIT:pharmaceutical_transformation_of: - operation: delete -NCIT:procedure_has_completely_excised_anatomy: - operation: keep - core_predicate: biolink:located_in -NCIT:procedure_has_excised_anatomy: - operation: keep - core_predicate: biolink:located_in -NCIT:procedure_has_imaged_anatomy: - operation: keep - core_predicate: biolink:located_in -NCIT:procedure_has_partially_excised_anatomy: - operation: keep - core_predicate: biolink:located_in -NCIT:procedure_has_target_anatomy: - operation: keep - core_predicate: biolink:located_in -NCIT:procedure_may_have_completely_excised_anatomy: - operation: keep - core_predicate: biolink:located_in -NCIT:procedure_may_have_excised_anatomy: - operation: keep - core_predicate: biolink:located_in -NCIT:procedure_may_have_partially_excised_anatomy: - operation: keep - core_predicate: biolink:located_in -NCIT:process_altered_by_allele: - operation: delete -NCIT:process_includes_biological_process: - operation: keep - core_predicate: biolink:has_participant -NCIT:process_initiates_biological_process: - operation: keep - core_predicate: biolink:causes -NCIT:process_involves_gene: - operation: keep - core_predicate: biolink:has_participant -NCIT:qualifier_applies_to: - operation: keep - core_predicate: biolink:related_to -NCIT:regimen_has_accepted_use_for_disease: - operation: keep - core_predicate: biolink:treats -NCIT:related_to_genetic_biomarker: - operation: delete -NCIT:role_has_domain: - operation: keep - core_predicate: biolink:related_to -NCIT:role_has_parent: - operation: keep - core_predicate: biolink:subclass_of -NCIT:role_has_range: - operation: keep - core_predicate: biolink:related_to -NCIT:role_is_parent_of: - operation: delete -NCIT:special_category_includes_neoplasm: - operation: delete -NCIT:subset_includes_concept: - operation: keep - core_predicate: biolink:superclass_of -NCIT:target_anatomy_has_procedure: - operation: delete -NCIT:tissue_is_expression_site_of_gene_product: - operation: delete -NCIT:tradename_of: - operation: keep - core_predicate: biolink:close_match -NCIT:value_set_is_paired_with: - operation: delete -NDDF:dose_form_of: - operation: delete -NDDF:has_dose_form: - operation: keep - core_predicate: biolink:subclass_of -NDDF:has_ingredient: - operation: keep - core_predicate: biolink:has_part -NDDF:ingredient_of: - operation: invert - core_predicate: biolink:has_part -OBI:0000293: - operation: keep - core_predicate: biolink:has_participant -OBI:0000295: - operation: invert - core_predicate: biolink:has_participant -OBI:0000299: - operation: keep - core_predicate: biolink:has_output -OBI:0000417: - operation: keep - core_predicate: biolink:has_output -OBI:0001927: - operation: invert - core_predicate: biolink:related_to -OBO:INO_0000154: - operation: keep - core_predicate: biolink:related_to -OBO:MF#manifestationOf: - operation: keep - core_predicate: biolink:manifestation_of -OBO:bspo#parallel_to: - operation: keep - core_predicate: biolink:coexists_with -# OBO:doid#has_symptom: -# operation: keep -# core_predicate: biolink:has_phenotype -OBO:envo#has_increased_levels_of: - operation: keep - core_predicate: biolink:affects -OBO:exo#interacts_with: - operation: keep - core_predicate: biolink:indirectly_physically_interacts_with -OBO:exo#interacts_with_an_exposure_receptor_via: - operation: keep - core_predicate: biolink:indirectly_physically_interacts_with -OBO:exo#interacts_with_an_exposure_stressor_via: - operation: keep - core_predicate: biolink:indirectly_physically_interacts_with -# OBO:exo.obo#interacts_with: -# operation: keep -# core_predicate: biolink:interacts_with -# OBO:exo.obo#interacts_with_an_exposure_receptor_via: -# operation: keep -# core_predicate: biolink:interacts_with -# OBO:exo.obo#interacts_with_an_exposure_stressor_via: -# operation: keep -# core_predicate: biolink:interacts_with -OBO:has_role: - operation: keep - core_predicate: biolink:related_to -OBO:HANCESTRO_0301: - operation: keep - core_predicate: biolink:related_to -OBO:HANCESTRO_0308: - operation: keep - core_predicate: biolink:related_to -OBO:HANCESTRO_0330: - operation: keep - core_predicate: biolink:related_to -OBO:nbo#by_means: - operation: invert - core_predicate: biolink:actively_involved_in -OBO:nbo#has_participant: - operation: keep - core_predicate: biolink:has_participant -OBO:nbo#in_response_to: - operation: invert - core_predicate: biolink:causes -OBO:nbo#is_about: - operation: keep - core_predicate: biolink:related_to -# OBO:uo#is_unit_of: -# operation: invert -# core_predicate: biolink:related_to -# OIO:hasDbXref: -# operation: keep -# core_predicate: biolink:close_match -OMIM:CHD: - operation: keep - core_predicate: biolink:subclass_of -OMIM:PAR: - operation: invert - core_predicate: biolink:subclass_of -OMIM:alias_of: - operation: keep - core_predicate: biolink:related_to -OMIM:allelic_variant_of: - operation: keep - core_predicate: biolink:is_sequence_variant_of -OMIM:entry_term_of: - operation: keep - core_predicate: biolink:related_to -OMIM:expanded_form_of: - operation: keep - core_predicate: biolink:close_match -OMIM:has_alias: - operation: keep - core_predicate: biolink:related_to -OMIM:has_allelic_variant: - operation: delete -OMIM:has_entry_term: - operation: keep - core_predicate: biolink:related_to -OMIM:has_expanded_form: - operation: keep - core_predicate: biolink:close_match -OMIM:has_inheritance_type: - operation: keep - core_predicate: biolink:related_to -OMIM:has_manifestation: - operation: invert - core_predicate: biolink:manifestation_of -OMIM:has_phenotype: - operation: keep - core_predicate: biolink:has_phenotype -OMIM:inheritance_type_of: - operation: delete -OMIM:manifestation_of: - operation: keep - core_predicate: biolink:manifestation_of -OMIM:phenotype_of: - operation: invert - core_predicate: biolink:has_phenotype -# ORPHA:317343: -# operation: keep -# core_predicate: biolink:causes -# ORPHA:317344: -# operation: keep -# core_predicate: biolink:causes -# ORPHA:317346: -# operation: keep -# core_predicate: biolink:causes -# ORPHANET:327767: -# operation: keep -# core_predicate: biolink:actively_involved_in -# ORPHA:410295: -# operation: keep -# core_predicate: biolink:causes -# ORPHA:410296: -# operation: keep -# core_predicate: biolink:causes -# ORPHA:465410: -# operation: keep -# core_predicate: biolink:biomarker_for -ORPHANET:317343: - operation: keep - core_predicate: biolink:causes -ORPHANET:317344: - operation: keep - core_predicate: biolink:causes -ORPHANET:317345: - operation: keep - core_predicate: biolink:correlated_with -orphanet:317346: - operation: keep - core_predicate: biolink:causes -ORPHANET:317346: - operation: keep - core_predicate: biolink:causes -ORPHANET:317348: - operation: keep - core_predicate: biolink:actively_involved_in -ORPHANET:317349: - operation: keep - core_predicate: biolink:actively_involved_in -ORPHANET:327767: - operation: keep - core_predicate: biolink:actively_involved_in -ORPHANET:410295: - operation: keep - core_predicate: biolink:causes -ORPHANET:410296: - operation: keep - core_predicate: biolink:causes -ORPHANET:465410: - operation: keep - core_predicate: biolink:biomarker_for -ORPHANET:C016: - operation: keep - core_predicate: biolink:related_to -ORPHANET:C017: - operation: keep - core_predicate: biolink:related_to -ORPHANET:C056: - operation: keep - core_predicate: biolink:close_match -ORPHANET:C057: - operation: keep - core_predicate: biolink:close_match -# PATO:0000085: -# operation: keep -# core_predicate: biolink:associated_with_sensitivity_to -# PATO:correlates_with: -# operation: keep -# core_predicate: biolink:correlated_with -PATO:decreased_in_magnitude_relative_to: - operation: keep - core_predicate: biolink:related_to -PATO:has_cross_section: - operation: keep - core_predicate: biolink:related_to -# PATO:has_relative_magnitude: -# operation: keep -# core_predicate: biolink:related_to -PATO:increased_in_magnitude_relative_to: - operation: keep - core_predicate: biolink:related_to -PATO:reciprocal_of: - operation: keep - core_predicate: biolink:related_to -# PATO:towards: -# operation: invert -# core_predicate: biolink:actively_involved_in -PDQ:SY: - operation: keep - core_predicate: biolink:close_match -PDQ:associated_disease: - operation: keep - core_predicate: biolink:correlated_with -PDQ:associated_genetic_condition: - operation: delete -PDQ:component_of: - operation: invert - core_predicate: biolink:has_part -PDQ:expanded_form_of: - operation: keep - core_predicate: biolink:close_match -PDQ:has_component: - operation: keep - core_predicate: biolink:has_part -PDQ:has_expanded_form: - operation: keep - core_predicate: biolink:close_match -PDQ:has_lab_number: - operation: delete -PDQ:has_tradename: - operation: keep - core_predicate: biolink:close_match -PDQ:inverse_isa: - operation: invert - core_predicate: biolink:subclass_of -PDQ:isa: - operation: keep - core_predicate: biolink:subclass_of -PDQ:lab_number_of: - operation: delete -PDQ:tradename_of: - operation: keep - core_predicate: biolink:close_match -PHAROS:drug_targets: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -PR:confers_resistance_to: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -PR:has_gene_template: - operation: keep - core_predicate: biolink:gene_product_of -PR:lacks_part: - operation: keep - core_predicate: biolink:lacks_part -PR:non-covalently_bound_to: - operation: keep - core_predicate: biolink:physically_interacts_with -PSY:CHD: - operation: keep - core_predicate: biolink:subclass_of -PSY:PAR: - operation: invert - core_predicate: biolink:subclass_of -PSY:RB: - operation: invert - core_predicate: biolink:subclass_of -PSY:RN: - operation: keep - core_predicate: biolink:subclass_of -PSY:RO: - operation: keep - core_predicate: biolink:related_to -PSY:has_member: - operation: keep - core_predicate: biolink:has_member -PSY:member_of: - operation: invert - core_predicate: biolink:has_member -PSY:use: - operation: keep - core_predicate: biolink:subclass_of -PSY:used_for: - operation: invert - core_predicate: biolink:has_input -PathWhiz:has_bound: - operation: keep - core_predicate: biolink:has_participant -PathWhiz:has_compound: - operation: keep - core_predicate: biolink:has_participant -PathWhiz:has_element_collection: - operation: keep - core_predicate: biolink:has_participant -PathWhiz:has_element_in_bound: - operation: keep - core_predicate: biolink:has_part -PathWhiz:has_enzyme: - operation: keep - core_predicate: biolink:has_participant -PathWhiz:has_left_element: - operation: keep - core_predicate: biolink:has_input -PathWhiz:has_location: - operation: keep - core_predicate: biolink:occurs_in -PathWhiz:has_nucleic_acid: - operation: keep - core_predicate: biolink:has_participant -PathWhiz:has_protein: - operation: keep - core_predicate: biolink:has_participant -PathWhiz:has_protein_in_complex: - operation: keep - core_predicate: biolink:has_part -PathWhiz:has_reaction: - operation: keep - core_predicate: biolink:has_participant -PathWhiz:has_right_element: - operation: keep - core_predicate: biolink:has_output -PathWhiz:in_species: - operation: keep - core_predicate: biolink:occurs_in -REACT:has_element: - operation: keep - core_predicate: biolink:has_part -REACT:has_event: - operation: keep - core_predicate: biolink:has_participant -REACT:has_input: - operation: keep - core_predicate: biolink:has_input -REACT:has_member: - operation: keep - core_predicate: biolink:has_part -REACT:has_output: - operation: keep - core_predicate: biolink:has_output -REACT:in_species: - operation: keep - core_predicate: biolink:occurs_in -REACT:is_requirement_for: # SAR: not sure if this is correct; need to look into it - operation: keep - core_predicate: biolink:regulates -REACT:linked_to_disease: - operation: keep - core_predicate: biolink:related_to -REACT:negatively_regulates: - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: downregulated -REACT:negatively_regulates_gene_expression: - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: downregulated -REACT:positively_regulates: - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: upregulated -REACT:positively_regulates_gene_expression: - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: upregulated -REACT:related_to: - operation: keep - core_predicate: biolink:related_to -REPODB:clinically_tested_approved_unknown_phase: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_suspended_phase_0: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_suspended_phase_1: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_suspended_phase_1_or_phase_2: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_suspended_phase_2: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_suspended_phase_2_or_phase_3: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_suspended_phase_3: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_terminated_phase_0: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_terminated_phase_1: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_terminated_phase_1_or_phase_2: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_terminated_phase_2: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_terminated_phase_2_or_phase_3: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_terminated_phase_3: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_withdrawn_phase_0: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_withdrawn_phase_1: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_withdrawn_phase_1_or_phase_2: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_withdrawn_phase_2: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_withdrawn_phase_2_or_phase_3: - operation: keep - core_predicate: biolink:treats -REPODB:clinically_tested_withdrawn_phase_3: - operation: keep - core_predicate: biolink:treats -RO:0000052: - operation: keep - core_predicate: biolink:related_to -RO:0000053: - operation: keep - core_predicate: biolink:related_to -RO:0000056: - operation: invert - core_predicate: biolink:has_participant -RO:0000057: - operation: keep - core_predicate: biolink:has_participant -RO:0000059: - operation: keep - core_predicate: biolink:related_to -# role of -RO:0000081: - operation: delete -RO:0000086: - operation: keep - core_predicate: biolink:related_to -RO:0000087: - operation: keep - core_predicate: biolink:related_to -# RO:00002325: -# operation: keep -# core_predicate: biolink:colocalizes_with -RO:0001000: - operation: keep - core_predicate: biolink:derives_from -# RO:0001001: -# operation: invert -# core_predicate: biolink:derives_from -RO:0001015: - operation: invert - core_predicate: biolink:located_in -# RO:0001018: -# operation: invert -# core_predicate: biolink:has_part -RO:0001019: - operation: keep - core_predicate: biolink:has_part -RO:0001022: - operation: invert - core_predicate: biolink:causes -RO:0001025: - operation: keep - core_predicate: biolink:located_in -RO:0002001: - operation: keep - core_predicate: biolink:related_to -RO:0002002: - operation: keep - core_predicate: biolink:related_to -# RO:0002003: -# operation: keep -# core_predicate: biolink:related_to -RO:0002005: - operation: keep - core_predicate: biolink:related_to -RO:0002007: - operation: invert - core_predicate: biolink:has_part -RO:0002008: - operation: keep - core_predicate: biolink:related_to -RO:0002082: - operation: keep - core_predicate: biolink:temporally_related_to -RO:0002083: - operation: keep - core_predicate: biolink:temporally_related_to -# RO:0002084: -# operation: keep -# core_predicate: biolink:related_to -RO:0002087: - operation: invert - core_predicate: biolink:precedes -RO:0002090: - operation: keep - core_predicate: biolink:precedes -RO:0002092: - operation: keep - core_predicate: biolink:related_to -RO:0002093: - operation: keep - core_predicate: biolink:related_to -RO:0002100: - operation: keep - core_predicate: biolink:overlaps -RO:0002101: - operation: keep - core_predicate: biolink:overlaps -RO:0002102: - operation: keep - core_predicate: biolink:overlaps -RO:0002103: # synapsed by - operation: keep - core_predicate: biolink:physically_interacts_with -RO:0002104: - operation: keep - core_predicate: biolink:has_plasma_membrane_part -RO:0002120: # synapsed to - operation: keep - core_predicate: biolink:physically_interacts_with -RO:0002130: # has synaptic terminal in - operation: keep - core_predicate: biolink:indirectly_physically_interacts_with -RO:0002131: - operation: keep - core_predicate: biolink:overlaps -RO:0002134: - operation: keep - core_predicate: biolink:related_to -RO:0002150: - operation: keep - core_predicate: biolink:related_to -RO:0002159: - operation: keep - core_predicate: biolink:related_to -RO:0002160: - operation: keep - core_predicate: biolink:in_taxon -RO:0002162: - operation: keep - core_predicate: biolink:in_taxon -RO:0002170: - operation: keep - core_predicate: biolink:related_to -RO:0002176: - operation: keep - core_predicate: biolink:related_to -RO:0002177: - operation: keep - core_predicate: biolink:related_to -RO:0002178: - operation: keep - core_predicate: biolink:related_to -RO:0002179: - operation: keep - core_predicate: biolink:related_to -RO:0002180: - operation: keep - core_predicate: biolink:has_part -RO:0002200: - operation: keep - core_predicate: biolink:has_phenotype -RO:0002202: - operation: keep - core_predicate: biolink:develops_from -RO:0002203: - operation: keep - core_predicate: biolink:develops_from -# RO:0002205: -# operation: invert -# core_predicate: biolink:gene_product_of -RO:0002207: - operation: keep - core_predicate: biolink:develops_from -RO:0002211: # regulates - operation: keep - core_predicate: biolink:regulates -RO:0002212: # negatively regulates - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: downregulated -RO:0002213: # positively regulates - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: upregulated -RO:0002215: - operation: keep - core_predicate: biolink:capable_of -RO:0002216: - operation: invert - core_predicate: biolink:has_participant -RO:0002219: - operation: keep - core_predicate: biolink:coexists_with -RO:0002220: - operation: keep - core_predicate: biolink:coexists_with -RO:0002221: - operation: keep - core_predicate: biolink:coexists_with -RO:0002223: - operation: keep - core_predicate: biolink:temporally_related_to -RO:0002224: - operation: keep - core_predicate: biolink:temporally_related_to -RO:0002225: - operation: keep - core_predicate: biolink:develops_from -RO:0002226: - operation: keep - core_predicate: biolink:develops_from -RO:0002229: - operation: keep - core_predicate: biolink:temporally_related_to -RO:0002230: - operation: keep - core_predicate: biolink:temporally_related_to -RO:0002231: - operation: keep - core_predicate: biolink:occurs_in -RO:0002232: - operation: keep - core_predicate: biolink:occurs_in -RO:0002233: - operation: keep - core_predicate: biolink:has_input -RO:0002234: - operation: keep - core_predicate: biolink:has_output -# RO:0002241: -# operation: keep -# core_predicate: biolink:related_to -RO:0002254: - operation: keep - core_predicate: biolink:related_to -# RO:0002255: -# operation: keep -# core_predicate: biolink:contributes_to -RO:0002256: - operation: keep - core_predicate: biolink:causes -# RO:0002263: -# operation: keep -# core_predicate: biolink:acts_upstream_of -# RO:0002264: -# operation: keep -# core_predicate: biolink:acts_upstream_of_or_within -RO:0002285: - operation: invert - core_predicate: biolink:precedes -RO:0002292: - operation: invert - core_predicate: biolink:expressed_in -RO:0002295: # results in developmental progression of - operation: keep - core_predicate: biolink:regulates -RO:0002296: # results in development of - operation: keep - core_predicate: biolink:has_output -RO:0002297: - operation: keep - core_predicate: biolink:has_output -RO:0002298: - operation: keep - core_predicate: biolink:has_output -RO:0002299: - operation: keep - core_predicate: biolink:has_output -# RO:0002302: -# operation: invert -# core_predicate: biolink:treats -RO:0002303: - operation: keep - core_predicate: biolink:located_in -RO:0002309: - operation: keep - core_predicate: biolink:related_to -# RO:0002313: -# operation: keep -# core_predicate: biolink:affects -# qualified_predicate: biolink:causes -# qualifiers: -# object_aspect: transport -# object_direction: increased -RO:0002314: - operation: keep - core_predicate: biolink:related_to -RO:0002315: - operation: keep - core_predicate: biolink:causes -RO:0002322: - operation: keep - core_predicate: biolink:related_to -# RO:0002326: -# operation: keep -# core_predicate: biolink:contributes_to -RO:0002328: - operation: keep - core_predicate: biolink:related_to -RO:0002331: - operation: keep - core_predicate: biolink:actively_involved_in -RO:0002332: - operation: keep - core_predicate: biolink:related_to -# RO:0002333: -# operation: invert -# core_predicate: biolink:enables -RO:0002334: # regulated by - operation: invert - core_predicate: biolink:regulates -RO:0002336: # positively regulated by - operation: invert - core_predicate: biolink:regulates -RO:0002338: - operation: keep - core_predicate: biolink:related_to -RO:0002339: - operation: keep - core_predicate: biolink:related_to -# RO:0002340: -# operation: keep -# core_predicate: biolink:affects -# qualified_predicate: biolink:causes -# qualifiers: -# object_aspect: transport -# object_direction: increased -RO:0002341: - operation: keep - core_predicate: biolink:related_to -RO:0002342: - operation: keep - core_predicate: biolink:related_to -RO:0002343: - operation: keep - core_predicate: biolink:affects -RO:0002344: - operation: keep - core_predicate: biolink:related_to -# RO:0002345: -# operation: keep -# core_predicate: biolink:affects -# qualified_predicate: biolink:causes -# qualifiers: -# object_aspect: transport -# object_direction: increased -RO:0002348: - operation: keep - core_predicate: biolink:related_to -RO:0002349: - operation: keep - core_predicate: biolink:related_to -RO:0002350: - operation: invert - core_predicate: biolink:has_member -RO:0002351: - operation: keep - core_predicate: biolink:has_member -RO:0002352: - operation: invert - core_predicate: biolink:has_input -RO:0002353: - operation: invert - core_predicate: biolink:has_output -RO:0002354: - operation: invert - core_predicate: biolink:has_output -RO:0002355: - operation: keep - core_predicate: biolink:affects -RO:0002356: - operation: keep - core_predicate: biolink:related_to -RO:0002371: - operation: keep - core_predicate: biolink:related_to -RO:0002372: - operation: keep - core_predicate: biolink:related_to -RO:0002373: - operation: keep - core_predicate: biolink:related_to -RO:0002374: - operation: keep - core_predicate: biolink:related_to -RO:0002376: - operation: invert - core_predicate: biolink:has_part -RO:0002380: - operation: invert - core_predicate: biolink:has_part -RO:0002385: - operation: keep - core_predicate: biolink:related_to -RO:0002387: - operation: keep - core_predicate: biolink:related_to -RO:0002388: - operation: delete -# RO:0002410: -# operation: keep -# core_predicate: biolink:causes -RO:0002411: - operation: keep - core_predicate: biolink:precedes -RO:0002412: - operation: keep - core_predicate: biolink:precedes -RO:0002428: - operation: keep - core_predicate: biolink:regulates -# RO:0002432: -# operation: keep -# core_predicate: biolink:active_in -RO:0002433: - operation: keep - core_predicate: biolink:overlaps -# RO:0002434: -# operation: keep -# core_predicate: biolink:interacts_with -# RO:0002435: -# operation: keep -# core_predicate: biolink:genetically_interacts_with -RO:0002436: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -# RO:0002448: -# operation: keep -# core_predicate: biolink:regulates -# RO:0002449: -# operation: keep -# core_predicate: biolink:regulates -# qualified_predicate: biolink:causes -# qualifiers: -# object_direction: downregulated -# RO:0002450: -# operation: keep -# core_predicate: biolink:regulates -# qualified_predicate: biolink:causes -# qualifiers: -# object_direction: upregulated -RO:0002451: - operation: keep - core_predicate: biolink:related_to -RO:0002452: - operation: keep - core_predicate: biolink:has_phenotype -RO:0002470: - operation: keep - core_predicate: biolink:related_to -RO:0002473: - operation: keep - core_predicate: biolink:composed_primarily_of -RO:0002488: - operation: keep - core_predicate: biolink:temporally_related_to -RO:0002489: - operation: keep - core_predicate: biolink:temporally_related_to -RO:0002491: - operation: keep - core_predicate: biolink:coexists_with -RO:0002492: - operation: keep - core_predicate: biolink:temporally_related_to -RO:0002493: - operation: keep - core_predicate: biolink:temporally_related_to -RO:0002494: - operation: keep - core_predicate: biolink:related_to -RO:0002495: - operation: keep - core_predicate: biolink:related_to -RO:0002496: - operation: keep - core_predicate: biolink:temporally_related_to -RO:0002497: - operation: keep - core_predicate: biolink:temporally_related_to -RO:0002500: - operation: keep - core_predicate: biolink:capable_of -RO:0002503: - operation: keep - core_predicate: biolink:actively_involved_in -RO:0002505: - operation: invert - core_predicate: biolink:has_participant -# RO:0002506: -# operation: keep -# core_predicate: biolink:causes -RO:0002507: - operation: keep - core_predicate: biolink:causes -RO:0002509: - operation: keep - core_predicate: biolink:causes -# RO:0002510: -# operation: keep -# core_predicate: biolink:transcribed_from -# RO:0002511: -# operation: invert -# core_predicate: biolink:transcribed_from -RO:0002524: - operation: keep - core_predicate: biolink:has_part -RO:0002551: - operation: keep - core_predicate: biolink:has_part -RO:0002565: - operation: invert - core_predicate: biolink:has_participant -RO:0002568: - operation: keep - core_predicate: biolink:related_to -RO:0002570: # conduit for - operation: keep - core_predicate: biolink:related_to -RO:0002571: - operation: invert - core_predicate: biolink:has_part -RO:0002572: - operation: invert - core_predicate: biolink:has_part -RO:0002573: - operation: keep - core_predicate: biolink:related_to -RO:0002576: - operation: invert - core_predicate: biolink:has_part -RO:0002578: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -RO:0002588: - operation: keep - core_predicate: biolink:has_output -RO:0002590: - operation: keep - core_predicate: biolink:has_input -RO:0002591: - operation: keep - core_predicate: biolink:affects -RO:0002592: - operation: keep - core_predicate: biolink:affects -RO:0002596: # capable of regulating - operation: keep - core_predicate: biolink:regulates -# RO:0002599: -# operation: keep -# core_predicate: biolink:prevents -# RO:0002604: -# operation: keep -# core_predicate: biolink:opposite_of -# RO:0002606: -# operation: keep -# core_predicate: biolink:treats -# RO:0002607: -# operation: keep -# core_predicate: biolink:biomarker_for -RO:0002608: - operation: invert - core_predicate: biolink:causes -RO:0002610: - operation: keep - core_predicate: biolink:correlated_with -RO:0002629: # directly positively regulates - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: upregulated -RO:0002630: # directly negatively regulates - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: downregulated -RO:0003000: - operation: keep - core_predicate: biolink:produces -RO:0003001: - operation: invert - core_predicate: biolink:produces -# RO:0003002: -# operation: keep -# core_predicate: biolink:affects -# qualified_predicate: biolink:causes -# qualifiers: -# object_aspect: expression -# object_direction: decreased -# RO:0003003: -# operation: keep -# core_predicate: biolink:affects -# qualified_predicate: biolink:causes -# qualifiers: -# object_aspect: expression -# object_direction: increased -# RO:0003301: -# operation: keep -# core_predicate: biolink:model_of -# RO:0003303: -# operation: keep -# core_predicate: biolink:causes -RO:0003304: - operation: keep - core_predicate: biolink:contributes_to -# RO:0003307: -# operation: keep -# core_predicate: biolink:ameliorates -# RO:0003309: -# operation: keep -# core_predicate: biolink:exacerbates -RO:0004001: - operation: keep - core_predicate: biolink:causes -# has material basis in germline mutation in -RO:0004003: - operation: keep - core_predicate: biolink:related_to -# has material basis in somatic mutation in -RO:0004004: - operation: keep - core_predicate: biolink:related_to -RO:0004007: - operation: keep - core_predicate: biolink:has_participant -RO:0004008: - operation: keep - core_predicate: biolink:has_output -RO:0004009: - operation: keep - core_predicate: biolink:has_input -RO:0004019: - operation: invert - core_predicate: biolink:causes -RO:0004020: - operation: invert - core_predicate: biolink:causes -RO:0004021: - operation: keep - core_predicate: biolink:has_participant -RO:0004022: - operation: keep - core_predicate: biolink:has_phenotype -RO:0004024: - operation: keep - core_predicate: biolink:disrupts -RO:0004025: - operation: keep - core_predicate: biolink:disrupts -RO:0004026: - operation: keep - core_predicate: biolink:disease_has_location -RO:0004027: - operation: keep - core_predicate: biolink:related_to -RO:0004028: - operation: invert - core_predicate: biolink:causes -RO:0004029: - operation: keep - core_predicate: biolink:associated_with -RO:0004030: - operation: invert - core_predicate: biolink:causes -# RO:0004032: -# operation: keep -# core_predicate: biolink:acts_upstream_of_or_within_positive_effect -# RO:0004033: -# operation: keep -# core_predicate: biolink:acts_upstream_of_or_within_negative_effect -# RO:0004034: -# operation: keep -# core_predicate: biolink:acts_upstream_of_positive_effect -# RO:0004035: -# operation: keep -# core_predicate: biolink:acts_upstream_of_negative_effect -# has disease driver -RO:0007001: - operation: keep - core_predicate: biolink:related_to -RO:0009001: - operation: keep - core_predicate: biolink:related_to -RO:0009003: # immersed_in - operation: keep - core_predicate: biolink:related_to -RO:0009004: - operation: keep - core_predicate: biolink:related_to -RO:0009501: - operation: invert - core_predicate: biolink:causes -RO:0012003: - operation: keep - core_predicate: biolink:affects -RO:0012008: - operation: keep - core_predicate: biolink:affects -RO:0013001: - operation: keep - core_predicate: biolink:related_to -RO:0013007: - operation: keep - core_predicate: biolink:overlaps -RO:0014001: - operation: keep - core_predicate: biolink:related_to -# increased in magnitude relative to -RO:0015007: - operation: delete -# decreased in magnitude relative to -RO:0015008: - operation: delete -# has relative magnitude -RO:0015010: - operation: delete -# has cross section -RO:0015011: - operation: delete -# reciprocal of -RO:0015012: - operation: keep - core_predicate: biolink:related_to -# has high plasma membrane amount -RO:0015015: - operation: keep - core_predicate: biolink:has_increased_amount -# has low plasma membrane amount -RO:0015016: - operation: keep - core_predicate: biolink:has_decreased_amount -# regulates characteristic -RO:0019000: - operation: keep - core_predicate: biolink:regulates -# positively regulates characteristic -RO:0019001: - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: upregulated -# negatively regulates characteristic -RO:0019002: - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: downregulated -RO:0040036: - operation: delete -# RO:HOM0000000: -# operation: keep -# core_predicate: biolink:similar_to -# RO:has_participant: -# operation: keep -# core_predicate: biolink:has_participant -RO:participates_in: - operation: invert - core_predicate: biolink:has_participant -RXNORM:SY: - operation: keep - core_predicate: biolink:close_match -RXNORM:consists_of: - operation: keep - core_predicate: biolink:has_part -RXNORM:constitutes: - operation: invert - core_predicate: biolink:has_part -RXNORM:contained_in: - operation: invert - core_predicate: biolink:has_part -RXNORM:contains: - operation: keep - core_predicate: biolink:has_part -RXNORM:dose_form_of: - operation: delete -RXNORM:doseformgroup_of: - operation: delete -RXNORM:form_of: - operation: delete -RXNORM:has_dose_form: - operation: keep - core_predicate: biolink:subclass_of -RXNORM:has_doseformgroup: - operation: keep - core_predicate: biolink:subclass_of -RXNORM:has_form: - operation: keep - core_predicate: biolink:related_to -RXNORM:has_ingredient: - operation: keep - core_predicate: biolink:has_part -RXNORM:has_ingredients: - operation: delete -RXNORM:has_part: - operation: keep - core_predicate: biolink:has_part -RXNORM:has_precise_ingredient: - operation: delete -RXNORM:has_quantified_form: - operation: keep - core_predicate: biolink:close_match -RXNORM:has_tradename: - operation: keep - core_predicate: biolink:related_to -RXNORM:included_in: - operation: keep - core_predicate: biolink:related_to -RXNORM:includes: - operation: keep - core_predicate: biolink:related_to -RXNORM:ingredient_of: - operation: invert - core_predicate: biolink:has_part -RXNORM:ingredients_of: - operation: invert - core_predicate: biolink:has_part -RXNORM:inverse_isa: - operation: invert - core_predicate: biolink:subclass_of -RXNORM:isa: - operation: keep - core_predicate: biolink:subclass_of -RXNORM:part_of: - operation: invert - core_predicate: biolink:has_part -RXNORM:precise_ingredient_of: - operation: invert - core_predicate: biolink:has_part -RXNORM:quantified_form_of: - operation: delete -RXNORM:reformulated_to: - operation: keep - core_predicate: biolink:related_to -RXNORM:reformulation_of: - operation: delete -RXNORM:tradename_of: - operation: delete -SEMMEDDB:1532: - operation: delete -SEMMEDDB:ADMINISTERED_TO: - operation: keep - core_predicate: biolink:related_to -SEMMEDDB:administered_to: - operation: keep - core_predicate: biolink:related_to -SEMMEDDB:AFFECTS: - operation: keep - core_predicate: biolink:affects -SEMMEDDB:affects: - operation: keep - core_predicate: biolink:affects -SEMMEDDB:ASSOCIATED_WITH: - operation: keep - core_predicate: biolink:related_to -SEMMEDDB:associated_with: - operation: keep - core_predicate: biolink:related_to -SEMMEDDB:AUGMENTS: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity_or_abundance - object_direction: increased -SEMMEDDB:augments: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity_or_abundance - object_direction: increased -SEMMEDDB:CAUSES: - operation: keep - core_predicate: biolink:causes -SEMMEDDB:causes: - operation: keep - core_predicate: biolink:causes -SEMMEDDB:COEXISTS_WITH: - operation: keep - core_predicate: biolink:coexists_with -SEMMEDDB:coexists_with: - operation: keep - core_predicate: biolink:coexists_with -SEMMEDDB:COMPARED_WITH: - operation: keep - core_predicate: biolink:related_to -SEMMEDDB:compared_with: - operation: keep - core_predicate: biolink:related_to -SEMMEDDB:COMPLICATES: - operation: keep - core_predicate: biolink:exacerbates -SEMMEDDB:complicates: - operation: keep - core_predicate: biolink:exacerbates -SEMMEDDB:CONVERTS_TO: - operation: invert - core_predicate: biolink:derives_from -SEMMEDDB:converts_to: - operation: invert - core_predicate: biolink:derives_from -SEMMEDDB:DIAGNOSES: - operation: keep - core_predicate: biolink:diagnoses -SEMMEDDB:diagnoses: - operation: keep - core_predicate: biolink:diagnoses -SEMMEDDB:DISRUPTS: - operation: keep - core_predicate: biolink:disrupts -SEMMEDDB:disrupts: - operation: keep - core_predicate: biolink:disrupts -SEMMEDDB:HIGHER_THAN: - operation: keep - core_predicate: biolink:related_to -SEMMEDDB:higher_than: - operation: keep - core_predicate: biolink:related_to -SEMMEDDB:INHIBITS: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -SEMMEDDB:inhibits: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: decreased -SEMMEDDB:INTERACTS_WITH: - operation: keep - core_predicate: biolink:physically_interacts_with -SEMMEDDB:interacts_with: - operation: keep - core_predicate: biolink:physically_interacts_with -SEMMEDDB:ISA: - operation: keep - core_predicate: biolink:subclass_of -SEMMEDDB:isa: - operation: keep - core_predicate: biolink:subclass_of -SEMMEDDB:LOCATION_OF: - operation: invert - core_predicate: biolink:located_in -SEMMEDDB:location_of: - operation: invert - core_predicate: biolink:located_in -SEMMEDDB:LOWER_THAN: - operation: keep - core_predicate: biolink:related_to -SEMMEDDB:lower_than: - operation: keep - core_predicate: biolink:related_to -SEMMEDDB:MANIFESTATION_OF: - operation: keep - core_predicate: biolink:manifestation_of -SEMMEDDB:manifestation_of: - operation: keep - core_predicate: biolink:manifestation_of -SEMMEDDB:MEASUREMENT_OF: - operation: delete -SEMMEDDB:measurement_of: - operation: delete -SEMMEDDB:MEASURES: - operation: keep - core_predicate: biolink:related_to -SEMMEDDB:measures: - operation: keep - core_predicate: biolink:related_to -SEMMEDDB:METHOD_OF: - operation: delete -SEMMEDDB:method_of: - operation: delete -SEMMEDDB:NOM: - operation: delete -SEMMEDDB:nom: - operation: delete -SEMMEDDB:OCCURS_IN: - operation: keep - core_predicate: biolink:occurs_in -SEMMEDDB:occurs_in: - operation: keep - core_predicate: biolink:occurs_in -SEMMEDDB:PART_OF: - operation: invert - core_predicate: biolink:has_part -SEMMEDDB:part_of: - operation: invert - core_predicate: biolink:has_part -SEMMEDDB:PRECEDES: - operation: keep - core_predicate: biolink:precedes -SEMMEDDB:precedes: - operation: keep - core_predicate: biolink:precedes -SEMMEDDB:PREDISPOSES: - operation: keep - core_predicate: biolink:predisposes -SEMMEDDB:predisposes: - operation: keep - core_predicate: biolink:predisposes -SEMMEDDB:PREP: - operation: delete -SEMMEDDB:prep: - operation: delete -SEMMEDDB:PREVENTS: - operation: keep - core_predicate: biolink:prevents -SEMMEDDB:prevents: - operation: keep - core_predicate: biolink:prevents -SEMMEDDB:PROCESS_OF: - operation: keep - core_predicate: biolink:occurs_in -SEMMEDDB:process_of: - operation: keep - core_predicate: biolink:occurs_in -SEMMEDDB:PRODUCES: - operation: keep - core_predicate: biolink:produces -SEMMEDDB:produces: - operation: keep - core_predicate: biolink:produces -SEMMEDDB:SAME_AS: - operation: keep - core_predicate: biolink:close_match -SEMMEDDB:same_as: - operation: keep - core_predicate: biolink:close_match -SEMMEDDB:STIMULATES: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -SEMMEDDB:stimulates: - operation: keep - core_predicate: biolink:affects - qualified_predicate: biolink:causes - qualifiers: - object_aspect: activity - object_direction: increased -SEMMEDDB:TREATS: - operation: keep - core_predicate: biolink:treats -SEMMEDDB:treats: - operation: keep - core_predicate: biolink:treats -SEMMEDDB:USES: - operation: keep - core_predicate: biolink:has_input -SEMMEDDB:uses: - operation: keep - core_predicate: biolink:has_input -SEMMEDDB:VERB: - operation: delete -SEMMEDDB:verb: - operation: delete -SEMMEDDB:XREF: - operation: keep - core_predicate: biolink:related_to -SEMMEDDB:xref: - operation: keep - core_predicate: biolink:related_to -SIO:000001: - operation: delete -SIO:000203: - operation: keep - core_predicate: biolink:directly_physically_interacts_with -# SIO:000628: -# operation: keep -# core_predicate: biolink:mentions -# SIO:000983: -# operation: keep -# core_predicate: biolink:biomarker_for -# SIO:001331: -# operation: keep -# core_predicate: biolink:diagnoses -# SIO:010080: -# operation: invert -# core_predicate: biolink:transcribed_from -# SIO:010081: -# operation: keep -# core_predicate: biolink:transcribed_from -# SIO:010285: -# operation: keep -# core_predicate: biolink:in_complex_with -# SO:0001583: -# operation: keep -# core_predicate: biolink:is_missense_variant_of -# SO:0001589: -# operation: keep -# core_predicate: biolink:is_frameshift_variant_of -# SO:0001629: -# operation: keep -# core_predicate: biolink:is_splice_site_variant_of -# SO:0001819: -# operation: keep -# core_predicate: biolink:is_synonymous_variant_of -# SO:0002054: -# operation: keep -# core_predicate: biolink:is_nonsense_variant_of -SO:has_origin: - operation: keep - core_predicate: biolink:coexists_with -# SO:similar_to: -# operation: keep -# core_predicate: biolink:similar_to -# UBERON:anastomoses_with: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:anteriorly_connected_to: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:channel_for: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:channels_from: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:channels_into: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:conduit_for: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:distally_connected_to: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:existence_starts_and_ends_during: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:extends_fibers_into: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:filtered_through: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:in_central_side_of: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:in_innermost_side_of: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:in_outermost_side_of: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:indirectly_supplies: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:posteriorly_connected_to: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:protects: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:proximally_connected_to: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:sexually_homologous_to: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON:site_of: -# operation: invert -# core_predicate: biolink:occurs_in -# UBERON:subdivision_of: -# operation: invert -# core_predicate: biolink:has_part -# UBERON:synapsed_by: -# operation: keep -# core_predicate: biolink:related_to -UBERON_CORE:anastomoses_with: - operation: keep - core_predicate: biolink:coexists_with -UBERON_CORE:anteriorly_connected_to: - operation: keep - core_predicate: biolink:coexists_with -UBERON_CORE:channel_for: - operation: keep - core_predicate: biolink:coexists_with -UBERON_CORE:channels_from: - operation: keep - core_predicate: biolink:coexists_with -UBERON_CORE:channels_into: - operation: keep - core_predicate: biolink:coexists_with -UBERON_CORE:conduit_for: - operation: keep - core_predicate: biolink:coexists_with -UBERON_CORE:distally_connected_to: - operation: keep - core_predicate: biolink:coexists_with -UBERON_CORE:extends_fibers_into: - operation: keep - core_predicate: biolink:coexists_with -UBERON_CORE:filtered_through: - operation: keep - core_predicate: biolink:coexists_with -UBERON_CORE:in_central_side_of: - operation: keep - core_predicate: biolink:located_in -UBERON_CORE:in_innermost_side_of: - operation: keep - core_predicate: biolink:located_in -UBERON_CORE:in_outermost_side_of: - operation: keep - core_predicate: biolink:located_in -UBERON_CORE:indirectly_supplies: - operation: keep - core_predicate: biolink:coexists_with -# UBERON_CORE:layer_part_of: -# operation: invert -# core_predicate: biolink:has_part -UBERON_CORE:posteriorly_connected_to: - operation: keep - core_predicate: biolink:coexists_with -UBERON_CORE:protects: - operation: keep - core_predicate: biolink:related_to -UBERON_CORE:proximally_connected_to: - operation: keep - core_predicate: biolink:coexists_with -UBERON_CORE:sexually_homologous_to: - operation: keep - core_predicate: biolink:homologous_to -UBERON_CORE:site_of: - operation: keep - core_predicate: biolink:occurs_in -UBERON_CORE:subdivision_of: - operation: invert - core_predicate: biolink:has_part -UBERON_CORE:synapsed_by: - operation: keep - core_predicate: biolink:coexists_with -# UBERON_CORE:transitively_anteriorly_connected_to: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON_CORE:transitively_connected_to: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON_CORE:transitively_distally_connected_to: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON_CORE:transitively_proximally_connected_to: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON_CORE:trunk_part_of: -# operation: invert -# core_predicate: biolink:has_part -# UBERON_NONAMESPACE:connected_to: -# operation: keep -# core_predicate: biolink:related_to -# UBERON_NONAMESPACE:distally_connected_to: -# operation: keep -# core_predicate: biolink:coexists_with -# UBERON_NONAMESPACE:innervated_by: -# operation: keep -# core_predicate: biolink:related_to -# UBERON_NONAMESPACE:subdivision_of: -# operation: keep -# core_predicate: biolink:coexists_with -UMLS:CHD: - operation: keep - core_predicate: biolink:subclass_of -UMLS:PAR: - operation: invert - core_predicate: biolink:subclass_of -UMLS:RB: - operation: invert - core_predicate: biolink:subclass_of -UMLS:RN: - operation: keep - core_predicate: biolink:subclass_of -UMLS:RO: - operation: keep - core_predicate: biolink:related_to -UMLS:RQ: - operation: keep - core_predicate: biolink:related_to -# UMLS:SIB: -# operation: delete -UMLS:SY: - operation: keep - core_predicate: biolink:close_match -UMLS:active_metabolites_of: - operation: invert - core_predicate: biolink:has_metabolite -UMLS:class_code_classified_by: - operation: keep - core_predicate: biolink:related_to -UMLS:classifies_class_code: - operation: delete -UMLS:component_of: - operation: invert - core_predicate: biolink:has_part -UMLS:context_binding_of: - operation: delete -UMLS:contraindicated_class_of: # Consider mapping this to drug interaction if and when that biolink predicate becomes available - operation: keep - core_predicate: biolink:related_to -UMLS:contraindicated_mechanism_of_action_of: - operation: keep - core_predicate: biolink:related_to -UMLS:contraindicated_physiologic_effect_of: - operation: keep - core_predicate: biolink:related_to -UMLS:contraindicated_with_disease: - operation: keep - core_predicate: biolink:related_to -UMLS:effect_may_be_inhibited_by: - operation: keep - core_predicate: biolink:related_to -UMLS:exhibited_by: - operation: keep - core_predicate: biolink:related_to -UMLS:exhibits: - operation: delete -UMLS:form_of: - operation: delete -UMLS:has_active_metabolites: - operation: keep - core_predicate: biolink:related_to -UMLS:has_component: - operation: keep - core_predicate: biolink:has_part -UMLS:has_context_binding: - operation: keep - core_predicate: biolink:related_to -UMLS:has_contraindicated_class: - operation: keep - core_predicate: biolink:related_to -UMLS:has_contraindicated_drug: - operation: keep - core_predicate: biolink:related_to -UMLS:has_contraindicated_mechanism_of_action: - operation: keep - core_predicate: biolink:related_to -UMLS:has_contraindicated_physiologic_effect: - operation: keep - core_predicate: biolink:related_to -UMLS:has_form: - operation: keep - core_predicate: biolink:related_to -UMLS:has_mapping_qualifier: - operation: keep - core_predicate: biolink:related_to -UMLS:has_mechanism_of_action: - operation: keep - core_predicate: biolink:related_to -UMLS:has_owning_affiliate: - operation: invert - core_predicate: biolink:has_part -UMLS:has_owning_section: - operation: delete -UMLS:has_owning_subsection: - operation: delete -UMLS:has_parent: - operation: keep - core_predicate: biolink:subclass_of -UMLS:has_pharmacokinetics: - operation: keep - core_predicate: biolink:related_to -UMLS:has_physiologic_effect: - operation: keep - core_predicate: biolink:causes -UMLS:has_structural_class: - operation: keep - core_predicate: biolink:related_to -UMLS:has_supported_concept_property: - operation: keep - core_predicate: biolink:related_to -UMLS:has_supported_concept_relationship: - operation: keep - core_predicate: biolink:related_to -UMLS:has_therapeutic_class: # Come back to this one at another time, might have a chance to use has_member - operation: keep - core_predicate: biolink:related_to -UMLS:induced_by: - operation: keep - core_predicate: biolink:related_to -UMLS:induces: - operation: keep - core_predicate: biolink:related_to -UMLS:larger_than: - operation: keep - core_predicate: biolink:related_to -UMLS:mapped_from: - operation: delete -UMLS:mapping_qualifier_of: - operation: delete -UMLS:mapped_to: - operation: keep - core_predicate: biolink:related_to -UMLS:may_be_diagnosed_by: - operation: keep - core_predicate: biolink:related_to -UMLS:may_be_prevented_by: - operation: keep - core_predicate: biolink:related_to -UMLS:may_be_qualified_by: - operation: keep - core_predicate: biolink:related_to -UMLS:may_be_treated_by: - operation: keep - core_predicate: biolink:related_to -UMLS:may_diagnose: - operation: keep - core_predicate: biolink:related_to -UMLS:may_inhibit_effect_of: - operation: keep - core_predicate: biolink:related_to -UMLS:may_prevent: - operation: keep - core_predicate: biolink:related_to -UMLS:may_qualify: - operation: delete -UMLS:may_treat: - operation: keep - core_predicate: biolink:related_to -UMLS:measured_by: - operation: delete -UMLS:measures: - operation: keep - core_predicate: biolink:related_to -UMLS:mechanism_of_action_of: - operation: keep - core_predicate: biolink:related_to -UMLS:metabolic_site_of: - operation: keep - core_predicate: biolink:related_to -UMLS:owning_affiliate_of: - operation: delete -UMLS:owning_section_of: - operation: keep - core_predicate: biolink:related_to -UMLS:owning_subsection_of: - operation: invert - core_predicate: biolink:has_part -UMLS:parent_of: - operation: invert - core_predicate: biolink:subclass_of -UMLS:pharmacokinetics_of: - operation: keep - core_predicate: biolink:related_to -UMLS:physiologic_effect_of: - operation: keep - core_predicate: biolink:related_to -UMLS:related_to: - operation: keep - core_predicate: biolink:related_to -UMLS:site_of_metabolism: - operation: keep - core_predicate: biolink:related_to -UMLS:smaller_than: - operation: keep - core_predicate: biolink:related_to -UMLS:structural_class_of: - operation: keep - core_predicate: biolink:related_to -UMLS:supported_concept_property_in: - operation: delete -UMLS:supported_concept_relationship_in: - operation: delete -UMLS:therapeutic_class_of: # Look into this at a later time, there might be an opportunity to use has_member - operation: keep - core_predicate: biolink:related_to -UMLS:xref: - operation: keep - core_predicate: biolink:close_match -# UO-PROPERTY:is_unit_of: -# operation: keep -# core_predicate: biolink:related_to -# UPHENO:0000001: -# operation: keep -# core_predicate: biolink:affects -VANDF:has_ingredient: - operation: keep - core_predicate: biolink:has_part -VANDF:has_print_name: - operation: keep - core_predicate: biolink:close_match -VANDF:ingredient_of: - operation: invert - core_predicate: biolink:has_part -VANDF:inverse_isa: - operation: invert - core_predicate: biolink:subclass_of -VANDF:isa: - operation: keep - core_predicate: biolink:subclass_of -VANDF:print_name_of: - operation: keep - core_predicate: biolink:close_match -# WIKIDATA:P2888: -# operation: keep -# core_predicate: biolink:exact_match -# WIKIDATA:P3433: -# operation: keep -# core_predicate: biolink:is_sequence_variant_of -# WIKIDATA:Q181394: -# operation: keep -# core_predicate: biolink:has_nutrient -# WIKIDATA:Q39893449: -# operation: keep -# core_predicate: biolink:exact_match -# WIKIDATA:Q39893967: -# operation: invert -# core_predicate: biolink:broad_match -# WIKIDATA:Q39894595: -# operation: keep -# core_predicate: biolink:broad_match -# WIKIDATA:Q66088480: -# operation: invert -# core_predicate: biolink:subclass_of -# WIKIDATA_PROPERTY:P123: -# operation: keep -# core_predicate: biolink:publisher -# WIKIDATA_PROPERTY:P128: -# operation: keep -# core_predicate: biolink:regulates -# WIKIDATA_PROPERTY:P129: -# operation: keep -# core_predicate: biolink:physically_interacts_with -# WIKIDATA_PROPERTY:P1056: -# operation: keep -# core_predicate: biolink:produces -# WIKIDATA_PROPERTY:P1542: -# operation: keep -# core_predicate: biolink:causes -# WIKIDATA_PROPERTY:P1557: -# operation: keep -# core_predicate: biolink:manifestation_of -# WIKIDATA_PROPERTY:P156: -# operation: keep -# core_predicate: biolink:precedes -# WIKIDATA_PROPERTY:P2175: -# operation: keep -# core_predicate: biolink:treats -# WIKIDATA_PROPERTY:P2176: -# operation: invert -# core_predicate: biolink:treats -# WIKIDATA_PROPERTY:P2293: -# operation: keep -# core_predicate: biolink:genetic_association -# WIKIDATA_PROPERTY:P276: -# operation: invert -# core_predicate: biolink:located_in -# WIKIDATA_PROPERTY:P279: -# operation: keep -# core_predicate: biolink:subclass_of -# WIKIDATA_PROPERTY:P361: -# operation: invert -# core_predicate: biolink:has_part -# WIKIDATA_PROPERTY:P50: -# operation: keep -# core_predicate: biolink:author -# WIKIDATA_PROPERTY:P527: -# operation: keep -# core_predicate: biolink:has_part -# WIKIDATA_PROPERTY:P688: -# operation: invert -# core_predicate: biolink:gene_product_of -# WIKIDATA_PROPERTY:P703: -# operation: keep -# core_predicate: biolink:in_taxon -# WIKIDATA_PROPERTY:P828: -# operation: invert -# core_predicate: biolink:causes -# WIKIDATA_PROPERTY:P98: -# operation: keep -# core_predicate: biolink:editor -biolink:in_taxon: - operation: keep - core_predicate: biolink:subclass_of -biolink:part_of: - operation: invert - core_predicate: biolink:has_part -biolink:subclass_of: - operation: invert - core_predicate: biolink:has_part -# dct:contributor: -# operation: keep -# core_predicate: biolink:contributor -# dct:creator: -# operation: keep -# core_predicate: biolink:author -# dct:publisher: -# operation: keep -# core_predicate: biolink:publisher -# faldo:location: -# operation: keep -# core_predicate: biolink:has_sequence_location -oboFormat:xref: - operation: keep - core_predicate: biolink:close_match -owl:inverseOf: - operation: keep - core_predicate: biolink:related_to -owl:sameAs: - operation: keep - core_predicate: biolink:same_as -# owl:topObjectProperty: -# operation: keep -# core_predicate: biolink:related_to -rdf:type: - operation: keep - core_predicate: biolink:related_to -rdfs:negatively_regulates: - operation: keep - core_predicate: biolink:regulates - qualified_predicate: biolink:causes - qualifiers: - object_direction: downregulated -rdfs:subClassOf: - operation: keep - core_predicate: biolink:subclass_of -rdfs:subPropertyOf: - operation: keep - core_predicate: biolink:subclass_of -# skos:broadMatch: -# operation: keep -# core_predicate: biolink:broad_match -# skos:closeMatch: -# operation: keep -# core_predicate: biolink:close_match -# skos:exactMatch: -# operation: keep -# core_predicate: biolink:exact_match -skos:member: - operation: keep - core_predicate: biolink:has_member -# skos:narrowMatch: -# operation: invert -# core_predicate: biolink:broad_match -# skos:relatedMatch: -# operation: keep -# core_predicate: biolink:related_to diff --git a/data/semmed_sentence_data.csv b/data/semmed_sentence_data.csv deleted file mode 100644 index 7653844..0000000 --- a/data/semmed_sentence_data.csv +++ /dev/null @@ -1,329 +0,0 @@ -6,16530473,ti,1,21,Fluoride-selective colorimetric sensor based on thiourea binding site and anthraquinone reporter.,119,,, -7,16530473,ab,1,125,"A structurally simple colorimetric sensor, N-4-nitrobenzene-N'-1'-anthraquinone-thiourea (1), for anions was synthesized and characterized by (1)H NMR, ESI mass and IR methods.",302,,, -8,16530473,ab,2,302,"In acetonitrile, the addition of F(-) changed 1 solution from colorless to yellow.",385,,, -9,16530473,ab,3,385,"In the presence of other anions such as CH(3)CO(2)(-), H(2)PO(4)(-), HSO(4)(-) and Cl(-), however, the absorption spectrum of 1 was slightly red shifted with no obvious color changes observed.",578,,, -10,16530473,ab,4,578,"The association constants of anionic complexes followed the order of F(-)>>CH(3)CO(2)(-)>H(2)PO(4)(-)>HSO(4)(-)>Cl(-)>Br(-), which was different from the order of anion basicity.",757,,, -11,16530473,ab,5,757,AM1 calculation results indicated that the most stable configuration of 1 existed in the Z-E-conformation with a six-membered ring via intramolecular hydrogen bond.,922,,, -12,16530473,ab,6,922,"This made thiourea moiety of 1 in an unfavorable conformation to bond with oxygen-anionic substrates such as CH(3)CO(2)(-) and H(2)PO(4)(-), thus leading to a high selectivity and sensitivity for the detection of F(-).",1140,,, -16,16530475,ti,1,21,Seroprevalence of tick-borne and mosquito-borne arboviruses in European brown hares in Northern and Western Germany.,138,,, -17,16530475,ab,1,144,"Tribec virus (Kemerovo serogroup, genus Orbivirus), Eyach virus (genus Coltivirus), and Tahyna virus (California encephalitis serogroup, genus Bunyavirus) are arthropod-borne viruses known to occur in Germany.",354,,, -18,16530475,ab,2,354,These viruses are also suspected to cause human disease.,411,,, -19,16530475,ab,3,411,"So far, no information is available on their geographical distribution in Germany and their natural transmission cycles.",532,,, -20,16530475,ab,4,532,"A total of 166 sera from European brown hares (Lepus europaeus) collected in seven districts of the Federal State of Schleswig-Holstein and in four districts of the Federal State of North Rhine-Westphalia was tested by plaque reduction neutralization test (PRNT) for antibodies against Tribec virus, Eyach virus, Tahyna virus, and Central European encephalitis virus.",900,,, -21,16530475,ab,5,900,One out of 22 sera (4.5%) collected in the district Nord-Friesland in Schleswig-Holstein was found positive (PRNT(90) 1:10) against Tribec virus.,1046,,, -22,16530475,ab,6,1046,Neither did sera from other regions of Schleswig-Holstein nor from hares from North Rhine-Westphalia react against any of the arboviruses tested.,1192,,, -23,16530475,ab,7,1192,"For the first time, antibodies against Tribec virus could be found in a European brown hare in Germany.",1296,,, -24,16530475,ab,8,1296,The negative serological results for Central European encephalitis virus are in line with the current knowledge of its natural distribution within Germany.,1452,,, -25,16530475,ab,9,1452,The negative serological results for Tahyna virus or Eyach virus argue against an autochthonous circulation of these viruses in the regions tested.,1599,,, -26,16530476,ti,1,21,"Structure-function mapping of BbCRASP-1, the key complement factor H and FHL-1 binding protein of Borrelia burgdorferi.",141,,, -27,16530476,ab,1,147,"Borrelia burgdorferi, a spirochaete transmitted to human hosts during feeding of infected Ixodes ticks, is the causative agent of Lyme disease, the most frequent vector-borne disease in Eurasia and North America.",360,,, -28,16530476,ab,2,360,"Sporadically Lyme disease develops into a chronic, multisystemic disorder.",435,,, -29,16530476,ab,3,435,Serum-resistant B. burgdorferi strains bind complement factor H (FH) and FH-like protein 1 (FHL-1) on the spirochaete surface.,562,,, -30,16530476,ab,4,562,This binding is dependent on the expression of proteins termed complement-regulator acquiring surface proteins (CRASPs).,683,,, -31,16530476,ab,5,683,"The atomic structure of BbCRASP-1, the key FHL-1/FH-binding protein of B. burgdorferi, has recently been determined.",800,,, -32,16530476,ab,6,800,Our analysis indicates that its protein topology apparently evolved to provide a high affinity interaction site for FH/FHL-1 and leads to an atomic-level hypothesis for the functioning of BbCRASP-1.,999,,, -33,16530476,ab,7,999,This work demonstrates that pathogens interact with complement regulators in ways that are distinct from the mechanisms used by the host and are thus obvious targets for drug design.,1181,,, -34,16530477,ti,1,21,Functionality of Borrelia burgdorferi LuxS: the Lyme disease spirochete produces and responds to the pheromone autoinducer-2 and lacks a complete activated-methyl cycle.,191,,, -35,16530477,ab,1,197,"Borrelia burgdorferi produces Pfs and LuxS enzymes for breakdown of the toxic byproducts of methylation reactions, producing 4,5-dihydroxy-2,3-pentanedione (DPD), adenine, and homocysteine.",387,,, -36,16530477,ab,2,387,DPD and its spontaneously rearranged derivatives constitute a class of bacterial pheromones named autoinducer-2 (AI-2).,507,,, -37,16530477,ab,3,507,We describe that B. burgdorferi produces DPD during laboratory cultivation.,583,,, -38,16530477,ab,4,583,"Furthermore, addition of in vitro synthesized DPD to cultured B. burgdorferi resulted in altered expression levels of a specific set of bacterial proteins, among which is the outer surface lipoprotein VlsE.",790,,, -39,16530477,ab,5,790,"While a large number of bacteria utilize homocysteine, the other LuxS product, for synthesis of methionine as part of the activated-methyl cycle, B. burgdorferi was found to lack that ability.",983,,, -40,16530477,ab,6,983,We propose that the main function of B. burgdorferi LuxS is to synthesize DPD and that the Lyme disease spirochete utilizes a form of DPD as a pheromone to control gene expression.,1163,,, -41,16530478,ti,1,21,Prevalence of Borrelia burgdorferi s.l.,61,,, -42,16530478,ti,2,61,OspA types in Ixodes ricinus ticks from selected localities in Slovakia and Poland.,145,,, -43,16530478,ab,1,151,"In this study, 746 questing Ixodes (I.) ricinus ticks from eastern Slovakia and 187 ticks from southern Poland were investigated for infection with Borrelia (B.) burgdorferi sensu lato and different outer surface protein A (OspA) types by an improved restriction fragment length polymorphism (RFLP) analysis of the ospA gene.",477,,, -44,16530478,ab,2,477,The method enables differentiation of both single and multiple infections with B. burgdorferi s.s.,576,,, -45,16530478,ab,3,576,"(OspA type 1), B. afzelii (OspA type 2), B. garinii (OspA types 3-8), B. valaisiana (subgroups I and II), B. lusitaniae, B. bissettii, and the recently described genospecies A14S.",756,,, -46,16530478,ab,4,756,"Broad heterogeneity in B. burgdorferi s.l. was found including all species and subtypes except for B. lusitaniae, B. bissettii, and genospecies A14S.",906,,, -47,16530478,ab,5,906,Regional prevalence of B. burgdorferi s.l. varied between 8% and 22.5%.,978,,, -48,16530478,ab,6,978,"The most frequent species were B. garinii (45.4%) and, notably, B. burgdorferi s.s.",1062,,, -49,16530478,ab,7,1062,(31.3%).,1071,,, -50,16530478,ab,8,1071,"I. ricinus nymphs harbored almost exclusively B. burgdorferi s.s. and B. garinii OspA type 4, while in adults a broad variety of B. burgdorferi s.l. types was found.",1237,,, -51,16530478,ab,9,1237,Mixed infections were significantly more often in nymphs than in adult ticks.,1315,,, -52,16530478,ab,10,1315,"In all mixed infected nymphs, B. burgdorferi s.s. with OspA type 4 was present.",1395,,, -53,16530478,ab,11,1395,These data strongly suggest that B. burgdorferi s.s. and B. garinii OspA type 4 are maintained in these areas by specific transmission cycles involving a so far undetermined vertebrate host which is frequently fed on by I. ricinus larvae.,1634,,, -54,16530478,ab,12,1634,"This improved method provides a reliable tool for epidemiological studies on the heterogeneity of B. burgdorferi species and OspA types, an important prerequisite for improved local risk assessment and for test- and vaccine development for Europe.",1881,,, -55,16530479,ti,1,21,Monitoring of antimicrobial resistance in pathogenic bacteria from livestock animals.,107,,, -56,16530479,ab,1,113,"Facing the problem of development and spreading of bacterial resistance, preventive strategies are considered the most appropriate means to counteract.",265,,, -57,16530479,ab,2,265,The establishment of corresponding management options relies on scientifically defensible efforts to obtain objective data on the prevalence of bacterial resistance in healthy and diseased livestock.,465,,, -58,16530479,ab,3,465,"Additionally, detailed statistics are needed on the overall amount of antimicrobial agents dispensed in Germany.",578,,, -59,16530479,ab,4,578,The collection of valid data on the prevalence of resistance requires representative and cross-sectional studies.,692,,, -60,16530479,ab,5,692,"The German national antimicrobial resistance monitoring of the Federal Office of Consumer Protection and Food Safety (BVL) determines the current quantitative resistance level of life-stock pathogens, in order to permit the evaluation and surveillance of the distribution of resistances on a valid basis.",997,,, -61,16530479,ab,6,997,Essential key features determining the design of these studies comprise (1) a statistically valid sampling program.,1113,,, -62,16530479,ab,7,1113,"This incorporates regional differences in animal population density, (2) the avoidance of \""copy strains\", (3) testing of no more than two bacterial strains belonging to one species per herd, (4) testing only if no antimicrobial therapy preceded sample collection," and (5) the use of standardized methods [e.g. microdilution broth method to determine the minimal inhibitory concentration (MIC)].""",1508 -63,16530479,ab,8,1508,"The analysis and interpretation of this data permits reliable identification and definition of epidemiological characteristics of resistance and its development in animal associated bacteria, such as geographically and time wise differentiated profiles on its prevalence, the emergence of unknown phenotypes of resistance and an assessment of the threat resistant bacteria from animals pose for humans.",1911,,, -64,16530479,ab,9,1911,"In applied antimicrobial therapy, the data can serve as a decision guidance in choosing the antimicrobial agent most adapted to the prevailing epidemiological situation.",2081,,, -65,16530479,ab,10,2081,"The susceptibility testing performed by the BVL suggests substantially lower degrees of resistance in bacteria isolated from cattle (mastitis: Escherichia coli, Staphylococcus spp., Streptococcus spp.; respiratory disease: Pasteurella multocida, Mannheimia haemolytica) and pigs (respiratory disease: Pasteurella multocida, Bordetella bronchiseptica) in comparison to data published for Germany so far.",2484,,, -66,16530479,ab,11,2484,This includes results for substances that have given cause for frequent debate.,2564,,, -67,16530479,ab,12,2564,"Only rare cases of resistance to enrofloxacin (fluoroquinolone) could be detected, and only 3% of bacterial strains tested proved resistant to 3rd and 4th generation cephalosporins, including substances prescribed in human medicine.",2796,,, -68,16530480,ti,1,21,Tick-borne encephalitis in the Baltic States: identifying risk factors in space and time.,111,,, -69,16530480,ab,1,117,"This paper presents preliminary results in our investigations of the biological (abiotic and biotic) and non-biological causes of the spatial heterogeneity and temporal change of tick-borne encephalitis (TBE), both within and between Estonia, Latvia, and Lithuania.",383,,, -70,16530480,ab,2,383,Spatial analysis revealed that the land cover and precise seasonal patterns of climatic indices (temperature and normalized difference vegetation index) can explain 55% of the observed spatial variation in TBE incidence over the period 1993-98 across all the Baltic States.,657,,, -71,16530480,ab,3,657,Temporal analysis of climatic variables indicates a very specific change in spring temperature conditions from 1993 onwards that could enhance the transmission of TBE virus.,831,,, -72,16530480,ab,4,831,"Further time series analysis of climate, together with analysis of biotic factors, socio-economic conditions, and human behaviour is being undertaken to explain the epidemiological patterns more fully.",1032,,, -73,16530481,ti,1,21,Etiology of tick-borne febrile illnesses in adult residents of North-Eastern Poland: report from a prospective clinical study.,148,,, -74,16530481,ab,1,154,Febrile tick-borne diseases can be caused by different pathogens.,220,,, -75,16530481,ab,2,220,"The study objective was to prospectively determine the etiology of infection among adults exposed to tick bite and to detect acute human granulocytic anaplasmosis (HGA), a recently emerging infection, in north-eastern Poland.",446,,, -76,16530481,ab,3,446,"We evaluated 68 patients (34 males and 34 females, mean age 44.2+/-15 years) who had fever within 4 weeks after a tick bite.",571,,, -77,16530481,ab,4,571,"Paired sera were tested for antibodies against tick-borne encephalitis virus, Borrelia burgdorferi and Anaplasma phagocytophilum.",701,,, -78,16530481,ab,5,701,Microscopic examination of EDTA whole blood and nested PCR targeting A. phagocytophilum 16S rDNA gene fragment were carried out at enrolment.,843,,, -79,16530481,ab,6,843,Tick-borne infections were diagnosed in 57 individuals (84%).,905,,, -80,16530481,ab,7,905,Sixty-four patients were hospitalised.,944,,, -81,16530481,ab,8,944,"Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.",1263,,, -82,16530481,ab,9,1263,Diagnosis of HGA was confirmed in one patient by PCR and in another one by seroconversion.,1354,,, -83,16530481,ab,10,1354,"In two further individuals, A. phagocytophilum infection was confirmed by immunofluorescence (antibody titers > or = 1:128), which, however, does not fulfil the ESCAR (European Society of Clinical Microbiology and Infectious Diseases Study Group on Coxiella, Anaplasma, Rickettsia, and Bartonella) criteria for HGA case definition.",1686,,, -84,16530481,ab,11,1686,Lyme borreliosis was diagnosed in 16 patients, in six of them as a single infection.,1771,, -85,16530481,ab,12,1771,Both confirmed HGA cases and seropositive individuals had A. phagocytophilum infection concurrent either with Lyme borreliosis (two cases) or with TBE (two cases).,1935,,, -86,16530481,ab,13,1935,"The clinical course was severe in three and moderate to mild in the remaining TBE cases, as well as in all Lyme borreliosis and HGA cases.",2074,,, -87,16530481,ab,14,2074,TBE was found the most prevalent disease among adults with febrile illnesses occurring after a tick bite in north-eastern Poland.,2204,,, -88,16530481,ab,15,2204,Concurrent tick-borne infections were frequent with multiple pathogens involved.,2285,,, -89,16530481,ab,16,2285,Two confirmed acute HGA cases (fulfilling the European case definition criteria defined by ESCAR) were detected for the first time in a prospective manner in Poland.,2450,,, -90,16530482,ti,1,21,Molecular analysis of decorin-binding protein A (DbpA) reveals five major groups among European Borrelia burgdorferi sensu lato strains with impact for the development of serological assays and indicates lateral gene transfer of the dbpA gene.,265,,, -91,16530482,ab,1,271,The Borrelia (B.) burgdorferi adhesin DbpA (decorin-binding protein A) is a valuable antigen for serodiagnosis of Lyme borreliosis and a promising candidate for a vaccine.,443,,, -92,16530482,ab,2,443,"To investigate the heterogeneity of DbpA, we aligned DNA sequences of 83 different dbpA genes (37 from the database, where the majority of sequences belong to B. burgdorferi sensu stricto and 46 were newly sequenced).",661,,, -93,16530482,ab,3,661,"Analysis of 25 sequences from the species B. burgdorferi s.s., 16 from B. afzelii, 40 from B. garinii, and two from the recently described human pathogenic genospecies A14S revealed five distinct DbpA groups.",870,,, -94,16530482,ab,4,870,Group I comprises B. burgdorferi s.s. and group II B. afzelii.,933,,, -95,16530482,ab,5,933,"B. garinii is divided into groups III and IV, whereas A14S strains form group V.",1014,,, -96,16530482,ab,6,1014,Formation of groups is mainly due to insertions of whole sequence sections.,1090,,, -97,16530482,ab,7,1090,Comparison of dbpA sequences with ospC sequences from a subset of 59 strains revealed all kinds of cross-connections indicating processes of lateral gene transfer among strains.,1268,,, -98,16530482,ab,8,1268,"The extent of sequence identity within the dbpA genes decreases from the DNA (67%) to the amino acid (AA) level (44%) by about 23%, in contrast ospC sequence identities differed only by about 10%.",1465,,, -99,16530482,ab,9,1465,This might be an indication that DbpA plays an important role in immune escape.,1545,,, -100,16530482,ab,10,1545,Immunoblots using four recombinant DbpAs representing groups I-IV show that DbpA proteins are sensitive and specific antigens and complement one another in their reactivity.,1719,,, -101,16530482,ab,11,1719,Part of the sera showed group-specific reactivity which could also be demonstrated with monoclonal antibodies.,1829,,, -102,16530483,ti,1,21,"A neuropeptide in immune-mediated inflammation, Y?",72,,, -103,16530483,ab,1,78,Disturbances in crosstalk between the immune system and the sympathetic nervous system (SNS) can contribute to the pathogenesis of Th1-mediated autoimmunity.,236,,, -104,16530483,ab,2,236,Recent studies indicate that neuropeptide Y (NPY) has a major role in the regulation of Th1 responses.,339,,, -105,16530483,ab,3,339,"The precise role of NPY has been an enigma, but a recent study provides a breakthrough, demonstrating that NPY has a bimodal role as a negative regulator of T cells and an activator of antigen-presenting cell function.",557,,, -106,16530484,ti,1,21,Innate sensing of self and non-self RNAs by Toll-like receptors.,86,,, -107,16530484,ab,1,92,Toll-like receptors (TLRs) have an important role in innate immunity in mammals by recognizing conserved microbial components that are known as pathogen-associated molecular patterns (PAMPs).,284,,, -108,16530484,ab,2,284,"Although the majority of these receptors sense pathogen components on the cell surface, a subset of them (TLR3, TLR7, TLR8 and TLR9) senses viral and bacterial nucleic acids in endosomal compartments.",485,,, -109,16530484,ab,3,485,"Of considerable interest is the recent finding that TLR7 and TLR8 can also recognize small interfering RNA (siRNA), which is the main effector in RNA interference.",649,,, -110,16530484,ab,4,649,This immune activation by siRNAs can be abrogated by the 2'-ribose modification of uridines.,742,,, -111,16530484,ab,5,742,"Here, we discuss the recent developments that have expanded the understanding of self-non-self discrimination of RNAs by the innate immune system, and consider future directions for therapeutic applications of these findings.",967,,, -112,16530485,ti,1,21,E2F1-induced apoptosis: turning killers into therapeutics.,80,,, -113,16530485,ab,1,86,The cellular transcription factor E2F1 is part of an anti-tumor safeguard mechanism: it engages cell-death pathways either alone or in cooperation with p53 to protect organisms from the development of tumors.,295,,, -114,16530485,ab,2,295,"E2F1 activates downstream factors, which in turn produce secondary changes in gene expression that trigger apoptosis.",413,,, -115,16530485,ab,3,413,"Although the mechanisms are incompletely understood, several studies have demonstrated that E2F1 is involved in many different aspects of programmed cell death depending on the cellular background.",611,,, -116,16530485,ab,4,611,"Here, these findings are highlighted in the context of the most recent follow-up studies that have used apoptotic E2F1 genes as new therapeutics or drug targets, thereby providing insight into the basic mechanisms of E2F1-induced apoptosis and its possible clinical implications.",890,,, -117,16530487,ti,1,21,An emerging consensus on recommendations to facilitate clinical gene transfer.,99,,, -123,16530488,ti,1,21,Protein and gene expression of VTG in response to 4-nonylphenol in rockfish (Sebastes schlegeli).,119,,, -124,16530488,ab,1,125,"To investigate the in vivo estrogenic activity of 4-nonylphenol (4-NP) on reproductive function, we have measured the expression level of rockfish vitellogenin (rVTG) mRNA, concentration of plasma VTG and levels of plasma estradiol-17beta(E(2)) and testosterone (T) by radioimmunoassay (RIA).",418,,, -125,16530488,ab,2,418,"An rVTG mRNA transcript of approximately 4.0 kb was extracted from hepatic tissue for Northern blot analysis, and the effects of 4-NP on rVTG mRNA expression in vivo with both male and female juvenile rockfish were examined.",643,,, -126,16530488,ab,3,643,The level of rVTG mRNA expression was increased 48 h after injection with 4-NP of 10 mg/kg body mass and after injection in both male and female rockfish.,798,,, -127,16530488,ab,4,798,"The level of rVTG mRNA expression was increased 24 h after injection in male rockfish injected with 4-NP of 25 mg/kg body mass, while the level of rVTG mRNA expression was increased 12h after injection in female injected with same dosage.",1037,,, -128,16530488,ab,5,1037,"Concentrations of plasma rVTG in female injected with 4-NP of 10 and 25 mg/kg b.w. were increased 72 h after injection and reached 35 and 66 mg/mL, respectively.",1199,,, -129,16530488,ab,6,1199,"In male, rVTG concentrations with the dosage of 25 mg/kg body mass were increased 72 h after injection and reached to 14 and 65 mg/mL at 168 h, respectively.",1357,,, -130,16530488,ab,7,1357,Plasma concentrations of T and E(2) in female and male injected with 4-NP were not significantly different between two 4-NP dosages.,1490,,, -131,16530488,ab,8,1490,These results suggest that 4-NP may disrupt the reproductive system of immature rockfish by acting directly on vitellogenesis.,1617,,, -132,16530488,ab,9,1617,"Immature females injected with 4-NP were more sensitive than immature males, but VTG in immature males is likely to return to normal conditions slowly.",1769,,, -133,16530488,ab,10,1769,There are obviously large interspecies differences in response of fish to 4-NP.,1848,,, -134,16530489,ti,1,21,A framework for systematic evaluation of health information infrastructure progress in communities.,121,,, -135,16530489,ab,1,127,"It is widely agreed that major improvements in the safety, quality, and efficiency of health care in the US require a National Health Information Infrastructure.",289,,, -136,16530489,ab,2,289,"To accomplish this, efforts are now underway in many communities to build local or regional health information infrastructures (HIIs) that provide secure, ubiquitous access to complete health care information.",499,,, -137,16530489,ab,3,499,"To facilitate the assessment and monitoring of the progress of operational HIIs toward completion, we propose a framework of four key measures of requirements that must be ultimately be met: (1) completeness of information, (2) degree of usage, (3) types of usage, and (4) financial sustainability.",798,,, -138,16530489,ab,4,798,"To evaluate the framework, it was used by the authors to qualitatively assess HII projects in cooperation with four leading communities, resulting in ratings of 78% for Bellingham, WA, 63% for Indianapolis, IN, 60% for South Bend, IN, and 74% for Spokane, WA.",1058,,, -139,16530489,ab,5,1058,"Qualitative assessment of community HII systems may be helpful in monitoring progress, comparing projects, and understanding the remaining tasks needed for completion.",1226,,, -140,16530489,ab,6,1226,Additional testing and refinement of the proposed framework is needed to further understand and improve HII progress measurement capabilities.,1368,,, -141,16530490,ti,1,21,"Developmental expression of HpNanos, the Hemicentrotus pulcherrimus homologue of nanos.",109,,, -142,16530490,ab,1,115,"The Hemicentrotus pulcherrimus homologue of nanos (HpNanos), that encodes a protein containing two CCHC zinc finger motifs, was isolated from a gastrula cDNA library.",282,,, -143,16530490,ab,2,282,The accumulation of HpNanos mRNA during embryonic development and the spatial expression pattern are reported.,393,,, -144,16530490,ab,3,393,"Developmental northern blot analysis revealed that HpNanos mRNA markedly accumulated during the blastula stages, and then decreased in abundance at the mesenchyme blastula stage.",572,,, -145,16530490,ab,4,572,"The second phase of HpNanos mRNA expression occurred during gastrulation, after which the expression returned to a low level.",698,,, -146,16530490,ab,5,698,Whole-mount in situ hybridization showed that the HpNanos was exclusively expressed in four to six small micromere-descendant cells at the blastula stage.,853,,, -147,16530490,ab,6,853,"The expression of HpNanos was restricted to the coelomic pouch, which gives rise to the mesoderm of the ventral surface of the adult rudiment, at the prism stage.",1016,,, -148,16530490,ab,7,1016,These results suggest that HpNanos expression will be instrumental for future analyses of the function of small micromere-descendant cells and of the origin of germ cells during sea urchin development.,1217,,, -149,16530491,ti,1,21,Germ line specific expression of a protein phosphatase Y interacting protein (PPYR1) in Drosophila.,121,,, -150,16530491,ab,1,127,"PPYR1, the product of the CG15031 gene, was identified as a protein phosphatase Y (PPY) interacting protein in Drosophila melanogaster using a yeast two-hybrid screen.",295,,, -151,16530491,ab,2,295,"PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.",544,,, -152,16530491,ab,3,544,"The maternal and zygotic gene products differ from each other in their size having apparent molecular masses of 47 and 66 kDa, respectively.",685,,, -153,16530491,ab,4,685,The maternal PPYR1 is localized in the cytoplasm of the follicular and nurse cells and is deposited as a ribonucleoprotein complex in the oocyte.,831,,, -154,16530491,ab,5,831,"In the early embryos, the PPYR1 is distributed evenly, and it gradually diminishes during embryonic development.",944,,, -155,16530491,ab,6,944,"Zygotic PPYR1 is expressed exclusively in the testes, predominantly in the cytoplasm of the spermatocytes.",1051,,, -156,16530491,ab,7,1051,PPY is localized in the nuclei of the same cells.,1101,,, -157,16530491,ab,8,1101,Our results suggest that PPYR1 has two distinct developmental isoforms: a maternal protein the expression of which is independent of PPY and a zygotic protein which is co-expressed with PPY.,1291,,, -158,16530492,ti,1,21,Determination of AKF-PD in whole blood of rat by HPLC-UV.,79,,, -159,16530492,ab,1,85,An HPLC-UV method was developed and validated for the determination of AKF-PD in whole blood of rat.,186,,, -160,16530492,ab,2,186,"Phenacetin was chosen as the internal standard, and the separation was achieved on a C18 column with methanol and 0.02 M phosphate buffer (pH 3.2) as mobile phase.",350,,, -161,16530492,ab,3,350,"The obtained calibration graphs were linear (r = 0.9999, n = 9) in the range of 0.203-52.0 microg ml(-1).",456,,, -162,16530492,ab,4,456,The low limit of quantitation was 0.203 microg ml(-1).,511,,, -163,16530492,ab,5,511,This method can be used to study the pharmacokinetics of AKF-PD in rat.,582,,, -164,16530493,ti,1,21,Electrophoretic approaches to the analysis of complex polysaccharides.,92,,, -165,16530493,ab,1,98,"Complex polysaccharides, glycosaminoglycans (GAGs), are a class of ubiquitous macromolecules exhibiting a wide range of biological functions.",240,,, -166,16530493,ab,2,240,They are widely distributed as sidechains of proteoglycans (PGs) in the extracellular matrix and at cellular level.,356,,, -167,16530493,ab,3,356,The recent emergence of enhanced analytical tools for their study has triggered a virtual explosion in the field of glycomics.,483,,, -168,16530493,ab,4,483,"Analytical electrophoretic separation techniques, including agarose-gel, capillary electrophoresis (HPCE) and fluorophore-assisted carbohydrate electrophoresis (FACE), of GAGs and GAG-derived oligosaccharides have been employed for the structural analysis and quantification of hyaluronic acid (HA), chondroitin sulfate (CS), dermatan sulfate (DS), keratan sulfate (KS), heparan sulfate (HS), heparin (Hep) and acidic bacterial polysaccharides.",928,,, -169,16530493,ab,5,928,"Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.",1302,,, -170,16530493,ab,6,1302,"In this paper, the electromigration procedures developed to analyze and characterize complex polysaccharides are reviewed.",1425,,, -171,16530493,ab,7,1425,"Moreover, a critical evaluation of the biological relevance of the results obtained by these electrophoresis approaches is presented.",1558,,, -172,16530494,ti,1,21,Lactulose and mannitol intestinal permeability detected by capillary electrophoresis.,107,,, -173,16530494,ab,1,113,"Aim of this study was to set up a method by capillary electrophoresis to detect lactulose and mannitol in urine after an oral load, and to estimate the intestinal permeability in controls and in type I diabetes patients.",334,,, -174,16530494,ab,2,334,"The underivatized carbohydrates were monitored by indirect UV detection using sorbate, cetyltrimethylammonium bromide and LiOH as background electrolyte.",488,,, -175,16530494,ab,3,488,"Urines were purified by solid phase extraction, shaken with cation exchange resin, filtered and analysed.",594,,, -176,16530494,ab,4,594,Carbohydrates migrated in <10 min in relation to their pK(a) and M(r).,665,,, -177,16530494,ab,5,665,"Controls (n = 33) and patients (n = 23) had an excretion ratio lactulose/mannitol 0.025 (0.018-0.051) and 0.067 (0.050-0.127), respectively (p < 0.01, median, interquartile range).",845,,, -178,16530495,ti,1,21,Cardiac arrhythmias in the fetus and newborn.,67,,, -179,16530495,ab,1,73,Arrhythmias are potentially life-threatening problems in the fetus and newborn.,153,,, -180,16530495,ab,2,153,Appropriate management depends on accurate diagnosis.,207,,, -181,16530495,ab,3,207,Atrioventricular re-entry is the most common type of supraventricular tachycardia in both the fetus and newborn.,320,,, -182,16530495,ab,4,320,"It should be distinguished from other types of tachycardia - such as atrial flutter, atrial ectopic tachycardia, permanent junctional re-entry tachycardia, and ventricular tachycardia.",505,,, -183,16530495,ab,5,505,Neonatal and fetal bradycardias are less common clinical problems.,572,,, -184,16530495,ab,6,572,Sustained bradycardia is most often caused by complete atrioventricular block.,651,,, -185,16530495,ab,7,651,It can be mimicked by the more common but benign occurrence of non-conducted atrial premature beats.,751,,, -186,16530496,ti,1,21,"Primary hyperparathyroidism and malignancy: \""studies by nature\"".",86,,, -187,16530496,ab,1,92,"The American Food and Drug Administration approval of parathyroid hormone (PTH) administration for osteoporosis as well as the possibility for its future therapeutic applications requires an examination of the suggested association between PTH and cancer, particularly osteosarcomas.",376,,, -188,16530496,ab,2,376,"The objective was to evaluate such a connection by collecting observational data from two groups of patients, designated as \""studies by nature\"".",521,,, -189,16530496,ab,3,521,"Cohort 1: Medical records of all patients with primary hyperparathyroidism that were treated in a referral center during a 12-year period were retrospectively reviewed for malignancy before, at the time or after diagnosis.",744,,, -190,16530496,ab,4,744,"Cohort 2: Records of patients with osteosarcomas that were treated in referral centers during 15 years were retrospectively reviewed for hyperparathyroidism, as indicated by history or laboratory results.",949,,, -191,16530496,ab,5,949,There were 582 patients with primary hyperparathyroidism.,1007,,, -192,16530496,ab,6,1007,"While 56 (9.6%) had malignancy, 47 (8%) developed cancer after diagnosis with hyperparathyroidism during 6.1 years of documentation.",1140,,, -193,16530496,ab,7,1140,This rate did not exceed the incidence of developing cancer among the general population.,1230,,, -194,16530496,ab,8,1230,"Although thyroid cancer was about 4 times the incidence in the general population, this may be attributed to a high level of detection while work-up, treating and following the parathyroid disease.",1428,,, -195,16530496,ab,9,1428,None had osteosarcoma.,1451,,, -196,16530496,ab,10,1451,None of the 126 patients with osteosarcoma had documentation of primary hyperparathyroidism or had biochemical evidence of hyperparathyroidism.,1595,,, -197,16530496,ab,11,1595,No obvious association was found between primary hyperparathyroidism and cancer.,1676,,, -198,16530496,ab,12,1676,"Similarly, there was no demonstrable relationship between osteosarcomas and hyperthyroidism biochemical stigmata.",1790,,, -199,16530496,ab,13,1790,"Since PTH may contribute to tumor invasiveness, screening for existing neoplasms, especially prostate and breast, before PTH treatment may be of importance.",1946,,, -200,16530497,ti,1,21,"Multilocus analysis of estrogen-related genes in Spanish postmenopausal women suggests an interactive role of ESR1, ESR2 and NRIP1 genes in the pathogenesis of osteoporosis.",195,,, -201,16530497,ab,1,201,Osteoporosis is a common disease with multiple environmental and genetic risk factors involved.,297,,, -202,16530497,ab,2,297,"Using a marker-by-marker approach, the role of different estrogen-related genes has been analyzed in different populations, but most of these studies ignore the complex multigenic nature of human osteoporosis.",507,,, -203,16530497,ab,3,507,"Looking for markers related to osteoporosis, we have analyzed five single nucleotide polymorphisms located in genes related to the estrogen pathway, Follicle Stimulating Hormone Receptor (FSHR) gene, the CYP19 aromatase (CYP19A1) gene, the Estrogen Receptor alpha (ESR1) gene, the Estrogen Receptor beta (ESR2) gene and the Nuclear Receptor Interacting Protein 1 (NRIP1) gene in 265 unrelated postmenopausal women.",922,,, -204,16530497,ab,4,922,"We have obtained nominal P values for the NRIP1 Gly75Gly and ESR2 *39A>G markers (P=0.013 and P=0.02 respectively), but no gene seems to be associated after multiple test corrections.",1106,,, -205,16530497,ab,5,1106,Reanalysis of this study using 437 postmenopausal women confirmed our results and only detect marginal effects for ESR2 marker (P=0.045).,1244,,, -206,16530497,ab,6,1244,"By contrast, multilocus analysis predicted epistatic interactions between ESR1, ESR2 and NRIP1 loci and its involvement in postmenopausal osteoporosis (P=0.003).",1406,,, -207,16530497,ab,7,1406,We detected two digenic genotypes involving ESR2-NRIP1 and ESR2-ESR1 genes strongly associated with osteoporosis (P=0.007).,1530,,, -208,16530497,ab,8,1530,Replication of multilocus studies using 437 patients confirmed the detected interactions (P<0.01).,1629,,, -209,16530497,ab,9,1629,We proposed a non-additive non-multiplicative oligogenic model including ESR2 AG genotype modulated by NRIP1 A+ or ESR1 TT genotypes involved in osteoporosis.,1788,,, -210,16530497,ab,10,1788,Our results reaffirm the polygenic nature and the genetic complexity of osteoporosis trait adding a new candidate gene (NRIP1) for association studies of bone-related traits.,1962,,, -211,16530501,ti,1,21,Pledges of $1.9 billion at avian influenza conference.,75,,, -212,16530502,ti,1,21,Gastrointestinal surgery for obesity: a question of life and death and expertise.,102,,, -282,16530529,ti,1,21,Hepatocanalicular transport defects: pathophysiologic mechanisms of rare diseases.,104,,, -283,16530529,ab,1,110,The apical membrane of the hepatocyte fulfils a unique function in the formation of primary bile.,208,,, -284,16530529,ab,2,208,For all important biliary constituents a primary active transporter is present that extrudes or translocates its substrate toward the canalicular lumen.,361,,, -285,16530529,ab,3,361,Most of these transporters are ATP-binding cassette (ABC) transporters.,433,,, -286,16530529,ab,4,433,"Two types of transporters can be recognized: those having endogenous metabolites as substrates (which could be referred to as \""physiologic\"" transporters) and those involved in the elimination of drugs, toxins, and waste products.",663,,, -287,16530529,ab,5,663,It should be emphasized that this distinction cannot be strictly made as some endogenous metabolites can be regarded as toxins as well.,799,,, -288,16530529,ab,6,799,The importance of the canalicular transporters has been recognized by the pathologic consequence of their genetic defects.,922,,, -289,16530529,ab,7,922,For each of the physiologic transporter genes an inherited disease has now been identified and most of these diseases have a quite serious clinical phenotype.,1081,,, -290,16530529,ab,8,1081,"Strikingly, complete defects in drug transporter function have not been recognized (yet) or only cause a mild phenotype.",1202,,, -291,16530529,ab,9,1202,"In this review we only briefly discuss the inherited defects in transporter function, and we focus on the pathophysiologic concepts that these diseases have generated.",1369,,, -293,16530531,ti,1,21,"American Gastroenterological Association Institute medical position statement on corticosteroids, immunomodulators, and infliximab in inflammatory bowel disease.",182,,, -294,16530532,ti,1,21,"American Gastroenterological Association Institute technical review on corticosteroids, immunomodulators, and infliximab in inflammatory bowel disease.",172,,, -299,16530537,ti,1,21,"Environment, genetics, and fish?",54,,, -300,16530537,ti,2,54,Answers to the cancer riddle.,83,,, -301,16530538,ti,1,21,GRK2 makes trouble: a no-NO in portal hypertension.,72,,, -302,16530540,ti,1,21,"Phospholipid in UC: novel, safe and works--is it too good to be true?",90,,, -303,16530542,ti,1,21,Prophylaxis with beta blockers as a performance measure of quality health care in cirrhosis.,113,,, -304,16530543,ti,1,21,Cyst fluid analysis to diagnose pancreatic cystic lesions: an as yet unfulfilled promise.,110,,, -305,16530546,ti,1,21,Projected national impact of colorectal cancer screening on clinical and economic outcomes and health services demand.,139,,, -307,16530549,ti,1,21,Is NAFLD an incidentaloma?,47,,, -308,16530550,ti,1,21,Are we overestimating the risks of NASH?,61,,, -309,16530553,ti,1,21,Pancreatic cancer proteome.,48,,, -310,16530555,ti,1,21,"\""There is too much sex in Scotland\"".",57,,, -311,16530554,ti,1,21,Seeing red about HIV.,42,,, -312,16530556,ti,1,21,An ode to hospitals.,41,,, -313,16530557,ti,1,21,Progress in the treatment of multiple myeloma.,67,,, -314,16530558,ti,1,21,Clotting in the air.,41,,, -315,16530559,ti,1,21,Registration problems for antiretrovirals in Africa.,73,,, -316,16530560,ti,1,21,Drive to eliminate the burden of type 1 diabetes.,70,,, -317,16530561,ti,1,21,Dairy food and ovarian cancer risk.,56,,, -318,16530562,ti,1,21,Clinical pharmacology--too young to die?,61,,, -319,16530563,ti,1,21,Assessing outcomes in individually-tailored interventions.,79,,, -320,16530564,ti,1,21,Ram Sasisekharan.,39,,, -321,16530564,ti,2,39,Interview.,49,,, -322,16530565,ti,1,21,Infanticide.,33,,, -323,16530566,ti,1,21,Clopidogrel and metoprolol in myocardial infarction.,73,,, -324,16530567,ti,1,21,Forcefeeding and restraint of Guantanamo Bay hunger strikers.,82,,, -325,16530568,ti,1,21,Clopidogrel and metoprolol in myocardial infarction.,73,,, -326,16530569,ti,1,21,Clopidogrel and metoprolol in myocardial infarction.,73,,, -328,16530572,ti,1,21,Harm reduction for sex workers.,52,,, -342,16530579,ti,1,21,Type 1 diabetes.,38,,, -343,16530579,ab,1,44,"Type 1 diabetes accounts for only about 5-10% of all cases of diabetes; however, its incidence continues to increase worldwide and it has serious short-term and long-term implications.",229,,, -344,16530579,ab,2,229,"The disorder has a strong genetic component, inherited mainly through the HLA complex, but the factors that trigger onset of clinical disease remain largely unknown.",395,,, -345,16530579,ab,3,395,"Management of type 1 diabetes is best undertaken in the context of a multidisciplinary health team and requires continuing attention to many aspects, including insulin administration, blood glucose monitoring, meal planning, and screening for comorbid conditions and diabetes-related complications.",694,,, -346,16530579,ab,4,694,"These complications consist of microvascular and macrovascular disease, which account for the major morbidity and mortality associated with type 1 diabetes.",851,,, -347,16530579,ab,5,851,Newer treatment approaches have facilitated improved outcomes in terms of both glycaemic control and reduced risks for development of complications.,1000,,, -348,16530579,ab,6,1000,"Nonetheless, major challenges remain in the development of approaches to the prevention and management of type 1 diabetes and its complications.",1144,,, -349,16530580,ti,1,21,Climate change and human health: present and future risks.,80,,, -350,16530580,ab,1,86,There is near unanimous scientific consensus that greenhouse gas emissions generated by human activity will change Earth's climate.,218,,, -351,16530580,ab,2,218,The recent (globally averaged) warming by 0.5 degrees C is partly attributable to such anthropogenic emissions.,330,,, -352,16530580,ab,3,330,Climate change will affect human health in many ways-mostly adversely.,401,,, -353,16530580,ab,4,401,"Here, we summarise the epidemiological evidence of how climate variations and trends affect various health outcomes.",518,,, -354,16530580,ab,5,518,We assess the little evidence there is that recent global warming has already affected some health outcomes.,627,,, -355,16530580,ab,6,627,We review the published estimates of future health effects of climate change over coming decades.,725,,, -356,16530580,ab,7,725,"Research so far has mostly focused on thermal stress, extreme weather events, and infectious diseases, with some attention to estimates of future regional food yields and hunger prevalence.",915,,, -357,16530580,ab,8,915,"An emerging broader approach addresses a wider spectrum of health risks due to the social, demographic, and economic disruptions of climate change.",1063,,, -358,16530580,ab,9,1063,"Evidence and anticipation of adverse health effects will strengthen the case for pre-emptive policies, and will also guide priorities for planned adaptive strategies.",1229,,, -359,16530581,ti,1,21,Cytotoxic therapy for severe avian influenza A (H5N1) infection.,86,,, -360,16530581,ab,1,92,"The mortality rate in documented avian influenza A virus subtype H5N1 infection is still high, which is currently reported by WHO at about 50%.",236,,, -361,16530581,ab,2,236,Post-mortem analyses in affected patients have revealed haemophagocytosis similar to that found in patients with haemophagocytic lymphohistiocytosis (HLH); such haemophagocytosis could be a very prominent post-mortem feature in H5N1 infection.,480,,, -362,16530581,ab,3,480,"There are also clinical similarities between H5N1 infection and HLH, such as massive hypercytokinaemia, cytopenia, and acute encephalitis.",619,,, -363,16530581,ab,4,619,"Importantly, patients with another severe viral infection that may be complicated by secondary HLH, severe Epstein-Barr-virus-associated HLH, have significantly better survival if specific HLH therapy (including the cytotoxic and pro-apoptotic drug etoposide) is initiated early, with survival reported to rise from about 50% to 90%.",953,,, -364,16530581,ab,5,953,"With this notable improvement in survival, specific HLH treatment, including cytotoxic therapy, could be considered in patients with severe avian influenza A infection complicated by secondary HLH.",1150,,, -365,16530582,ti,1,21,The first Japanese case of variant Creutzfeldt-Jakob disease showing periodic electroencephalogram.,120,,, -366,16530583,ti,1,21,Why should you read these articles on dissociative processes?,82,,, -367,16530584,ti,1,21,A new model of dissociative identity disorder.,67,,, -368,16530585,ti,1,21,How metaphors shape the concept and treatment of dissociation.,83,,, -369,16530586,ti,1,21,Normative dissociation.,44,,, -370,16530587,ti,1,21,From infant attachment disorganization to adult dissociation: relational adaptations or traumatic experiences?,131,,, -371,16530588,ti,1,21,Posttraumatic personality disorder: a reformulation of complex posttraumatic stress disorder and borderline personality disorder.,150,,, -372,16530589,ti,1,21,Neurobiology of dissociation: unity and disunity in mind-body-brain.,89,,, -373,16530590,ti,1,21,Dissociative disorders as a confounding factor in psychiatric research.,92,,, -374,16530591,ti,1,21,Psychological assessment of patients with dissociative identity disorder.,94,,, -375,16530592,ti,1,21,The forensic evaluation of dissociation and persons diagnosed with dissociative identity disorder: searching for convergence.,146,,, -376,16530593,ti,1,21,Why conversion seizures should be classified as a dissociative disorder.,93,,, -377,16530594,ti,1,21,Culture-bound dissociation: a comparative analysis.,72,,, -378,16530595,ti,1,21,The scope of dissociative disorders: an international perspective.,87,,, -379,16530596,ti,1,21,Therapeutic interventions in the treatment of dissociative disorders.,90,,, -380,16530597,ti,1,21,A sensorimotor approach to the treatment of trauma and dissociation.,89,,, -381,16530598,ti,1,21,Dealing with alters: a pragmatic clinical perspective.,75,,, -382,16530599,ti,1,21,DID 101: a hands-on clinical guide to the stabilization phase of dissociative identity disorder treatment.,127,,, -383,16530601,ti,1,21,Focal and segmental glomerulosclerosis: varying biologic mechanisms underlie a final histopathologic end point.,133,,, -384,16530601,ab,1,139,Focal and segmental glomerulosclerosis (FSGS) is a pathologic entity that is a common and increasing cause of end-stage renal disease.,274,,, -385,16530601,ab,2,274,"Typical manifestations include proteinuria, hypertension, worsening renal insufficiency, and, frequently, renal failure.",395,,, -386,16530601,ab,3,395,"The etiology, however, remains unknown in a majority of patients.",461,,, -387,16530601,ab,4,461,"There is an estimated recurrence rate of 30% to 40% in renal transplant patients, suggesting that the pathogenesis is not solely a result of intrinsic kidney disease.",628,,, -388,16530601,ab,5,628,"Although some of its characteristics have been reported, the precise identification of a circulating factor associated with FSGS has not been made.",776,,, -389,16530601,ab,6,776,Remarkable progress has been made in recent years regarding biologic mechanisms surrounding FSGS and proteinuria.,890,,, -390,16530601,ab,7,890,Insight into the pathogenesis of FSGS has been gained through the study of hereditary forms of FSGS and nephrotic syndromes.,1015,,, -391,16530601,ab,8,1015,Mutations in cytoskeletal proteins that affect podocyte structure have been the target until recently.,1118,,, -392,16530601,ab,9,1118,Here we review the current understanding of this glomerular disease and areas for future concentration.,1221,,, -393,16530602,ti,1,21,Lupus nephritis.,38,,, -394,16530602,ab,1,44,"Lupus nephritis is one of the more serious manifestations of the systemic autoimmune disease, systemic lupus erythematosus, and is associated with considerable morbidity and even mortality.",234,,, -395,16530602,ab,2,234,"Treatment remains problematic, particularly in terms of controlling the underlying disease process while at the same time preventing unacceptable side effects of therapy.",405,,, -396,16530602,ab,3,405,"In recent years, clinical trials have started to define optimum regimens of the immunosuppressive agents presently in use.",528,,, -397,16530602,ab,4,528,The etiology and pathogenesis of systemic lupus erythematosus and lupus nephritis still are understood incompletely.,645,,, -398,16530602,ab,5,645,"Nevertheless, insights gained from basic science research in both animals and human beings now are being translated into newer therapies that have the potential to be safer and more specific than those currently available.",867,,, -399,16530603,ti,1,21,Acute renal failure: much more than a kidney disease.,75,,, -400,16530603,ab,1,81,"Acute renal failure is a frequent clinical problem with an increasing incidence, an unacceptably high mortality rate that has not improved in more than 40 years, and no specific treatment, yet renal failure is not the usual cause of death.",321,,, -401,16530603,ab,2,321,The role of inflammation has been documented in both acute renal injury and cardiac dysfunction.,418,,, -402,16530603,ab,3,418,Several investigators have shown that congestive heart failure is associated with increased mortality in patients with acute renal failure.,558,,, -403,16530603,ab,4,558,This article reviews some of the cardiac and other distant organ effects of acute renal injury that may be important in the morbidity and mortality observed clinically.,727,,, -404,16530603,ab,5,727,"Cardiac changes after experimental renal ischemia include cytokine induction, leukocyte infiltration, cell death by apoptosis, and impaired function.",877,,, -405,16530603,ab,6,877,I propose that the extrarenal effects of kidney injury must be considered in designing therapies.,975,,, -406,16530603,ab,7,975,Acute renal failure has systemic consequences and must be thought of as more than a kidney disease.,1074,,, -407,16530604,ti,1,21,Quality of life for children with chronic kidney disease.,79,,, -408,16530604,ab,1,85,"Medical care advancements for children with chronic kidney disease (CKD) receiving hemodialysis, peritoneal dialysis, or with a renal transplant have resulted in relatively improved long-term patient survival compared with adult patients with CKD.",333,,, -409,16530604,ab,2,333,"Optimal care for the pediatric patient with CKD requires attention not only to medical management, but also the psychosocial and developmental factors that either will ensure or prevent a pediatric patient's successful transition into adulthood.",579,,, -410,16530604,ab,3,579,"We review the range of issues that impact pediatric CKD patients' health-related quality of life (HRQOL), the history of pediatric CKD patients' HRQOL investigation, and the instruments currently available to assess HRQOL.",801,,, -411,16530605,ti,1,21,Epidemiology of dialysis patients and heart failure patients.,83,,, -412,16530605,ab,1,89,The epidemiology of maintenance dialysis patients and heart failure patients has striking similarities.,193,,, -413,16530605,ab,2,193,"Both groups have a high prevalence of comorbid conditions, a high hospitalization rate, a low self-reported quality of life, and an excessively high mortality risk, mostly because of cardiovascular causes.",399,,, -414,16530605,ab,3,399,"Observational studies in both dialysis and heart failure patients have indicated the lack of a significant association between the traditional cardiovascular risk factors and mortality, or the existence of a paradoxic or reverse association, in that obesity, hypercholesterolemia, and hypertension appear to confer survival advantages.",735,,, -415,16530605,ab,4,735,"The time discrepancy between the 2 sets of risk factors, that is, overnutrition (long-term killer) versus undernutrition (short-term killer) may explain the overwhelming role of malnutrition, inflammation, and cachexia in causing the reverse epidemiology, which may exist in more than 20 million Americans.",1042,,, -416,16530605,ab,5,1042,"We have reviewed the opposing views about the concept of reverse epidemiology in dialysis and heart failure patients, the recent Die Deutsche Diabetes Dialyze study findings, and the possible role of racial disparities.",1262,,, -417,16530605,ab,6,1262,Contradictory findings on hyperhomocysteinemia in dialysis patients are reviewed in greater details as a possible example of publication bias.,1405,,, -418,16530605,ab,7,1405,"Additional findings related to intravenous iron and serum ferritin, calcium, and leptin levels in dialysis patients may enhance our understanding of the new paradigm.",1572,,, -419,16530605,ab,8,1572,The association between obesity and increased death risk in kidney transplanted patients is reviewed as an example of the reversal of reverse epidemiology.,1728,,, -420,16530605,ab,9,1728,Studying the epidemiology of dialysis patients as the archetypical population with such paradoxic associations may lead to the development of population-specific guidelines and treatment strategies beyond the current Framingham cardiovascular risk factor paradigm.,1992,,, -421,16530606,ti,1,21,Nutrition and metabolism in kidney disease.,65,,, -422,16530606,ab,1,71,Nutritional and metabolic derangements are highly prevalent in patients with chronic kidney disease (CKD) and patients on renal replacement therapy.,220,,, -423,16530606,ab,2,220,"These derangements, which can be termed uremic malnutrition, significantly affect the high morbidity and mortality rates observed in this patient population.",378,,, -424,16530606,ab,3,378,Uremic malnutrition clearly is related to multiple factors encountered during the predialysis stage and during chronic dialysis therapy.,515,,, -425,16530606,ab,4,515,"Several preliminary studies suggested that interventions to improve the nutritional status and metabolic status of uremic patients actually may improve the expected outcome in these patients, although their long-term efficacy is not well established.",766,,, -426,16530606,ab,5,766,"It therefore is important to emphasize that uremic malnutrition is a major comorbid condition in CKD and renal replacement therapy patients, and that all efforts should be made to try to understand better and treat these conditions effectively to improve not only mortality but also the quality of life of chronically uremic patients.",1101,,, -427,16530606,ab,6,1101,"In this article we review the current state of knowledge in the field of nutrition and metabolism in all stages of CKD and renal replacement therapy, including kidney transplant.",1280,,, -428,16530606,ab,7,1280,We also address questions that face investigators in this field and suggest where future research might be headed.,1394,,, -429,16530607,ti,1,21,Amino Acid and protein kinetics in renal failure: an integrated approach.,95,,, -430,16530607,ab,1,101,Even apparently healthy patients on dialysis have significant loss of lean body mass.,187,,, -431,16530607,ab,2,187,"Patients with chronic renal failure without coexisting metabolic acidosis or inflammation have decreased protein turnover, with balanced reduction in protein synthesis and breakdown.",370,,, diff --git a/data/semmed_triple_data.csv b/data/semmed_triple_data.csv deleted file mode 100644 index 3ba0a5c..0000000 --- a/data/semmed_triple_data.csv +++ /dev/null @@ -1,200 +0,0 @@ -10592604,16,16530475,PROCESS_OF,C0003725,Arboviruses,virs,1,C0999630,Lepus capensis,mamm,1,\N,\N,\N -10592697,17,16530475,ISA,C0039258,Tahyna virus,virs,1,C0446169,California Group Viruses,virs,1,\N,\N,\N -10592728,17,16530475,ISA,C0318627,Eyach virus,virs,1,C0206590,Coltivirus,virs,1,\N,\N,\N -10592759,17,16530475,ISA,C0446169,California Group Viruses,virs,1,C0003725,Arboviruses,virs,1,\N,\N,\N -10592832,18,16530475,PROCESS_OF,C0012634,Disease,dsyn,0,C0020114,Human,humn,0,\N,\N,\N -10592873,18,16530475,CAUSES,C0042776,Virus,virs,1,C0012634,Disease,dsyn,0,\N,\N,\N -10593057,23,16530475,LOCATION_OF,C0999630,Lepus capensis,mamm,1,C0003241,Antibodies,aapp,1,\N,\N,\N -10593208,26,16530476,PART_OF,C0242210,Binding Protein,bacs,1,2273,FHL1,aapp,1,\N,\N,\N -10593243,26,16530476,PART_OF,C0056207|3075,COMPLEMENT FACTOR H|CFH,aapp,1,C0006034,Borrelia burgdorferi,bact,1,\N,\N,\N -10593287,26,16530476,PART_OF,C0242210,Binding Protein,aapp,1,C0006034,Borrelia burgdorferi,bact,1,\N,\N,\N -10593621,34,16530477,PART_OF,7523,XS,gngm,1,C0006034,Borrelia burgdorferi,bact,1,\N,\N,\N -10593815,39,16530477,PRODUCES,7523,XS,gngm,1,C0019878,homocysteine,aapp,1,\N,\N,\N -10593856,39,16530477,INTERACTS_WITH,C0004611,Bacteria,bact,1,C0025646,Methionine,aapp,1,\N,\N,\N -10593932,40,16530477,AFFECTS,C0031516,Pheromone,bacs,1,C0017262,Gene Expression,genf,1,\N,\N,\N -10594285,50,16530478,TREATS,C0718782,B.S.S.,phsu,1,C0001675,Adult,aggp,1,\N,\N,\N -10594435,53,16530478,PART_OF,C1167395,host,celc,1,C0042567,Vertebrates,vtbt,0,\N,\N,\N -10594472,53,16530478,AFFECTS,C0718782,B.S.S.,inch,1,C1167395,host,celc,1,\N,\N,\N -10594584,55,16530479,ISA,C0162318,Farm Animals,anim,1,C0003062,Animals,anim,0,\N,\N,\N -10594689,57,16530479,PROCESS_OF,C0012634,Disease,dsyn,0,C0162318,Farm Animals,anim,1,\N,\N,\N -10594898,62,16530479,USES,C0087111,Therapeutic procedure,topp,0,C1136254,Microbicides,phsu,1,\N,\N,\N -10595006,64,16530479,USES,C0087111,Therapeutic procedure,topp,0,C1136254,Microbicides,phsu,1,\N,\N,\N -10595160,67,16530479,ISA,C0059374,enrofloxacin,antb,1,C0949665,Fluoroquinolones,orch,1,\N,\N,\N -10595193,67,16530479,COEXISTS_WITH,C0059374,enrofloxacin,antb,1,C0013227,Pharmaceutical Preparations,phsu,0,\N,\N,\N -10595361,70,16530480,TREATS,C0180153,Covers,medd,1,C0014061,Tick-Borne Encephalitis,dsyn,1,\N,\N,\N -10595474,72,16530480,PROCESS_OF,C0004927,Behavior,inbe,0,C0020114,Human,humn,0,\N,\N,\N -10595632,75,16530481,PROCESS_OF,C0021311,Infection,dsyn,1,C0001675,Adult,humn,1,\N,\N,\N -10595725,76,16530481,PROCESS_OF,C0015967,Fever,fndg,1,C0030705,Patients,humn,0,\N,\N,\N -10595759,76,16530481,PROCESS_OF,C0015967,Fever,fndg,1,C0086287,Females,humn,1,\N,\N,\N -10595794,76,16530481,PROCESS_OF,C0015967,Fever,fndg,1,C0086582,Males,humn,1,\N,\N,\N -10595906,78,16530481,PART_OF,C0012931,Recombinant DNA,bacs,1,C1552130,16s,bpoc,0,\N,\N,\N -10595985,79,16530481,PROCESS_OF,C0162699,Tick-Borne Infections,dsyn,1,C0237401,Individual,humn,0,\N,\N,\N -10596143,81,16530481,PROCESS_OF,C0017677,"Glossitis, Benign Migratory",dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10596167,81,16530481,ISA,C0017677,"Glossitis, Benign Migratory",dsyn,1,C1457887,Symptoms,sosy,0,\N,\N,\N -10596199,81,16530481,PROCESS_OF,C0017677,"Glossitis, Benign Migratory",dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10596244,81,16530481,PROCESS_OF,C1457887,Symptoms,sosy,0,C0030705,Patients,humn,0,\N,\N,\N -10596294,81,16530481,PROCESS_OF,C0024198,Lyme Disease,dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10596383,82,16530481,TREATS,C0011900,Diagnosis,hlca,0,C0030705,Patients,humn,0,\N,\N,\N -10596492,83,16530481,DIAGNOSES,C0079603,Immunofluorescence,lbpr,1,C0021311,Infection,dsyn,1,\N,\N,\N -10596565,84,16530481,PROCESS_OF,C0024198,Lyme Disease,dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10596660,85,16530481,PROCESS_OF,C0024198,Lyme Disease,dsyn,1,C0237401,Individual,humn,0,\N,\N,\N -10596772,87,16530481,PROCESS_OF,C0012634,Disease,dsyn,0,C0001675,Adult,humn,1,\N,\N,\N -10596805,87,16530481,PROCESS_OF,C0743841,Disorder characterized by fever,dsyn,1,C0001675,Adult,humn,1,\N,\N,\N -10597199,97,16530482,compared_with,C0638611,"4,5-dibromo-2-pyrrolic acid",orch,1,C0089701,1-oleoyl-2-stearoylphosphatidylcholine,lipd,1,\N,\N,\N -10597287,98,16530482,INHIBITS,C0638611,"4,5-dibromo-2-pyrrolic acid",orch,1,C0012854,DNA,bacs,1,\N,\N,\N -10597421,100,16530482,INTERACTS_WITH,C0638611,"4,5-dibromo-2-pyrrolic acid",orch,1,C0456981,Specific antigen,imft,1,\N,\N,\N -10597542,102,16530483,AFFECTS,C0027895,Neuropeptides,aapp,1,C0021368,Inflammation,patf,1,\N,\N,\N -10597633,103,16530483,CAUSES,C1504598,Crosstalk,inpo,1,C0004368,Autoimmunity,patf,1,\N,\N,\N -10597756,105,16530483,INTERACTS_WITH,C0027893|4852,neuropeptide Y|NPY,gngm,1,C0039194,T-Lymphocyte,cell,1,\N,\N,\N -10597803,105,16530483,STIMULATES,C0027893|4852,neuropeptide Y|NPY,aapp,1,C0003315,Antigen-Presenting Cells,cell,1,\N,\N,\N -10597925,107,16530484,LOCATION_OF,C0024660,Mammals,mamm,0,C0670896,Toll-like receptors,aapp,1,\N,\N,\N -10598015,108,16530484,LOCATION_OF,C0034850,Endosomes,celc,1,C1185625,Compartments,bsoj,0,\N,\N,\N -10598051,108,16530484,LOCATION_OF,C0699040,Cell surface,celc,1,C0597357,receptor,aapp,1,\N,\N,\N -10598148,110,16530484,INTERACTS_WITH,C1099354,"RNA, Small Interfering",bacs,1,C0035549,Ribose,bacs,1,\N,\N,\N -10598263,112,16530485,CAUSES,C0812258|1869|7332,E2F1 gene|E2F1|UBE2L3,gngm,1,C0162638,Apoptosis,celf,1,\N,\N,\N -10598476,116,16530485,INTERACTS_WITH,C0812258|1869|7332,E2F1 gene|E2F1|UBE2L3,gngm,1,C0013227,Pharmaceutical Preparations,phsu,0,\N,\N,\N -10598517,116,16530485,CAUSES,C0812258|1869|7332,E2F1 gene|E2F1|UBE2L3,gngm,1,C0162638,Apoptosis,celf,1,\N,\N,\N -10599076,123,16530488,PROCESS_OF,C0017262,Gene Expression,genf,1,C0998896,Scorpaenidae,fish,1,\N,\N,\N -10599190,124,16530488,PART_OF,C0042896,Vitellogenins,gngm,1,C0998896,Scorpaenidae,fish,1,\N,\N,\N -10599329,125,16530488,PART_OF,C0042896,Vitellogenins,gngm,1,C0998896,Scorpaenidae,fish,1,\N,\N,\N -10599368,125,16530488,PART_OF,C0042896,Vitellogenins,gngm,1,C0998896,Scorpaenidae,fish,1,\N,\N,\N -10599395,125,16530488,AFFECTS,C0042896,Vitellogenins,aapp,1,C0332124,No past history,fndg,1,\N,\N,\N -10599484,126,16530488,PART_OF,C0042896,Vitellogenins,gngm,1,C0998896,Scorpaenidae,fish,1,\N,\N,\N -10599560,127,16530488,PART_OF,C0042896,Vitellogenins,gngm,1,C0998896,Scorpaenidae,fish,1,\N,\N,\N -10599602,127,16530488,PART_OF,C0042896,Vitellogenins,gngm,1,C0998896,Scorpaenidae,fish,1,\N,\N,\N -10599653,127,16530488,TREATS,C1533685,Injection procedure,topp,1,C0015780,Female,orga,1,\N,\N,\N -10599747,128,16530488,PART_OF,C0042896,Vitellogenins,gngm,1,C0998896,Scorpaenidae,fish,1,\N,\N,\N -10599840,129,16530488,PART_OF,C0042896,Vitellogenins,gngm,1,C0998896,Scorpaenidae,fish,1,\N,\N,\N -10600338,141,16530490,PART_OF,C1334043,Homologous Gene,gngm,1,C0998689,Hemicentrotus pulcherrimus,invt,1,\N,\N,\N -10600422,142,16530490,PART_OF,C0751608,cDNA Library,gngm,1,C0017199,Gastrula,emst,1,\N,\N,\N -10600456,142,16530490,PART_OF,C1334043,Homologous Gene,gngm,1,C0998689,Hemicentrotus pulcherrimus,invt,1,\N,\N,\N -10600542,144,16530490,PART_OF,C1281743,Blastocyst structure,emst,1,C0162415,Mesenchyma,emst,1,\N,\N,\N -10600645,146,16530490,USES,C0162788,In Situ Hybridization,lbpr,1,C0181909,Mounts,medd,1,\N,\N,\N -10600813,151,16530491,LOCATION_OF,C0013935,Embryo,emst,1,5539,PPY,aapp,1,\N,\N,\N -10600845,151,16530491,PART_OF,C0021358,Inferior Colliculus,bpoc,1,C0086582,Males,humn,1,\N,\N,\N -10600962,153,16530491,PART_OF,5539,PPY,gngm,1,C0026591,Mothers,humn,1,\N,\N,\N -10600997,153,16530491,PART_OF,C0007634,Cells,cell,0,C0028661,Nurses,humn,1,\N,\N,\N -10601037,153,16530491,LOCATION_OF,C0010834,Cytoplasm,celc,1,5539,PPY,aapp,1,\N,\N,\N -10601150,155,16530491,PART_OF,C0010834,Cytoplasm,celc,1,C0037863,Spermatocytes,cell,1,\N,\N,\N -10601184,155,16530491,LOCATION_OF,C0021358,Inferior Colliculus,bpoc,1,5539,PPY,aapp,1,\N,\N,\N -10601265,156,16530491,PART_OF,C0007610,Cell Nucleus,celc,1,C0007634,Cells,cell,0,\N,\N,\N -10601441,160,16530492,LOCATION_OF,C1185738,Column,bpoc,1,C0036679,Diastasis,patf,1,\N,\N,\N -10601592,163,16530492,PROCESS_OF,C0031327,Drug Kinetics,phsf,0,C0034693,Rattus norvegicus,mamm,1,\N,\N,\N -10601714,165,16530493,ISA,C0017973,Glycosaminoglycans,bacs,1,C0032594,Polysaccharides,carb,1,\N,\N,\N -10601803,166,16530493,LOCATION_OF,C0015350,Extracellular Matrix,tisu,1,C0033692,Proteoglycan,aapp,1,\N,\N,\N -10601941,168,16530493,CONVERTS_TO,C0017346,GAG Gene,gngm,1,C0017973,Glycosaminoglycans,carb,1,\N,\N,\N -10601994,168,16530493,CONVERTS_TO,C0017346,GAG Gene,gngm,1,C0028959,Oligosaccharides,carb,1,\N,\N,\N -10602026,168,16530493,USES,C0013855,Electrophoresis,lbpr,1,C0204514,Structural analysis,topp,1,\N,\N,\N -10602109,169,16530493,INTERACTS_WITH,C0014442,Enzymes,enzy,0,C0017973,Glycosaminoglycans,bacs,1,\N,\N,\N -10602147,169,16530493,INTERACTS_WITH,C0220806,Chemicals,chem,1,C0017973,Glycosaminoglycans,bacs,1,\N,\N,\N -10602185,169,16530493,CONVERTS_TO,C0017973,Glycosaminoglycans,bacs,1,C0012611,Disaccharides,carb,1,\N,\N,\N -10602215,169,16530493,CONVERTS_TO,C0017973,Glycosaminoglycans,bacs,1,C0028959,Oligosaccharides,carb,1,\N,\N,\N -10602419,173,16530494,PROCESS_OF,C0011847,Diabetes,dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10602491,174,16530494,USES,C1511790,Detection,topp,1,C1533168,Sorbate,phsu,1,\N,\N,\N -10602733,182,16530495,ISA,C0004239,Atrial Flutter,patf,1,C0039231,Tachycardia,patf,1,\N,\N,\N -10602764,182,16530495,ISA,C0039234,"Tachycardia, Ectopic Atrial",dsyn,1,C0039231,Tachycardia,patf,1,\N,\N,\N -10602804,182,16530495,ISA,C0039235,"Tachycardia, Ectopic Junctional",dsyn,1,C0039231,Tachycardia,patf,1,\N,\N,\N -10602837,182,16530495,ISA,C0042514,"Tachycardia, Ventricular",patf,1,C0039231,Tachycardia,patf,1,\N,\N,\N -10603013,187,16530496,ASSOCIATED_WITH,C0020063|5741,"PTH protein, human|PTH",aapp,1,C0029463,osteosarcoma,neop,1,\N,\N,\N -10603029,187,16530496,ISA,C0029463,osteosarcoma,neop,1,C0006826,Malignant Neoplasms,neop,1,\N,\N,\N -10603069,187,16530496,ASSOCIATED_WITH,C0020063|5741,"PTH protein, human|PTH",aapp,1,C0006826,Malignant Neoplasms,neop,1,\N,\N,\N -10603164,189,16530496,PROCESS_OF,C0221002,"Hyperparathyroidism, Primary",dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10603247,190,16530496,PROCESS_OF,C0029463,osteosarcoma,neop,1,C0030705,Patients,humn,0,\N,\N,\N -10603339,191,16530496,PROCESS_OF,C0221002,"Hyperparathyroidism, Primary",dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10603447,193,16530496,NEG_OCCURS_IN,C0006826,Malignant Neoplasms,neop,1,C0683971,General Population,popg,0,\N,\N,\N -10603538,194,16530496,OCCURS_IN,C0012634,Disease,dsyn,0,C0683971,General Population,popg,0,\N,\N,\N -10603641,196,16530496,PROCESS_OF,C0029463,osteosarcoma,neop,1,C0030705,Patients,humn,0,\N,\N,\N -10603772,199,16530496,ISA,C0020063|5741,"PTH protein, human|PTH",aapp,1,C0087111,Therapeutic procedure,topp,0,\N,\N,\N -10603809,199,16530496,USES,C0087111,Therapeutic procedure,topp,0,C0020063|5741,"PTH protein, human|PTH",aapp,1,\N,\N,\N -10603857,199,16530496,TREATS,C0020063|5741,"PTH protein, human|PTH",horm,1,C0027651,Neoplasm,neop,1,\N,\N,\N -10603961,200,16530497,ASSOCIATED_WITH,C0699748,Pathogenesis,patf,1,C0017337,Genes,gngm,0,\N,\N,\N -10604007,200,16530497,ASSOCIATED_WITH,C0699748,Pathogenesis,patf,1,C1414461|2099,ESR1 gene|ESR1,gngm,1,\N,\N,\N -10604038,200,16530497,ASSOCIATED_WITH,C0699748,Pathogenesis,patf,1,C1414462|2100,ESR2 gene|ESR2,gngm,1,\N,\N,\N -10604108,201,16530497,ISA,C0029456,Osteoporosis,dsyn,1,C0012634,Disease,dsyn,0,\N,\N,\N -10604188,202,16530497,PROCESS_OF,C0029456,Osteoporosis,dsyn,1,C0020114,Human,humn,0,\N,\N,\N -10604268,203,16530497,COEXISTS_WITH,C0752046,Single Nucleotide Polymorphism,nusq,1,C0017337,Genes,gngm,0,\N,\N,\N -10604292,203,16530497,COEXISTS_WITH,C0017337,Genes,gngm,0,C0014939,Estrogens,horm,1,\N,\N,\N -10604325,203,16530497,PROCESS_OF,C0029456,Osteoporosis,dsyn,1,C0043210,Woman,humn,1,\N,\N,\N -10604461,206,16530497,INTERACTS_WITH,C1414462|2100,ESR2 gene|ESR2,gngm,1,C1414461|2099,ESR1 gene|ESR1,gngm,1,\N,\N,\N -10604551,207,16530497,ASSOCIATED_WITH,C1334904|8204,NRIP1 gene|NRIP1,gngm,1,C0029456,Osteoporosis,dsyn,1,\N,\N,\N -10604592,207,16530497,ASSOCIATED_WITH,C1414462|2100,ESR2 gene|ESR2,gngm,1,C0029456,Osteoporosis,dsyn,1,\N,\N,\N -10604700,209,16530497,ASSOCIATED_WITH,C1334904|8204,NRIP1 gene|NRIP1,gngm,1,C0029456,Osteoporosis,dsyn,1,\N,\N,\N -10604840,212,16530502,TREATS,C0524722,Gastrointestinal Surgical Procedure,topp,1,C0028754,Obesity,dsyn,1,\N,\N,\N -10609209,283,16530529,PART_OF,C0596119,apical membrane,celc,1,C0227525,Hepatocyte,cell,1,\N,\N,\N -10609362,286,16530529,ISA,C0040549,Toxin,bacs,1,C0013227,Pharmaceutical Preparations,phsu,0,\N,\N,\N -10609509,290,16530529,ISA,C0596902,Membrane Transport Proteins,aapp,1,C0013227,Pharmaceutical Preparations,phsu,0,\N,\N,\N -10609671,293,16530531,ASSOCIATED_WITH,C0001617,Adrenal Cortex Hormones,phsu,1,C0021390,Inflammatory Bowel Diseases,dsyn,1,\N,\N,\N -10609705,293,16530531,ASSOCIATED_WITH,C0666743,infliximab,aapp,1,C0021390,Inflammatory Bowel Diseases,dsyn,1,\N,\N,\N -10609737,293,16530531,ASSOCIATED_WITH,C1527392,Immunomodulators,imft,1,C0021390,Inflammatory Bowel Diseases,dsyn,1,\N,\N,\N -10609805,294,16530532,ASSOCIATED_WITH,C0001617,Adrenal Cortex Hormones,phsu,1,C0021390,Inflammatory Bowel Diseases,dsyn,1,\N,\N,\N -10609844,294,16530532,ASSOCIATED_WITH,C0666743,infliximab,aapp,1,C0021390,Inflammatory Bowel Diseases,dsyn,1,\N,\N,\N -10609883,294,16530532,ASSOCIATED_WITH,C1527392,Immunomodulators,imft,1,C0021390,Inflammatory Bowel Diseases,dsyn,1,\N,\N,\N -10610158,301,16530538,NEG_ASSOCIATED_WITH,C0753114|156,Beta-Adrenergic Receptor Kinase 1|GRK2,aapp,1,C0020541,"Hypertension, Portal",dsyn,1,\N,\N,\N -10610370,303,16530542,USES,C0199176,Prophylactic treatment,topp,1,C0001645,Adrenergic beta-Antagonists,phsu,1,\N,\N,\N -10610397,303,16530542,TREATS,C0086388,Health Care,hlca,0,C0016059,Fibrosis,patf,1,\N,\N,\N -10610453,304,16530543,LOCATION_OF,C0030274,Pancreas,bpoc,1,C1511606,Cystic Lesion,fndg,1,\N,\N,\N -10610626,309,16530553,PART_OF,C0751973,Proteome,gngm,1,C0235974,Pancreatic carcinoma,neop,1,\N,\N,\N -10610978,323,16530566,TREATS,C0025859,Metoprolol,phsu,1,C0027051,Myocardial Infarction,dsyn,1,\N,\N,\N -10611011,323,16530566,TREATS,C0070166,clopidogrel,orch,1,C0027051,Myocardial Infarction,dsyn,1,\N,\N,\N -10611110,325,16530568,TREATS,C0025859,Metoprolol,phsu,1,C0027051,Myocardial Infarction,dsyn,1,\N,\N,\N -10611138,325,16530568,TREATS,C0070166,clopidogrel,orch,1,C0027051,Myocardial Infarction,dsyn,1,\N,\N,\N -10611222,326,16530569,TREATS,C0025859,Metoprolol,phsu,1,C0027051,Myocardial Infarction,dsyn,1,\N,\N,\N -10611267,326,16530569,TREATS,C0070166,clopidogrel,orch,1,C0027051,Myocardial Infarction,dsyn,1,\N,\N,\N -10611529,328,16530572,TREATS,C0679771,Harm Reduction,topp,1,C0240816,Prostitute NOS,humn,1,\N,\N,\N -10612762,345,16530579,TREATS,C0220908,Screening procedure,hlca,1,C0342257,Complications of Diabetes Mellitus,patf,1,\N,\N,\N -10612795,345,16530579,TREATS,C0220908,Screening procedure,hlca,1,C1275743,Co-morbid conditions,fndg,1,\N,\N,\N -10612830,345,16530579,TREATS,C1170884,Blood Glucose Monitoring,medd,1,C0011854,"Diabetes Mellitus, Insulin-Dependent",dsyn,1,\N,\N,\N -10612915,346,16530579,COEXISTS_WITH,C0011854,"Diabetes Mellitus, Insulin-Dependent",dsyn,1,C0012634,Disease,dsyn,0,\N,\N,\N -10613117,350,16530580,AFFECTS,C0233929,Emission,orgf,1,C0008946,Climate,npop,1,\N,\N,\N -10613441,359,16530581,TREATS,C0677881,Cytotoxic Chemotherapy,topp,1,C0016627,Influenza in Birds,dsyn,1,\N,\N,\N -10613551,361,16530581,PROCESS_OF,C0024291,"Lymphohistiocytosis, Hemophagocytic",dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10613587,361,16530581,PROCESS_OF,C0876991,Histiocytosis haematophagic,dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10613621,361,16530581,COEXISTS_WITH,C0876991,Histiocytosis haematophagic,dsyn,1,C0021311,Infection,dsyn,1,\N,\N,\N -10613734,363,16530581,PROCESS_OF,C0042769,Virus Diseases,dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10613794,364,16530581,TREATS,C0677881,Cytotoxic Chemotherapy,topp,1,C0016627,Influenza in Birds,dsyn,1,\N,\N,\N -10613828,364,16530581,COMPLICATES,C0024291,"Lymphohistiocytosis, Hemophagocytic",dsyn,1,C0021311,Infection,dsyn,1,\N,\N,\N -10613863,364,16530581,PROCESS_OF,C0016627,Influenza in Birds,dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10613892,364,16530581,TREATS,C0677881,Cytotoxic Chemotherapy,topp,1,C0030705,Patients,podg,0,\N,\N,\N -10614109,370,16530587,PROCESS_OF,C0086168,Dissociation,mobd,1,C0001675,Adult,humn,1,\N,\N,\N -10614255,374,16530591,PROCESS_OF,C0026773,Multiple Personality Disorder,mobd,1,C0030705,Patients,humn,0,\N,\N,\N -10614343,375,16530592,PROCESS_OF,C0026773,Multiple Personality Disorder,mobd,1,C0027361,Persons,humn,0,\N,\N,\N -10614517,379,16530596,TREATS,C0087111,Therapeutic procedure,topp,0,C0012746,Dissociative disorder,mobd,1,\N,\N,\N -10614730,384,16530601,CAUSES,C0403425,Focal segmental glomerulosclerosis,dsyn,1,C1261469,End stage renal failure,dsyn,1,\N,\N,\N -10614846,385,16530601,COMPLICATES,C0020538,Hypertensive disease,dsyn,1,C1565489,Renal Insufficiency,dsyn,1,\N,\N,\N -10614959,387,16530601,CAUSES,C0022658,Kidney Diseases,dsyn,1,C0699748,Pathogenesis,patf,1,\N,\N,\N -10615143,391,16530601,PROCESS_OF,C0026882,Mutation,genf,1,C0010852,Cytoskeletal Proteins,gngm,1,\N,\N,\N -10615285,394,16530602,ISA,C0024143,Lupus Nephritis,dsyn,1,C0024141,"Lupus Erythematosus, Systemic",dsyn,1,\N,\N,\N -10615374,395,16530602,PREVENTS,C0087111,Therapeutic procedure,topp,0,C0879626,Adverse effects,patf,0,\N,\N,\N -10615525,398,16530602,PROCESS_OF,C0233820,Insight,menp,1,C0003062,Animals,anim,0,\N,\N,\N -10615565,398,16530602,PROCESS_OF,C0233820,Insight,menp,1,C0020114,Human,humn,0,\N,\N,\N -10615677,400,16530603,NEG_CAUSES,C0035078,Kidney Failure,dsyn,1,C0011065,Cessation of life,orgf,1,\N,\N,\N -10615760,401,16530603,COEXISTS_WITH,C0021368,Inflammation,patf,1,C0160420,Injury to kidney NOS,inpo,1,\N,\N,\N -10615805,401,16530603,COEXISTS_WITH,C0021368,Inflammation,patf,1,C0277785,Functional disorder,patf,0,\N,\N,\N -10615891,402,16530603,PROCESS_OF,C0022660,"Kidney Failure, Acute",dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10615926,402,16530603,PROCESS_OF,C0018802,Congestive heart failure,dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10616062,404,16530603,USES,C0857127,Induction,topp,1,C0079189,cytokine,aapp,1,\N,\N,\N -10616165,405,16530603,LOCATION_OF,C0022646,Kidney,bpoc,1,C0175677,Injury,inpo,1,\N,\N,\N -10616256,407,16530604,PROCESS_OF,C0022661,"Kidney Failure, Chronic",dsyn,1,C0008059,Child,humn,1,\N,\N,\N -10616333,408,16530604,PROCESS_OF,C0022661,"Kidney Failure, Chronic",dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10616429,409,16530604,PROCESS_OF,C0022661,"Kidney Failure, Chronic",dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10616568,411,16530605,PROCESS_OF,C0018801,Heart failure,dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10616652,412,16530605,PROCESS_OF,C0018801,Heart failure,dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10616794,414,16530605,PROCESS_OF,C0018801,Heart failure,dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10616936,416,16530605,PROCESS_OF,C0018801,Heart failure,dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10616975,417,16530605,PROCESS_OF,C0598608,Hyperhomocysteinemia,dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10617032,418,16530605,LOCATION_OF,C0229671,Serum,bdsu,1,C0015879,Ferritin,aapp,1,\N,\N,\N -10617065,418,16530605,TREATS,C0015879,Ferritin,aapp,1,C0030705,Patients,podg,0,\N,\N,\N -10617110,418,16530605,TREATS,C0299583,Leptin,horm,1,C0030705,Patients,podg,0,\N,\N,\N -10617141,418,16530605,TREATS,C0302583,Iron,phsu,1,C0030705,Patients,podg,0,\N,\N,\N -10617244,419,16530605,PROCESS_OF,C0011065,Cessation of life,orgf,1,C0030705,Patients,humn,0,\N,\N,\N -10617287,419,16530605,ASSOCIATED_WITH,C0011065,Cessation of life,orgf,1,C0028754,Obesity,dsyn,1,\N,\N,\N -10617413,421,16530606,ASSOCIATED_WITH,C0025519,Metabolism,orgf,1,C0022658,Kidney Diseases,dsyn,1,\N,\N,\N -10617485,422,16530606,PROCESS_OF,C0022661,"Kidney Failure, Chronic",dsyn,1,C0030705,Patients,humn,0,\N,\N,\N -10617563,423,16530606,ISA,C0030705,Patients,podg,0,C1257890,Population Group,popg,0,\N,\N,\N -10617609,423,16530606,PROCESS_OF,C0162429,Malnutrition,dsyn,1,C0030705,Patients,podg,0,\N,\N,\N -10617641,423,16530606,PROCESS_OF,C0162429,Malnutrition,dsyn,1,C1257890,Population Group,humn,0,\N,\N,\N -10617751,425,16530606,TREATS,C1273869,Intervention regimes,hlca,0,C0030705,Patients,humn,0,\N,\N,\N -10617828,426,16530606,COEXISTS_WITH,C1275743,Co-morbid conditions,fndg,1,C0022661,"Kidney Failure, Chronic",dsyn,1,\N,\N,\N -10617967,429,16530607,ASSOCIATED_WITH,C0002520,Amino Acids,aapp,1,C0035078,Kidney Failure,dsyn,1,\N,\N,\N -10618086,431,16530607,NEG_PROCESS_OF,C0597297,Protein Turnover,moft,1,C0030705,Patients,humn,0,\N,\N,\N -10618125,431,16530607,PROCESS_OF,C0021368,Inflammation,patf,1,C0030705,Patients,humn,0,\N,\N,\N diff --git a/data/test_df_gpt_3_5_turbo_icl.csv b/data/test_df_gpt_3_5_turbo_icl.csv deleted file mode 100644 index 4fd6e8e..0000000 --- a/data/test_df_gpt_3_5_turbo_icl.csv +++ /dev/null @@ -1,31 +0,0 @@ -Predicate ID,Triple,Sentence ID,Sentence,Question,Label,Reference -10601803,Extracellular Matrix location of Proteoglycan,166,They are widely distributed as sidechains of proteoglycans (PGs) in the extracellular matrix and at cellular level.,Is the triple 'Extracellular Matrix location of Proteoglycan' supported by the sentence: 'They are widely distributed as sidechains of proteoglycans (PGs) in the extracellular matrix and at cellular level.'?,True,https://www.frontiersin.org/articles/10.3389/fcell.2021.760532/full -10598263,E2F1 gene|E2F1|UBE2L3 causes Apoptosis,112,E2F1-induced apoptosis: turning killers into therapeutics.,Is the triple 'E2F1 gene|E2F1|UBE2L3 causes Apoptosis' supported by the sentence: 'E2F1-induced apoptosis: turning killers into therapeutics.'?,True,https://www.omim.org/entry/189971 -10600542,Blastocyst structure part of Mesenchyma,144,"Developmental northern blot analysis revealed that HpNanos mRNA markedly accumulated during the blastula stages, and then decreased in abundance at the mesenchyme blastula stage.","Is the triple 'Blastocyst structure part of Mesenchyma' supported by the sentence: 'Developmental northern blot analysis revealed that HpNanos mRNA markedly accumulated during the blastula stages, and then decreased in abundance at the mesenchyme blastula stage.'?",False,https://en.wikipedia.org/wiki/Blastocyst -10597542,Neuropeptides affects Inflammation,102,"A neuropeptide in immune-mediated inflammation, Y?","Is the triple 'Neuropeptides affects Inflammation' supported by the sentence: 'A neuropeptide in immune-mediated inflammation, Y?'?",False,https://link.springer.com/chapter/10.1007/978-94-011-2996-1_9 -10597421,"4,5-dibromo-2-pyrrolic acid interacts with Specific antigen",100,Immunoblots using four recombinant DbpAs representing groups I-IV show that DbpA proteins are sensitive and specific antigens and complement one another in their reactivity.,"Is the triple '4,5-dibromo-2-pyrrolic acid interacts with Specific antigen' supported by the sentence: 'Immunoblots using four recombinant DbpAs representing groups I-IV show that DbpA proteins are sensitive and specific antigens and complement one another in their reactivity.'?",True,https://link.springer.com/article/10.1007/s11094-022-02723-x -10596660,Lyme Disease process of Individual,85,Both confirmed HGA cases and seropositive individuals had A. phagocytophilum infection concurrent either with Lyme borreliosis (two cases) or with TBE (two cases).,Is the triple 'Lyme Disease process of Individual' supported by the sentence: 'Both confirmed HGA cases and seropositive individuals had A. phagocytophilum infection concurrent either with Lyme borreliosis (two cases) or with TBE (two cases).'?,True,https://www.mayoclinic.org/diseases-conditions/lyme-disease/symptoms-causes/syc-20374651 -10595193,enrofloxacin coexists with Pharmaceutical Preparations,67,"Only rare cases of resistance to enrofloxacin (fluoroquinolone) could be detected, and only 3% of bacterial strains tested proved resistant to 3rd and 4th generation cephalosporins, including substances prescribed in human medicine.","Is the triple 'enrofloxacin coexists with Pharmaceutical Preparations' supported by the sentence: 'Only rare cases of resistance to enrofloxacin (fluoroquinolone) could be detected, and only 3% of bacterial strains tested proved resistant to 3rd and 4th generation cephalosporins, including substances prescribed in human medicine.'?",False,https://www.mdpi.com/2076-2615/11/8/2312 -10601441,Column location of Diastasis,160,"Phenacetin was chosen as the internal standard, and the separation was achieved on a C18 column with methanol and 0.02 M phosphate buffer (pH 3.2) as mobile phase.","Is the triple 'Column location of Diastasis' supported by the sentence: 'Phenacetin was chosen as the internal standard, and the separation was achieved on a C18 column with methanol and 0.02 M phosphate buffer (pH 3.2) as mobile phase.'?",False,https://radiopaedia.org/articles/diastasis-recti -10593621,XS part of Borrelia burgdorferi,34,Functionality of Borrelia burgdorferi LuxS: the Lyme disease spirochete produces and responds to the pheromone autoinducer-2 and lacks a complete activated-methyl cycle.,Is the triple 'XS part of Borrelia burgdorferi' supported by the sentence: 'Functionality of Borrelia burgdorferi LuxS: the Lyme disease spirochete produces and responds to the pheromone autoinducer-2 and lacks a complete activated-methyl cycle.'?,True,https://europepmc.org/article/PMC/128172 -10592604,Arboviruses process of Lepus capensis,16,Seroprevalence of tick-borne and mosquito-borne arboviruses in European brown hares in Northern and Western Germany.,Is the triple 'Arboviruses process of Lepus capensis' supported by the sentence: 'Seroprevalence of tick-borne and mosquito-borne arboviruses in European brown hares in Northern and Western Germany.'?,False,https://eurekamag.com/research/004/525/004525561.php -10594689,Disease process of Farm Animals,57,The establishment of corresponding management options relies on scientifically defensible efforts to obtain objective data on the prevalence of bacterial resistance in healthy and diseased livestock.,Is the triple 'Disease process of Farm Animals' supported by the sentence: 'The establishment of corresponding management options relies on scientifically defensible efforts to obtain objective data on the prevalence of bacterial resistance in healthy and diseased livestock.'?,True,https://www.rvc.ac.uk/Media/Default/UoLW%20Distance%20Learning/Modules/Animal%20Disease%20%28Current%20Concepts%29.pdf -10595985,Tick-Borne Infections process of Individual,79,Tick-borne infections were diagnosed in 57 individuals (84%).,Is the triple 'Tick-Borne Infections process of Individual' supported by the sentence: 'Tick-borne infections were diagnosed in 57 individuals (84%).'?,False,https://www.cdc.gov/ticks/diseases/index.html -10600845,Inferior Colliculus part of Males,151,"PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.","Is the triple 'Inferior Colliculus part of Males' supported by the sentence: 'PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.'?",False,https://www.healthline.com/human-body-maps/inferior-colliculus -10596199,"Glossitis, Benign Migratory process of Patients",81,"Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.","Is the triple 'Glossitis, Benign Migratory process of Patients' supported by the sentence: 'Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.'?",False,https://dermnetnz.org/topics/geographic-tongue -10602215,Glycosaminoglycans converts to Oligosaccharides,169,"Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.","Is the triple 'Glycosaminoglycans converts to Oligosaccharides' supported by the sentence: 'Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.'?",True,https://link.springer.com/chapter/10.1007/978-3-662-63123-2_41 -10592832,Disease process of Human,18,These viruses are also suspected to cause human disease.,Is the triple 'Disease process of Human' supported by the sentence: 'These viruses are also suspected to cause human disease.'?,True,https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Introductory_Biology_(CK-12)/07%3A_Prokaryotes_and_Viruses/7.12%3A_Viruses_and_Human_Disease -10601037,Cytoplasm location of PPY,153,The maternal PPYR1 is localized in the cytoplasm of the follicular and nurse cells and is deposited as a ribonucleoprotein complex in the oocyte.,Is the triple 'Cytoplasm location of PPY' supported by the sentence: 'The maternal PPYR1 is localized in the cytoplasm of the follicular and nurse cells and is deposited as a ribonucleoprotein complex in the oocyte.'?,True,https://www.uniprot.org/uniprotkb/P01298/entry -10601150,Cytoplasm part of Spermatocytes,155,"Zygotic PPYR1 is expressed exclusively in the testes, predominantly in the cytoplasm of the spermatocytes.","Is the triple 'Cytoplasm part of Spermatocytes' supported by the sentence: 'Zygotic PPYR1 is expressed exclusively in the testes, predominantly in the cytoplasm of the spermatocytes.'?",True,https://www.frontiersin.org/articles/10.3389/fvets.2023.1188479/full -10593856,Bacteria interacts with Methionine,39,"While a large number of bacteria utilize homocysteine, the other LuxS product, for synthesis of methionine as part of the activated-methyl cycle, B. burgdorferi was found to lack that ability.","Is the triple 'Bacteria interacts with Methionine' supported by the sentence: 'While a large number of bacteria utilize homocysteine, the other LuxS product, for synthesis of methionine as part of the activated-methyl cycle, B. burgdorferi was found to lack that ability.'?",True,https://europepmc.org/article/MED/31383657 -10596143,"Glossitis, Benign Migratory process of Patients",81,"Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.","Is the triple 'Glossitis, Benign Migratory process of Patients' supported by the sentence: 'Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.'?",False,https://dermnetnz.org/topics/geographic-tongue -10598517,E2F1 gene|E2F1|UBE2L3 causes Apoptosis,116,"Here, these findings are highlighted in the context of the most recent follow-up studies that have used apoptotic E2F1 genes as new therapeutics or drug targets, thereby providing insight into the basic mechanisms of E2F1-induced apoptosis and its possible clinical implications.","Is the triple 'E2F1 gene|E2F1|UBE2L3 causes Apoptosis' supported by the sentence: 'Here, these findings are highlighted in the context of the most recent follow-up studies that have used apoptotic E2F1 genes as new therapeutics or drug targets, thereby providing insight into the basic mechanisms of E2F1-induced apoptosis and its possible clinical implications.'?",True,https://www.frontiersin.org/articles/10.3389/fmolb.2020.599332/full -10602147,Chemicals interacts with Glycosaminoglycans,169,"Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.","Is the triple 'Chemicals interacts with Glycosaminoglycans' supported by the sentence: 'Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.'?",True,https://www.frontiersin.org/articles/10.3389/fmolb.2021.639666/full -10595725,Fever process of Patients,76,"We evaluated 68 patients (34 males and 34 females, mean age 44.2+/-15 years) who had fever within 4 weeks after a tick bite.","Is the triple 'Fever process of Patients' supported by the sentence: 'We evaluated 68 patients (34 males and 34 females, mean age 44.2+/-15 years) who had fever within 4 weeks after a tick bite.'?",True,https://www.uptodate.com/contents/pathophysiology-and-treatment-of-fever-in-adults -10597199,"4,5-dibromo-2-pyrrolic acid compared with 1-oleoyl-2-stearoylphosphatidylcholine",97,Comparison of dbpA sequences with ospC sequences from a subset of 59 strains revealed all kinds of cross-connections indicating processes of lateral gene transfer among strains.,"Is the triple '4,5-dibromo-2-pyrrolic acid compared with 1-oleoyl-2-stearoylphosphatidylcholine' supported by the sentence: 'Comparison of dbpA sequences with ospC sequences from a subset of 59 strains revealed all kinds of cross-connections indicating processes of lateral gene transfer among strains.'?",False,https://www.sigmaaldrich.com/UA/en/product/aldrich/656291 -10600456,Homologous Gene part of Hemicentrotus pulcherrimus,142,"The Hemicentrotus pulcherrimus homologue of nanos (HpNanos), that encodes a protein containing two CCHC zinc finger motifs, was isolated from a gastrula cDNA library.","Is the triple 'Homologous Gene part of Hemicentrotus pulcherrimus' supported by the sentence: 'The Hemicentrotus pulcherrimus homologue of nanos (HpNanos), that encodes a protein containing two CCHC zinc finger motifs, was isolated from a gastrula cDNA library.'?",False,https://db.cngb.org/stomics/publications/16530490 -10594435,host part of Vertebrates,53,These data strongly suggest that B. burgdorferi s.s. and B. garinii OspA type 4 are maintained in these areas by specific transmission cycles involving a so far undetermined vertebrate host which is frequently fed on by I. ricinus larvae.,Is the triple 'host part of Vertebrates' supported by the sentence: 'These data strongly suggest that B. burgdorferi s.s. and B. garinii OspA type 4 are maintained in these areas by specific transmission cycles involving a so far undetermined vertebrate host which is frequently fed on by I. ricinus larvae.'?,False,https://zoo.sav.sk/data/people_publictions_106_Lencakova_et_al.2006.IJMM.pdf -10596772,Disease process of Adult,87,TBE was found the most prevalent disease among adults with febrile illnesses occurring after a tick bite in north-eastern Poland.,Is the triple 'Disease process of Adult' supported by the sentence: 'TBE was found the most prevalent disease among adults with febrile illnesses occurring after a tick bite in north-eastern Poland.'?,True,https://www.ecdc.europa.eu/en/tick-borne-encephalitis/facts/factsheet -10602837,"Tachycardia, Ventricular is a Tachycardia",182,"It should be distinguished from other types of tachycardia - such as atrial flutter, atrial ectopic tachycardia, permanent junctional re-entry tachycardia, and ventricular tachycardia.","Is the triple 'Tachycardia, Ventricular is a Tachycardia' supported by the sentence: 'It should be distinguished from other types of tachycardia - such as atrial flutter, atrial ectopic tachycardia, permanent junctional re-entry tachycardia, and ventricular tachycardia.'?",True,https://www.mayoclinic.org/diseases-conditions/ventricular-tachycardia/symptoms-causes/syc-20355138 -10593287,Binding Protein part of Borrelia burgdorferi,26,"Structure-function mapping of BbCRASP-1, the key complement factor H and FHL-1 binding protein of Borrelia burgdorferi.","Is the triple 'Binding Protein part of Borrelia burgdorferi' supported by the sentence: 'Structure-function mapping of BbCRASP-1, the key complement factor H and FHL-1 binding protein of Borrelia burgdorferi.'?",True,https://www.rcsb.org/structure/1W33 -10600813,Embryo location of PPY,151,"PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.","Is the triple 'Embryo location of PPY' supported by the sentence: 'PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.'?",True,https://www.proteinatlas.org/ENSG00000204174-NPY4R diff --git a/data/test_df_gpt_4_0_icl.csv b/data/test_df_gpt_4_0_icl.csv deleted file mode 100644 index 4fd6e8e..0000000 --- a/data/test_df_gpt_4_0_icl.csv +++ /dev/null @@ -1,31 +0,0 @@ -Predicate ID,Triple,Sentence ID,Sentence,Question,Label,Reference -10601803,Extracellular Matrix location of Proteoglycan,166,They are widely distributed as sidechains of proteoglycans (PGs) in the extracellular matrix and at cellular level.,Is the triple 'Extracellular Matrix location of Proteoglycan' supported by the sentence: 'They are widely distributed as sidechains of proteoglycans (PGs) in the extracellular matrix and at cellular level.'?,True,https://www.frontiersin.org/articles/10.3389/fcell.2021.760532/full -10598263,E2F1 gene|E2F1|UBE2L3 causes Apoptosis,112,E2F1-induced apoptosis: turning killers into therapeutics.,Is the triple 'E2F1 gene|E2F1|UBE2L3 causes Apoptosis' supported by the sentence: 'E2F1-induced apoptosis: turning killers into therapeutics.'?,True,https://www.omim.org/entry/189971 -10600542,Blastocyst structure part of Mesenchyma,144,"Developmental northern blot analysis revealed that HpNanos mRNA markedly accumulated during the blastula stages, and then decreased in abundance at the mesenchyme blastula stage.","Is the triple 'Blastocyst structure part of Mesenchyma' supported by the sentence: 'Developmental northern blot analysis revealed that HpNanos mRNA markedly accumulated during the blastula stages, and then decreased in abundance at the mesenchyme blastula stage.'?",False,https://en.wikipedia.org/wiki/Blastocyst -10597542,Neuropeptides affects Inflammation,102,"A neuropeptide in immune-mediated inflammation, Y?","Is the triple 'Neuropeptides affects Inflammation' supported by the sentence: 'A neuropeptide in immune-mediated inflammation, Y?'?",False,https://link.springer.com/chapter/10.1007/978-94-011-2996-1_9 -10597421,"4,5-dibromo-2-pyrrolic acid interacts with Specific antigen",100,Immunoblots using four recombinant DbpAs representing groups I-IV show that DbpA proteins are sensitive and specific antigens and complement one another in their reactivity.,"Is the triple '4,5-dibromo-2-pyrrolic acid interacts with Specific antigen' supported by the sentence: 'Immunoblots using four recombinant DbpAs representing groups I-IV show that DbpA proteins are sensitive and specific antigens and complement one another in their reactivity.'?",True,https://link.springer.com/article/10.1007/s11094-022-02723-x -10596660,Lyme Disease process of Individual,85,Both confirmed HGA cases and seropositive individuals had A. phagocytophilum infection concurrent either with Lyme borreliosis (two cases) or with TBE (two cases).,Is the triple 'Lyme Disease process of Individual' supported by the sentence: 'Both confirmed HGA cases and seropositive individuals had A. phagocytophilum infection concurrent either with Lyme borreliosis (two cases) or with TBE (two cases).'?,True,https://www.mayoclinic.org/diseases-conditions/lyme-disease/symptoms-causes/syc-20374651 -10595193,enrofloxacin coexists with Pharmaceutical Preparations,67,"Only rare cases of resistance to enrofloxacin (fluoroquinolone) could be detected, and only 3% of bacterial strains tested proved resistant to 3rd and 4th generation cephalosporins, including substances prescribed in human medicine.","Is the triple 'enrofloxacin coexists with Pharmaceutical Preparations' supported by the sentence: 'Only rare cases of resistance to enrofloxacin (fluoroquinolone) could be detected, and only 3% of bacterial strains tested proved resistant to 3rd and 4th generation cephalosporins, including substances prescribed in human medicine.'?",False,https://www.mdpi.com/2076-2615/11/8/2312 -10601441,Column location of Diastasis,160,"Phenacetin was chosen as the internal standard, and the separation was achieved on a C18 column with methanol and 0.02 M phosphate buffer (pH 3.2) as mobile phase.","Is the triple 'Column location of Diastasis' supported by the sentence: 'Phenacetin was chosen as the internal standard, and the separation was achieved on a C18 column with methanol and 0.02 M phosphate buffer (pH 3.2) as mobile phase.'?",False,https://radiopaedia.org/articles/diastasis-recti -10593621,XS part of Borrelia burgdorferi,34,Functionality of Borrelia burgdorferi LuxS: the Lyme disease spirochete produces and responds to the pheromone autoinducer-2 and lacks a complete activated-methyl cycle.,Is the triple 'XS part of Borrelia burgdorferi' supported by the sentence: 'Functionality of Borrelia burgdorferi LuxS: the Lyme disease spirochete produces and responds to the pheromone autoinducer-2 and lacks a complete activated-methyl cycle.'?,True,https://europepmc.org/article/PMC/128172 -10592604,Arboviruses process of Lepus capensis,16,Seroprevalence of tick-borne and mosquito-borne arboviruses in European brown hares in Northern and Western Germany.,Is the triple 'Arboviruses process of Lepus capensis' supported by the sentence: 'Seroprevalence of tick-borne and mosquito-borne arboviruses in European brown hares in Northern and Western Germany.'?,False,https://eurekamag.com/research/004/525/004525561.php -10594689,Disease process of Farm Animals,57,The establishment of corresponding management options relies on scientifically defensible efforts to obtain objective data on the prevalence of bacterial resistance in healthy and diseased livestock.,Is the triple 'Disease process of Farm Animals' supported by the sentence: 'The establishment of corresponding management options relies on scientifically defensible efforts to obtain objective data on the prevalence of bacterial resistance in healthy and diseased livestock.'?,True,https://www.rvc.ac.uk/Media/Default/UoLW%20Distance%20Learning/Modules/Animal%20Disease%20%28Current%20Concepts%29.pdf -10595985,Tick-Borne Infections process of Individual,79,Tick-borne infections were diagnosed in 57 individuals (84%).,Is the triple 'Tick-Borne Infections process of Individual' supported by the sentence: 'Tick-borne infections were diagnosed in 57 individuals (84%).'?,False,https://www.cdc.gov/ticks/diseases/index.html -10600845,Inferior Colliculus part of Males,151,"PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.","Is the triple 'Inferior Colliculus part of Males' supported by the sentence: 'PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.'?",False,https://www.healthline.com/human-body-maps/inferior-colliculus -10596199,"Glossitis, Benign Migratory process of Patients",81,"Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.","Is the triple 'Glossitis, Benign Migratory process of Patients' supported by the sentence: 'Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.'?",False,https://dermnetnz.org/topics/geographic-tongue -10602215,Glycosaminoglycans converts to Oligosaccharides,169,"Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.","Is the triple 'Glycosaminoglycans converts to Oligosaccharides' supported by the sentence: 'Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.'?",True,https://link.springer.com/chapter/10.1007/978-3-662-63123-2_41 -10592832,Disease process of Human,18,These viruses are also suspected to cause human disease.,Is the triple 'Disease process of Human' supported by the sentence: 'These viruses are also suspected to cause human disease.'?,True,https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Introductory_Biology_(CK-12)/07%3A_Prokaryotes_and_Viruses/7.12%3A_Viruses_and_Human_Disease -10601037,Cytoplasm location of PPY,153,The maternal PPYR1 is localized in the cytoplasm of the follicular and nurse cells and is deposited as a ribonucleoprotein complex in the oocyte.,Is the triple 'Cytoplasm location of PPY' supported by the sentence: 'The maternal PPYR1 is localized in the cytoplasm of the follicular and nurse cells and is deposited as a ribonucleoprotein complex in the oocyte.'?,True,https://www.uniprot.org/uniprotkb/P01298/entry -10601150,Cytoplasm part of Spermatocytes,155,"Zygotic PPYR1 is expressed exclusively in the testes, predominantly in the cytoplasm of the spermatocytes.","Is the triple 'Cytoplasm part of Spermatocytes' supported by the sentence: 'Zygotic PPYR1 is expressed exclusively in the testes, predominantly in the cytoplasm of the spermatocytes.'?",True,https://www.frontiersin.org/articles/10.3389/fvets.2023.1188479/full -10593856,Bacteria interacts with Methionine,39,"While a large number of bacteria utilize homocysteine, the other LuxS product, for synthesis of methionine as part of the activated-methyl cycle, B. burgdorferi was found to lack that ability.","Is the triple 'Bacteria interacts with Methionine' supported by the sentence: 'While a large number of bacteria utilize homocysteine, the other LuxS product, for synthesis of methionine as part of the activated-methyl cycle, B. burgdorferi was found to lack that ability.'?",True,https://europepmc.org/article/MED/31383657 -10596143,"Glossitis, Benign Migratory process of Patients",81,"Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.","Is the triple 'Glossitis, Benign Migratory process of Patients' supported by the sentence: 'Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.'?",False,https://dermnetnz.org/topics/geographic-tongue -10598517,E2F1 gene|E2F1|UBE2L3 causes Apoptosis,116,"Here, these findings are highlighted in the context of the most recent follow-up studies that have used apoptotic E2F1 genes as new therapeutics or drug targets, thereby providing insight into the basic mechanisms of E2F1-induced apoptosis and its possible clinical implications.","Is the triple 'E2F1 gene|E2F1|UBE2L3 causes Apoptosis' supported by the sentence: 'Here, these findings are highlighted in the context of the most recent follow-up studies that have used apoptotic E2F1 genes as new therapeutics or drug targets, thereby providing insight into the basic mechanisms of E2F1-induced apoptosis and its possible clinical implications.'?",True,https://www.frontiersin.org/articles/10.3389/fmolb.2020.599332/full -10602147,Chemicals interacts with Glycosaminoglycans,169,"Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.","Is the triple 'Chemicals interacts with Glycosaminoglycans' supported by the sentence: 'Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.'?",True,https://www.frontiersin.org/articles/10.3389/fmolb.2021.639666/full -10595725,Fever process of Patients,76,"We evaluated 68 patients (34 males and 34 females, mean age 44.2+/-15 years) who had fever within 4 weeks after a tick bite.","Is the triple 'Fever process of Patients' supported by the sentence: 'We evaluated 68 patients (34 males and 34 females, mean age 44.2+/-15 years) who had fever within 4 weeks after a tick bite.'?",True,https://www.uptodate.com/contents/pathophysiology-and-treatment-of-fever-in-adults -10597199,"4,5-dibromo-2-pyrrolic acid compared with 1-oleoyl-2-stearoylphosphatidylcholine",97,Comparison of dbpA sequences with ospC sequences from a subset of 59 strains revealed all kinds of cross-connections indicating processes of lateral gene transfer among strains.,"Is the triple '4,5-dibromo-2-pyrrolic acid compared with 1-oleoyl-2-stearoylphosphatidylcholine' supported by the sentence: 'Comparison of dbpA sequences with ospC sequences from a subset of 59 strains revealed all kinds of cross-connections indicating processes of lateral gene transfer among strains.'?",False,https://www.sigmaaldrich.com/UA/en/product/aldrich/656291 -10600456,Homologous Gene part of Hemicentrotus pulcherrimus,142,"The Hemicentrotus pulcherrimus homologue of nanos (HpNanos), that encodes a protein containing two CCHC zinc finger motifs, was isolated from a gastrula cDNA library.","Is the triple 'Homologous Gene part of Hemicentrotus pulcherrimus' supported by the sentence: 'The Hemicentrotus pulcherrimus homologue of nanos (HpNanos), that encodes a protein containing two CCHC zinc finger motifs, was isolated from a gastrula cDNA library.'?",False,https://db.cngb.org/stomics/publications/16530490 -10594435,host part of Vertebrates,53,These data strongly suggest that B. burgdorferi s.s. and B. garinii OspA type 4 are maintained in these areas by specific transmission cycles involving a so far undetermined vertebrate host which is frequently fed on by I. ricinus larvae.,Is the triple 'host part of Vertebrates' supported by the sentence: 'These data strongly suggest that B. burgdorferi s.s. and B. garinii OspA type 4 are maintained in these areas by specific transmission cycles involving a so far undetermined vertebrate host which is frequently fed on by I. ricinus larvae.'?,False,https://zoo.sav.sk/data/people_publictions_106_Lencakova_et_al.2006.IJMM.pdf -10596772,Disease process of Adult,87,TBE was found the most prevalent disease among adults with febrile illnesses occurring after a tick bite in north-eastern Poland.,Is the triple 'Disease process of Adult' supported by the sentence: 'TBE was found the most prevalent disease among adults with febrile illnesses occurring after a tick bite in north-eastern Poland.'?,True,https://www.ecdc.europa.eu/en/tick-borne-encephalitis/facts/factsheet -10602837,"Tachycardia, Ventricular is a Tachycardia",182,"It should be distinguished from other types of tachycardia - such as atrial flutter, atrial ectopic tachycardia, permanent junctional re-entry tachycardia, and ventricular tachycardia.","Is the triple 'Tachycardia, Ventricular is a Tachycardia' supported by the sentence: 'It should be distinguished from other types of tachycardia - such as atrial flutter, atrial ectopic tachycardia, permanent junctional re-entry tachycardia, and ventricular tachycardia.'?",True,https://www.mayoclinic.org/diseases-conditions/ventricular-tachycardia/symptoms-causes/syc-20355138 -10593287,Binding Protein part of Borrelia burgdorferi,26,"Structure-function mapping of BbCRASP-1, the key complement factor H and FHL-1 binding protein of Borrelia burgdorferi.","Is the triple 'Binding Protein part of Borrelia burgdorferi' supported by the sentence: 'Structure-function mapping of BbCRASP-1, the key complement factor H and FHL-1 binding protein of Borrelia burgdorferi.'?",True,https://www.rcsb.org/structure/1W33 -10600813,Embryo location of PPY,151,"PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.","Is the triple 'Embryo location of PPY' supported by the sentence: 'PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.'?",True,https://www.proteinatlas.org/ENSG00000204174-NPY4R diff --git a/data/test_df_llama_icl.csv b/data/test_df_llama_icl.csv deleted file mode 100644 index 4fd6e8e..0000000 --- a/data/test_df_llama_icl.csv +++ /dev/null @@ -1,31 +0,0 @@ -Predicate ID,Triple,Sentence ID,Sentence,Question,Label,Reference -10601803,Extracellular Matrix location of Proteoglycan,166,They are widely distributed as sidechains of proteoglycans (PGs) in the extracellular matrix and at cellular level.,Is the triple 'Extracellular Matrix location of Proteoglycan' supported by the sentence: 'They are widely distributed as sidechains of proteoglycans (PGs) in the extracellular matrix and at cellular level.'?,True,https://www.frontiersin.org/articles/10.3389/fcell.2021.760532/full -10598263,E2F1 gene|E2F1|UBE2L3 causes Apoptosis,112,E2F1-induced apoptosis: turning killers into therapeutics.,Is the triple 'E2F1 gene|E2F1|UBE2L3 causes Apoptosis' supported by the sentence: 'E2F1-induced apoptosis: turning killers into therapeutics.'?,True,https://www.omim.org/entry/189971 -10600542,Blastocyst structure part of Mesenchyma,144,"Developmental northern blot analysis revealed that HpNanos mRNA markedly accumulated during the blastula stages, and then decreased in abundance at the mesenchyme blastula stage.","Is the triple 'Blastocyst structure part of Mesenchyma' supported by the sentence: 'Developmental northern blot analysis revealed that HpNanos mRNA markedly accumulated during the blastula stages, and then decreased in abundance at the mesenchyme blastula stage.'?",False,https://en.wikipedia.org/wiki/Blastocyst -10597542,Neuropeptides affects Inflammation,102,"A neuropeptide in immune-mediated inflammation, Y?","Is the triple 'Neuropeptides affects Inflammation' supported by the sentence: 'A neuropeptide in immune-mediated inflammation, Y?'?",False,https://link.springer.com/chapter/10.1007/978-94-011-2996-1_9 -10597421,"4,5-dibromo-2-pyrrolic acid interacts with Specific antigen",100,Immunoblots using four recombinant DbpAs representing groups I-IV show that DbpA proteins are sensitive and specific antigens and complement one another in their reactivity.,"Is the triple '4,5-dibromo-2-pyrrolic acid interacts with Specific antigen' supported by the sentence: 'Immunoblots using four recombinant DbpAs representing groups I-IV show that DbpA proteins are sensitive and specific antigens and complement one another in their reactivity.'?",True,https://link.springer.com/article/10.1007/s11094-022-02723-x -10596660,Lyme Disease process of Individual,85,Both confirmed HGA cases and seropositive individuals had A. phagocytophilum infection concurrent either with Lyme borreliosis (two cases) or with TBE (two cases).,Is the triple 'Lyme Disease process of Individual' supported by the sentence: 'Both confirmed HGA cases and seropositive individuals had A. phagocytophilum infection concurrent either with Lyme borreliosis (two cases) or with TBE (two cases).'?,True,https://www.mayoclinic.org/diseases-conditions/lyme-disease/symptoms-causes/syc-20374651 -10595193,enrofloxacin coexists with Pharmaceutical Preparations,67,"Only rare cases of resistance to enrofloxacin (fluoroquinolone) could be detected, and only 3% of bacterial strains tested proved resistant to 3rd and 4th generation cephalosporins, including substances prescribed in human medicine.","Is the triple 'enrofloxacin coexists with Pharmaceutical Preparations' supported by the sentence: 'Only rare cases of resistance to enrofloxacin (fluoroquinolone) could be detected, and only 3% of bacterial strains tested proved resistant to 3rd and 4th generation cephalosporins, including substances prescribed in human medicine.'?",False,https://www.mdpi.com/2076-2615/11/8/2312 -10601441,Column location of Diastasis,160,"Phenacetin was chosen as the internal standard, and the separation was achieved on a C18 column with methanol and 0.02 M phosphate buffer (pH 3.2) as mobile phase.","Is the triple 'Column location of Diastasis' supported by the sentence: 'Phenacetin was chosen as the internal standard, and the separation was achieved on a C18 column with methanol and 0.02 M phosphate buffer (pH 3.2) as mobile phase.'?",False,https://radiopaedia.org/articles/diastasis-recti -10593621,XS part of Borrelia burgdorferi,34,Functionality of Borrelia burgdorferi LuxS: the Lyme disease spirochete produces and responds to the pheromone autoinducer-2 and lacks a complete activated-methyl cycle.,Is the triple 'XS part of Borrelia burgdorferi' supported by the sentence: 'Functionality of Borrelia burgdorferi LuxS: the Lyme disease spirochete produces and responds to the pheromone autoinducer-2 and lacks a complete activated-methyl cycle.'?,True,https://europepmc.org/article/PMC/128172 -10592604,Arboviruses process of Lepus capensis,16,Seroprevalence of tick-borne and mosquito-borne arboviruses in European brown hares in Northern and Western Germany.,Is the triple 'Arboviruses process of Lepus capensis' supported by the sentence: 'Seroprevalence of tick-borne and mosquito-borne arboviruses in European brown hares in Northern and Western Germany.'?,False,https://eurekamag.com/research/004/525/004525561.php -10594689,Disease process of Farm Animals,57,The establishment of corresponding management options relies on scientifically defensible efforts to obtain objective data on the prevalence of bacterial resistance in healthy and diseased livestock.,Is the triple 'Disease process of Farm Animals' supported by the sentence: 'The establishment of corresponding management options relies on scientifically defensible efforts to obtain objective data on the prevalence of bacterial resistance in healthy and diseased livestock.'?,True,https://www.rvc.ac.uk/Media/Default/UoLW%20Distance%20Learning/Modules/Animal%20Disease%20%28Current%20Concepts%29.pdf -10595985,Tick-Borne Infections process of Individual,79,Tick-borne infections were diagnosed in 57 individuals (84%).,Is the triple 'Tick-Borne Infections process of Individual' supported by the sentence: 'Tick-borne infections were diagnosed in 57 individuals (84%).'?,False,https://www.cdc.gov/ticks/diseases/index.html -10600845,Inferior Colliculus part of Males,151,"PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.","Is the triple 'Inferior Colliculus part of Males' supported by the sentence: 'PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.'?",False,https://www.healthline.com/human-body-maps/inferior-colliculus -10596199,"Glossitis, Benign Migratory process of Patients",81,"Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.","Is the triple 'Glossitis, Benign Migratory process of Patients' supported by the sentence: 'Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.'?",False,https://dermnetnz.org/topics/geographic-tongue -10602215,Glycosaminoglycans converts to Oligosaccharides,169,"Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.","Is the triple 'Glycosaminoglycans converts to Oligosaccharides' supported by the sentence: 'Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.'?",True,https://link.springer.com/chapter/10.1007/978-3-662-63123-2_41 -10592832,Disease process of Human,18,These viruses are also suspected to cause human disease.,Is the triple 'Disease process of Human' supported by the sentence: 'These viruses are also suspected to cause human disease.'?,True,https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Introductory_Biology_(CK-12)/07%3A_Prokaryotes_and_Viruses/7.12%3A_Viruses_and_Human_Disease -10601037,Cytoplasm location of PPY,153,The maternal PPYR1 is localized in the cytoplasm of the follicular and nurse cells and is deposited as a ribonucleoprotein complex in the oocyte.,Is the triple 'Cytoplasm location of PPY' supported by the sentence: 'The maternal PPYR1 is localized in the cytoplasm of the follicular and nurse cells and is deposited as a ribonucleoprotein complex in the oocyte.'?,True,https://www.uniprot.org/uniprotkb/P01298/entry -10601150,Cytoplasm part of Spermatocytes,155,"Zygotic PPYR1 is expressed exclusively in the testes, predominantly in the cytoplasm of the spermatocytes.","Is the triple 'Cytoplasm part of Spermatocytes' supported by the sentence: 'Zygotic PPYR1 is expressed exclusively in the testes, predominantly in the cytoplasm of the spermatocytes.'?",True,https://www.frontiersin.org/articles/10.3389/fvets.2023.1188479/full -10593856,Bacteria interacts with Methionine,39,"While a large number of bacteria utilize homocysteine, the other LuxS product, for synthesis of methionine as part of the activated-methyl cycle, B. burgdorferi was found to lack that ability.","Is the triple 'Bacteria interacts with Methionine' supported by the sentence: 'While a large number of bacteria utilize homocysteine, the other LuxS product, for synthesis of methionine as part of the activated-methyl cycle, B. burgdorferi was found to lack that ability.'?",True,https://europepmc.org/article/MED/31383657 -10596143,"Glossitis, Benign Migratory process of Patients",81,"Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.","Is the triple 'Glossitis, Benign Migratory process of Patients' supported by the sentence: 'Tick-borne encephalitis (TBE) was revealed in 49 cases; in 39 patients as a single infection, in three patients concurrent with erythema migrans or other Lyme borreliosis symptoms, in five patients concurrent with probable or possible Lyme borreliosis, and in two patients concurrent with A. phagocytophilum infection.'?",False,https://dermnetnz.org/topics/geographic-tongue -10598517,E2F1 gene|E2F1|UBE2L3 causes Apoptosis,116,"Here, these findings are highlighted in the context of the most recent follow-up studies that have used apoptotic E2F1 genes as new therapeutics or drug targets, thereby providing insight into the basic mechanisms of E2F1-induced apoptosis and its possible clinical implications.","Is the triple 'E2F1 gene|E2F1|UBE2L3 causes Apoptosis' supported by the sentence: 'Here, these findings are highlighted in the context of the most recent follow-up studies that have used apoptotic E2F1 genes as new therapeutics or drug targets, thereby providing insight into the basic mechanisms of E2F1-induced apoptosis and its possible clinical implications.'?",True,https://www.frontiersin.org/articles/10.3389/fmolb.2020.599332/full -10602147,Chemicals interacts with Glycosaminoglycans,169,"Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.","Is the triple 'Chemicals interacts with Glycosaminoglycans' supported by the sentence: 'Furthermore, recent developments in the electrophoretic separation and detection of unsaturated disaccharides and oligosaccharides derived from GAGs by enzymatic or chemical degradation have made it possible to examine alterations of GAGs with respect to their amounts and fine structural features in various pathological conditions, thus becoming applicable for diagnosis.'?",True,https://www.frontiersin.org/articles/10.3389/fmolb.2021.639666/full -10595725,Fever process of Patients,76,"We evaluated 68 patients (34 males and 34 females, mean age 44.2+/-15 years) who had fever within 4 weeks after a tick bite.","Is the triple 'Fever process of Patients' supported by the sentence: 'We evaluated 68 patients (34 males and 34 females, mean age 44.2+/-15 years) who had fever within 4 weeks after a tick bite.'?",True,https://www.uptodate.com/contents/pathophysiology-and-treatment-of-fever-in-adults -10597199,"4,5-dibromo-2-pyrrolic acid compared with 1-oleoyl-2-stearoylphosphatidylcholine",97,Comparison of dbpA sequences with ospC sequences from a subset of 59 strains revealed all kinds of cross-connections indicating processes of lateral gene transfer among strains.,"Is the triple '4,5-dibromo-2-pyrrolic acid compared with 1-oleoyl-2-stearoylphosphatidylcholine' supported by the sentence: 'Comparison of dbpA sequences with ospC sequences from a subset of 59 strains revealed all kinds of cross-connections indicating processes of lateral gene transfer among strains.'?",False,https://www.sigmaaldrich.com/UA/en/product/aldrich/656291 -10600456,Homologous Gene part of Hemicentrotus pulcherrimus,142,"The Hemicentrotus pulcherrimus homologue of nanos (HpNanos), that encodes a protein containing two CCHC zinc finger motifs, was isolated from a gastrula cDNA library.","Is the triple 'Homologous Gene part of Hemicentrotus pulcherrimus' supported by the sentence: 'The Hemicentrotus pulcherrimus homologue of nanos (HpNanos), that encodes a protein containing two CCHC zinc finger motifs, was isolated from a gastrula cDNA library.'?",False,https://db.cngb.org/stomics/publications/16530490 -10594435,host part of Vertebrates,53,These data strongly suggest that B. burgdorferi s.s. and B. garinii OspA type 4 are maintained in these areas by specific transmission cycles involving a so far undetermined vertebrate host which is frequently fed on by I. ricinus larvae.,Is the triple 'host part of Vertebrates' supported by the sentence: 'These data strongly suggest that B. burgdorferi s.s. and B. garinii OspA type 4 are maintained in these areas by specific transmission cycles involving a so far undetermined vertebrate host which is frequently fed on by I. ricinus larvae.'?,False,https://zoo.sav.sk/data/people_publictions_106_Lencakova_et_al.2006.IJMM.pdf -10596772,Disease process of Adult,87,TBE was found the most prevalent disease among adults with febrile illnesses occurring after a tick bite in north-eastern Poland.,Is the triple 'Disease process of Adult' supported by the sentence: 'TBE was found the most prevalent disease among adults with febrile illnesses occurring after a tick bite in north-eastern Poland.'?,True,https://www.ecdc.europa.eu/en/tick-borne-encephalitis/facts/factsheet -10602837,"Tachycardia, Ventricular is a Tachycardia",182,"It should be distinguished from other types of tachycardia - such as atrial flutter, atrial ectopic tachycardia, permanent junctional re-entry tachycardia, and ventricular tachycardia.","Is the triple 'Tachycardia, Ventricular is a Tachycardia' supported by the sentence: 'It should be distinguished from other types of tachycardia - such as atrial flutter, atrial ectopic tachycardia, permanent junctional re-entry tachycardia, and ventricular tachycardia.'?",True,https://www.mayoclinic.org/diseases-conditions/ventricular-tachycardia/symptoms-causes/syc-20355138 -10593287,Binding Protein part of Borrelia burgdorferi,26,"Structure-function mapping of BbCRASP-1, the key complement factor H and FHL-1 binding protein of Borrelia burgdorferi.","Is the triple 'Binding Protein part of Borrelia burgdorferi' supported by the sentence: 'Structure-function mapping of BbCRASP-1, the key complement factor H and FHL-1 binding protein of Borrelia burgdorferi.'?",True,https://www.rcsb.org/structure/1W33 -10600813,Embryo location of PPY,151,"PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.","Is the triple 'Embryo location of PPY' supported by the sentence: 'PPYR1 displays a biphasic expression pattern: the maternal protein is abundant in the developing egg chambers and in the early embryos, while the zygotic protein appears later in development and is localized specifically in the testes of the males.'?",True,https://www.proteinatlas.org/ENSG00000204174-NPY4R diff --git a/data/true_false_chembl_labeled.csv b/data/true_false_chembl_labeled.csv deleted file mode 100644 index 5561d0d..0000000 --- a/data/true_false_chembl_labeled.csv +++ /dev/null @@ -1,99 +0,0 @@ -Predicate ID,Triple,Sentence ID,Sentence,Question,Label,Reference -26452786,Fenbendazole causes helminthiasis,1001,Evaluation of granulated fenbendazole (22.2%) against induced and naturally occurring helminth infections in cats.,"Is the triple ""Fenbendazole causes helminthiasis"" supported by the sentence: ""Evaluation of granulated fenbendazole (22.2%) against induced and naturally occurring helminth infections in cats.""?",True, -24413653,Fenbendazole treats helminthiasis,1002,"This study investigated worm control practices by free-range egg farmers and the efficacy of the commercial anthelmintics levamisole (LEV), piperazine (PIP), flubendazole (FLBZ) and fenbendazole (FBZ) against gastrointestinal nematodes on two free-range layer farms in Australia.","Is the triple ""Fenbendazole treats helminthiasis"" supported by the sentence: ""This study investigated worm control practices by free-range egg farmers and the efficacy of the commercial anthelmintics levamisole (LEV), piperazine (PIP), flubendazole (FLBZ) and fenbendazole (FBZ) against gastrointestinal nematodes on two free-range layer farms in Australia.""?",True, -22762728,Fenbendazole prevents helminthiasis,1003,Fenbendazole resistance in O. ostertagi was confirmed with a total treatment failure in reducing worm burden: efficacy of 0%.,"Is the triple ""Fenbendazole prevents helminthiasis"" supported by the sentence: ""Fenbendazole resistance in O. ostertagi was confirmed with a total treatment failure in reducing worm burden: efficacy of 0%.""?",True, -9783282,Thiabendazole treats helminthiasis,1004,[The treatment of helminthiasis with thiabendazole].,"Is the triple ""Thiabendazole treats helminthiasis"" supported by the sentence: ""[The treatment of helminthiasis with thiabendazole].""?",True, -21848143,Albendazole causes helminthiasis,1005,Symptoms of perianal itching and visualization of visible motile worms persisted for 6 months despite being treated with multiple courses of albendazole causing a lot of frustration and distress to the caregivers.,"Is the triple ""Albendazole causes helminthiasis"" supported by the sentence: ""Symptoms of perianal itching and visualization of visible motile worms persisted for 6 months despite being treated with multiple courses of albendazole causing a lot of frustration and distress to the caregivers.""?",True, -25735916,Albendazole affects trichuriasis,1006,"Ovicidal effects of albendazole in human ascariasis, ancylostomiasis and trichuriasis.","Is the triple ""Albendazole affects trichuriasis"" supported by the sentence: ""Ovicidal effects of albendazole in human ascariasis, ancylostomiasis and trichuriasis.""?",True, -24685635,Albendazole affects filarial elephantiasis,1007,"A combination of drugs Ivermectin, Diethylcarbamazine citrate and Albendazole is recommended by WHO to accelerate the Global Programme to Eliminate Lymphatic Filariasis (GPELF).","Is the triple ""Albendazole affects filarial elephantiasis"" supported by the sentence: ""A combination of drugs Ivermectin, Diethylcarbamazine citrate and Albendazole is recommended by WHO to accelerate the Global Programme to Eliminate Lymphatic Filariasis (GPELF).""?",True, -18452252,Albendazole affects toxocariasis,1008,Effect of albendazole in experimental toxocariasis of mice.,"Is the triple ""Albendazole affects toxocariasis"" supported by the sentence: ""Effect of albendazole in experimental toxocariasis of mice.""?",True, -16658505,Albendazole affects malaria,1009,"Given the low helminth prevalence in our children, the effect of albendazole on malaria is likely to be direct.","Is the triple ""Albendazole affects malaria"" supported by the sentence: ""Given the low helminth prevalence in our children, the effect of albendazole on malaria is likely to be direct.""?",True, -13946207,Albendazole affects helminthiasis,1010,"Mass co-administration of ivermectin and albendazole by the LFEP had a significant effect on STH, which was further amplified by treatment with praziquantel and albendazole 4 months later.","Is the triple ""Albendazole affects helminthiasis"" supported by the sentence: ""Mass co-administration of ivermectin and albendazole by the LFEP had a significant effect on STH, which was further amplified by treatment with praziquantel and albendazole 4 months later.""?",True, -11239060,Albendazole affects filariasis,1011,The effect of single dose ivermectin alone or in combination with albendazole on Wuchereria bancrofti infection in primary school children in Tanzania.,"Is the triple ""Albendazole affects filariasis"" supported by the sentence: ""The effect of single dose ivermectin alone or in combination with albendazole on Wuchereria bancrofti infection in primary school children in Tanzania.""?",True, -22678969,Albendazole treats Infection,1012,The control of STH infections is based on preventive chemotherapy using either albendazole or mebendazole.,"Is the triple ""Albendazole treats Infection"" supported by the sentence: ""The control of STH infections is based on preventive chemotherapy using either albendazole or mebendazole.""?",True, -10750815,Albendazole treats onchocerciasis,1013,"A double-blind clinical trial was conducted in Monagas State, Venezuela to assess the tolerance and efficacy of albendazole in the therapy of Onchocerca volvulus infection.","Is the triple ""Albendazole treats onchocerciasis"" supported by the sentence: ""A double-blind clinical trial was conducted in Monagas State, Venezuela to assess the tolerance and efficacy of albendazole in the therapy of Onchocerca volvulus infection.""?",True, -10114050,Albendazole treats toxocariasis,1014,"The treatment of cutaneous larva migrans and Toxocara infection relies on antihelminthic agents such as thiabendazole, albendazole and ivermectin.","Is the triple ""Albendazole treats toxocariasis"" supported by the sentence: ""The treatment of cutaneous larva migrans and Toxocara infection relies on antihelminthic agents such as thiabendazole, albendazole and ivermectin.""?",True, -9588560,Albendazole treats trichuriasis,1015,"Three randomized clinical studies were conducted in 2000 to evaluate the efficacy of nitazoxanide paediatric suspension compared to albendazole in the treatment of ascariasis and trichuriasis and praziquantel in the treatment of hymenolepiasis in children from Cajamarca, Peru.","Is the triple ""Albendazole treats trichuriasis"" supported by the sentence: ""Three randomized clinical studies were conducted in 2000 to evaluate the efficacy of nitazoxanide paediatric suspension compared to albendazole in the treatment of ascariasis and trichuriasis and praziquantel in the treatment of hymenolepiasis in children from Cajamarca, Peru.""?",True, -9492446,Albendazole treats filariasis,1016,"Today, the only way is the prophylactic control of Onchocerca vovulus infections and treating lymphatic filariosis with ivermectin, diethylcarbamacine, ivermectin/diethylcarbamazine. or ivermectin/albendazole combinations.","Is the triple ""Albendazole treats filariasis"" supported by the sentence: ""Today, the only way is the prophylactic control of Onchocerca vovulus infections and treating lymphatic filariosis with ivermectin, diethylcarbamacine, ivermectin/diethylcarbamazine. or ivermectin/albendazole combinations.""?",True, -8712067,Albendazole treats helminthiasis,1017,The study population was assessed for helminthic infection and those found to be positive were randomly assigned to either an albendazole treatment group or a control group who received a placebo.,"Is the triple ""Albendazole treats helminthiasis"" supported by the sentence: ""The study population was assessed for helminthic infection and those found to be positive were randomly assigned to either an albendazole treatment group or a control group who received a placebo.""?",True, -7789677,Albendazole treats strongyloidiasis,1018,"To determine the host factors involved in response to treatment, 46 patients with strongyloidiasis were treated with albendazole, followed-up for 1 year, and separated into two groups: cured and non-cured.","Is the triple ""Albendazole treats strongyloidiasis"" supported by the sentence: ""To determine the host factors involved in response to treatment, 46 patients with strongyloidiasis were treated with albendazole, followed-up for 1 year, and separated into two groups: cured and non-cured.""?",True, -7640018,Albendazole treats filarial elephantiasis,1019,The role of albendazole in programmes to eliminate lymphatic filariasis.,"Is the triple ""Albendazole treats filarial elephantiasis"" supported by the sentence: ""The role of albendazole in programmes to eliminate lymphatic filariasis.""?",True, -7620262,Albendazole treats Hookworm Infections,1020,On the basis of our results the single 400 mg dose of albendazole is the treatment of choice for hookworm infections in this region of Mali.,"Is the triple ""Albendazole treats Hookworm Infections"" supported by the sentence: ""On the basis of our results the single 400 mg dose of albendazole is the treatment of choice for hookworm infections in this region of Mali.""?",True, -7226097,Albendazole treats cysticercosis,1021,The efficacy of albendazole (15 mg/kg/d for 1 week) was compared with praziquantel (100 mg/kg in three divided doses at 2-hour intervals) for therapy of parenchymal brain cysticercosis.,"Is the triple ""Albendazole treats cysticercosis"" supported by the sentence: ""The efficacy of albendazole (15 mg/kg/d for 1 week) was compared with praziquantel (100 mg/kg in three divided doses at 2-hour intervals) for therapy of parenchymal brain cysticercosis.""?",True, -24729219,Albendazole disrupts helminthiasis,1022,"Additionally, compared with albendazole, it resulted in a significant reduction in adult worm and total larval counts; moreover, it caused a decrease in the number of larvae deposited in muscles, with a highly significant decrease in the inflammatory cell infiltrate around the larvae and a considerable decrease in the expression of the angiogenic marker vascular endothelial growth factor in muscles.","Is the triple ""Albendazole disrupts helminthiasis"" supported by the sentence: ""Additionally, compared with albendazole, it resulted in a significant reduction in adult worm and total larval counts; moreover, it caused a decrease in the number of larvae deposited in muscles, with a highly significant decrease in the inflammatory cell infiltrate around the larvae and a considerable decrease in the expression of the angiogenic marker vascular endothelial growth factor in muscles.""?",True, -16658503,Albendazole disrupts malaria,1023,"Quarterly albendazole during childhood was associated with reduced incidence of clinical malaria (HR 0.85 (95% CI 0.73-0.98), p = 0.03).","Is the triple ""Albendazole disrupts malaria"" supported by the sentence: ""Quarterly albendazole during childhood was associated with reduced incidence of clinical malaria (HR 0.85 (95% CI 0.73-0.98), p = 0.03).""?",True, -13637338,Albendazole disrupts Hookworm Infections,1024,CONCLUSIONS: Mebendazole and albendazole showed reduced efficacy against Ascaris lumbricoides and hookworm infections at the recommended doses.,"Is the triple ""Albendazole disrupts Hookworm Infections"" supported by the sentence: ""CONCLUSIONS: Mebendazole and albendazole showed reduced efficacy against Ascaris lumbricoides and hookworm infections at the recommended doses.""?",True, -15248433,Albendazole prevents filariasis,1025,Evaluation of effectiveness of diethylcarbamazine/albendazole combination in reduction of Wuchereria bancrofti infection using multiple infection parameters.,"Is the triple ""Albendazole prevents filariasis"" supported by the sentence: ""Evaluation of effectiveness of diethylcarbamazine/albendazole combination in reduction of Wuchereria bancrofti infection using multiple infection parameters.""?",True, -13732336,Albendazole prevents helminthiasis,1026,"Our evaluation suggests that although additional studies are needed to determine optimal treatment regimens for intestinal parasites, especially among young children and pregnant women, a five-day course of pre-departure albendazole was effective in reducing helminthic infection in treated refugees.","Is the triple ""Albendazole prevents helminthiasis"" supported by the sentence: ""Our evaluation suggests that although additional studies are needed to determine optimal treatment regimens for intestinal parasites, especially among young children and pregnant women, a five-day course of pre-departure albendazole was effective in reducing helminthic infection in treated refugees.""?",True, -25678577,Latamoxef treats bacterial infectious disease,1027,"Clinical efficacy and safety of a new oxacephem, moxalactam, in serious bacterial infections.","Is the triple ""Latamoxef treats bacterial infectious disease"" supported by the sentence: ""Clinical efficacy and safety of a new oxacephem, moxalactam, in serious bacterial infections.""?",True, -15316470,Ibuprofen subclass of 2-Hydroxyibuprofen,1028,"The purpose of this study was the development and validation of an LC-MS-MS method for simultaneous analysis of ibuprofen (IBP), 2-hydroxyibuprofen (2-OH-IBP) enantiomers, and carboxyibuprofen (COOH-IBP) stereoisomers in fungi culture medium, to investigate the ability of some endophytic fungi to biotransform the chiral drug IBP into its metabolites.","Is the triple ""Ibuprofen subclass of 2-Hydroxyibuprofen"" supported by the sentence: ""The purpose of this study was the development and validation of an LC-MS-MS method for simultaneous analysis of ibuprofen (IBP), 2-hydroxyibuprofen (2-OH-IBP) enantiomers, and carboxyibuprofen (COOH-IBP) stereoisomers in fungi culture medium, to investigate the ability of some endophytic fungi to biotransform the chiral drug IBP into its metabolites.""?",True, -16265626,Ibuprofen related to Arthralgia,1029,"AIMS: To carry out a randomized clinical trial to compare the effect of palmitoylethanolamide (PEA) versus ibuprofen, a nonsteroidal anti-inflammatory drug (NSAID), for pain relief in temporomandibular joint (TMJ) osteoarthritis or arthralgia.","Is the triple ""Ibuprofen related to Arthralgia"" supported by the sentence: ""AIMS: To carry out a randomized clinical trial to compare the effect of palmitoylethanolamide (PEA) versus ibuprofen, a nonsteroidal anti-inflammatory drug (NSAID), for pain relief in temporomandibular joint (TMJ) osteoarthritis or arthralgia.""?",True, -14582794,Ibuprofen related to Pain,1030,"We investigated the analgesic efficacy of single doses of ibuprofen, tramadol and pregabalin in menthol-evoked cold pain in a randomized, placebo-controlled four-way cross-over study in 20 healthy volunteers.","Is the triple ""Ibuprofen related to Pain"" supported by the sentence: ""We investigated the analgesic efficacy of single doses of ibuprofen, tramadol and pregabalin in menthol-evoked cold pain in a randomized, placebo-controlled four-way cross-over study in 20 healthy volunteers.""?",True, -11440746,Ibuprofen related to Toothache,1031,Double blind study on emorfazone and ibuprofen in dental pain and inflammation.,"Is the triple ""Ibuprofen related to Toothache"" supported by the sentence: ""Double blind study on emorfazone and ibuprofen in dental pain and inflammation.""?",True, -9106384,Ibuprofen related to osteoarthritis,1032,Glucosamine sulfate compared to ibuprofen in osteoarthritis of the knee.,"Is the triple ""Ibuprofen related to osteoarthritis"" supported by the sentence: ""Glucosamine sulfate compared to ibuprofen in osteoarthritis of the knee.""?",True, -8106985,Ibuprofen related to burn,1033,INTRODUCTION: The anti-inflammatory and anticoagulant effects of ibuprofen and heparin may enhance skin perfusion in cutaneous scald burns.,"Is the triple ""Ibuprofen related to burn"" supported by the sentence: ""INTRODUCTION: The anti-inflammatory and anticoagulant effects of ibuprofen and heparin may enhance skin perfusion in cutaneous scald burns.""?",True, -13726345,Ibuprofen causes patent ductus arteriosus,1034,"CONCLUSIONS: Ibuprofen-induced patent ductus arteriosus closure improved pulmonary mechanics, decreased total lung water, increased epithelial sodium channel expression, and decreased the detrimental effects of preterm birth on alveolarization.","Is the triple ""Ibuprofen causes patent ductus arteriosus"" supported by the sentence: ""CONCLUSIONS: Ibuprofen-induced patent ductus arteriosus closure improved pulmonary mechanics, decreased total lung water, increased epithelial sodium channel expression, and decreased the detrimental effects of preterm birth on alveolarization.""?",True, -13653982,Ibuprofen causes Alzheimer disease,1035,Protein profile in neuroblastoma cells incubated with S- and R-enantiomers of ibuprofen by iTRAQ-coupled 2-D LC-MS/MS analysis: possible action of induced proteins on Alzheimer's disease.,"Is the triple ""Ibuprofen causes Alzheimer disease"" supported by the sentence: ""Protein profile in neuroblastoma cells incubated with S- and R-enantiomers of ibuprofen by iTRAQ-coupled 2-D LC-MS/MS analysis: possible action of induced proteins on Alzheimer's disease.""?",True, -13133316,Ibuprofen causes peptic ulcer disease,1036,Protective effect of glucosamine against ibuprofen-induced peptic ulcer in rats.,"Is the triple ""Ibuprofen causes peptic ulcer disease"" supported by the sentence: ""Protective effect of glucosamine against ibuprofen-induced peptic ulcer in rats.""?",True, -12641386,Ibuprofen causes Fever,1037,Ibuprofen-induced fever in Sjogren's syndrome.,"Is the triple ""Ibuprofen causes Fever"" supported by the sentence: ""Ibuprofen-induced fever in Sjogren's syndrome.""?",True, -12482174,Ibuprofen causes pancreatitis,1038,There have been no prior definite cases reported of ibuprofen-induced pancreatitis.,"Is the triple ""Ibuprofen causes pancreatitis"" supported by the sentence: ""There have been no prior definite cases reported of ibuprofen-induced pancreatitis.""?",True, -12438812,Ibuprofen causes Toothache,1039,"RESULTS: None of the studies established any of the COX-2 inhibitors as clearly better than ibuprofen, the current gold standard for the treatment of surgically induced dental pain.","Is the triple ""Ibuprofen causes Toothache"" supported by the sentence: ""RESULTS: None of the studies established any of the COX-2 inhibitors as clearly better than ibuprofen, the current gold standard for the treatment of surgically induced dental pain.""?",True, -12079834,Ibuprofen causes adult acute respiratory distress syndrome,1040,Noncardiogenic pulmonary edema due to ibuprofen.,"Is the triple ""Ibuprofen causes adult acute respiratory distress syndrome"" supported by the sentence: ""Noncardiogenic pulmonary edema due to ibuprofen.""?",True, -11157616,Ibuprofen causes Pain,1041,"In a double-blind cross-over study on 22 healthy subjects the analgesic efficacies of the antipyretic analgesic drugs ibuprofen, dipyrone and paracetamol were tested against placebo using a model of experimentally induced pain.","Is the triple ""Ibuprofen causes Pain"" supported by the sentence: ""In a double-blind cross-over study on 22 healthy subjects the analgesic efficacies of the antipyretic analgesic drugs ibuprofen, dipyrone and paracetamol were tested against placebo using a model of experimentally induced pain.""?",True, -10429873,Ibuprofen causes Hemorrhage,1042,Unaltered ibuprofen-induced faecal blood loss upon coadministration of moclobemide.,"Is the triple ""Ibuprofen causes Hemorrhage"" supported by the sentence: ""Unaltered ibuprofen-induced faecal blood loss upon coadministration of moclobemide.""?",True, -9800201,Ibuprofen causes arthritic joint disease,1043,The C5a antagonist (1 or 3 mg/kg/day) and/or ibuprofen (30 mg/kg/day) were administered orally on a daily basis either before or after arthritis induction.,"Is the triple ""Ibuprofen causes arthritic joint disease"" supported by the sentence: ""The C5a antagonist (1 or 3 mg/kg/day) and/or ibuprofen (30 mg/kg/day) were administered orally on a daily basis either before or after arthritis induction.""?",True, -8163776,Ibuprofen causes injury,1044,RESULTS: Ketoprofen 50 mg t.d.s. suppressed prostaglandin synthesis to a significantly greater extent than ibuprofen and caused significantly more gastroduodenal injury.,"Is the triple ""Ibuprofen causes injury"" supported by the sentence: ""RESULTS: Ketoprofen 50 mg t.d.s. suppressed prostaglandin synthesis to a significantly greater extent than ibuprofen and caused significantly more gastroduodenal injury.""?",True, -26701175,Ibuprofen affects rheumatoid arthritis,1045,The duration of action of sustained-release ibuprofen ('Brufen Retard') was investigated in a 14-day double-blind study involving 14 osteoarthritis and 10 rheumatoid arthritis patients.,"Is the triple ""Ibuprofen affects rheumatoid arthritis"" supported by the sentence: ""The duration of action of sustained-release ibuprofen ('Brufen Retard') was investigated in a 14-day double-blind study involving 14 osteoarthritis and 10 rheumatoid arthritis patients.""?",True, -24384432,Ibuprofen affects migraine disorder,1046,This study attempts to investigate the effect of ibuprofen on reducing eye pain and migraine headaches caused by trochleitis.,"Is the triple ""Ibuprofen affects migraine disorder"" supported by the sentence: ""This study attempts to investigate the effect of ibuprofen on reducing eye pain and migraine headaches caused by trochleitis.""?",True, -23500890,Ibuprofen affects adult acute respiratory distress syndrome,1047,"Ibuprofen suppresses the production of various pro-inflammatory cytokines that are implicated in the ""cytokine storm"" and subsequent ARDS in COVID-19 disease.","Is the triple ""Ibuprofen affects adult acute respiratory distress syndrome"" supported by the sentence: ""Ibuprofen suppresses the production of various pro-inflammatory cytokines that are implicated in the ""cytokine storm"" and subsequent ARDS in COVID-19 disease.""?",True, -21214366,Ibuprofen affects bronchopulmonary dysplasia,1048,"After adjusting for covariates, the risk of BPD was associated independently with ibuprofen exposure (odds ratios (OR) 2.296, 95% confidence interval (CI): 1.166-4.522, p = 0.016).","Is the triple ""Ibuprofen affects bronchopulmonary dysplasia"" supported by the sentence: ""After adjusting for covariates, the risk of BPD was associated independently with ibuprofen exposure (odds ratios (OR) 2.296, 95% confidence interval (CI): 1.166-4.522, p = 0.016).""?",True, -20886939,Ibuprofen affects Cognitive impairment,1049,The opposite effect of ibuprofen on ethanol-induced cognitive impairment as measured by two lateralized functions is consistent with the reports in tissue and animal models that central nervous system effects of ethanol may be mediated at least in part by prostaglandins.,"Is the triple ""Ibuprofen affects Cognitive impairment"" supported by the sentence: ""The opposite effect of ibuprofen on ethanol-induced cognitive impairment as measured by two lateralized functions is consistent with the reports in tissue and animal models that central nervous system effects of ethanol may be mediated at least in part by prostaglandins.""?",True, -10385921,Provider treats Chronic pain,1,METHOD: These findings are extracted from a wider research study exploring congruence between service providers from a range of professional groups and service users regarding their endorsement of treatments for chronic pain.,"Is the triple ""Provider treats Chronic pain"" supported by the sentence: ""METHOD: These findings are extracted from a wider research study exploring congruence between service providers from a range of professional groups and service users regarding their endorsement of treatments for chronic pain.""?",True, -9014061,Provider treats obesity disorder,2,Recognition by the American Heart Association that obesity is a major modifiable risk factor for coronary heart disease has prompted health providers to take a more active role in obesity management.,"Is the triple ""Provider treats obesity disorder"" supported by the sentence: ""Recognition by the American Heart Association that obesity is a major modifiable risk factor for coronary heart disease has prompted health providers to take a more active role in obesity management.""?",True, -16543798,Provider treats osteoarthritis,3,"Descriptive analyses and qualitative constant comparison methodology revealed individuals use local recreational facilities, senior centers, shopping centers, religious organizations, medical providers, pharmacies and their social network for OA management.","Is the triple ""Provider treats osteoarthritis"" supported by the sentence: ""Descriptive analyses and qualitative constant comparison methodology revealed individuals use local recreational facilities, senior centers, shopping centers, religious organizations, medical providers, pharmacies and their social network for OA management.""?",True, -16923720,Provider treats cerebral palsy,4,"Partnerships between researchers, policy makers, service providers, and families must be developed to address system barriers and build capacity in youth with CP and their communities.","Is the triple ""Provider treats cerebral palsy"" supported by the sentence: ""Partnerships between researchers, policy makers, service providers, and families must be developed to address system barriers and build capacity in youth with CP and their communities.""?",True, -12558657,Provider treats stroke disorder,5,We report findings from a qualitative interview study with stroke service providers undertaken during an investigation of inequalities in stroke care.,"Is the triple ""Provider treats stroke disorder"" supported by the sentence: ""We report findings from a qualitative interview study with stroke service providers undertaken during an investigation of inequalities in stroke care.""?",True, -7248329,Provider treats heart disorder,6,"Mental health providers who just several years ago sought carve outs for their services now say psychological issues are critical factors in the treatment of diseases such as cancer and heart disease, and must be integrated with other clinical services to achieve optimum outcomes and financial savings.","Is the triple ""Provider treats heart disorder"" supported by the sentence: ""Mental health providers who just several years ago sought carve outs for their services now say psychological issues are critical factors in the treatment of diseases such as cancer and heart disease, and must be integrated with other clinical services to achieve optimum outcomes and financial savings.""?",True, -9133778,Provider treats asthma,7,The percentages of respondents who reported having visited a medical provider for asthma-like symptoms in the previous year did not differ.,"Is the triple ""Provider treats asthma"" supported by the sentence: ""The percentages of respondents who reported having visited a medical provider for asthma-like symptoms in the previous year did not differ.""?",True, -9228776,Provider treats Pain,8,Patients of trained providers had a significant reduction in usual pain over the 4 months of data collection compared with patients of untrained providers (t = 2.0; p = .05).,"Is the triple ""Provider treats Pain"" supported by the sentence: ""Patients of trained providers had a significant reduction in usual pain over the 4 months of data collection compared with patients of untrained providers (t = 2.0; p = .05).""?",True, -12643140,Fenbendazole treats infectious disease,9,"Treatment with fenbendazole at a dose of 10mg/kg for 3 consecutive days, successfully cleared the infection.","Is the triple ""Fenbendazole treats infectious disease"" supported by the sentence: ""Treatment with fenbendazole at a dose of 10mg/kg for 3 consecutive days, successfully cleared the infection.""?",True, -24413653,Fenbendazole treats helminthiasis,10,"This study investigated worm control practices by free-range egg farmers and the efficacy of the commercial anthelmintics levamisole (LEV), piperazine (PIP), flubendazole (FLBZ) and fenbendazole (FBZ) against gastrointestinal nematodes on two free-range layer farms in Australia.","Is the triple ""Fenbendazole treats helminthiasis"" supported by the sentence: ""This study investigated worm control practices by free-range egg farmers and the efficacy of the commercial anthelmintics levamisole (LEV), piperazine (PIP), flubendazole (FLBZ) and fenbendazole (FBZ) against gastrointestinal nematodes on two free-range layer farms in Australia.""?",True, -9347430,mebendazole treats infectious disease,11,"To investigate the pathogenetic contribution of the several parasitic factors involved, the following procedures were performed in rats: a) regarding the role of eggs, these were isolated and injected either into the peritoneal cavity or directly into the liver parenchyma; b) for worms alone, 15-day-old infection was treated with mebendazole, killing the parasites before oviposition started; c) for both eggs and worms, rats at the 30th day of infection were treated with either mebendazole or ivermectin.","Is the triple ""mebendazole treats infectious disease"" supported by the sentence: ""To investigate the pathogenetic contribution of the several parasitic factors involved, the following procedures were performed in rats: a) regarding the role of eggs, these were isolated and injected either into the peritoneal cavity or directly into the liver parenchyma; b) for worms alone, 15-day-old infection was treated with mebendazole, killing the parasites before oviposition started; c) for both eggs and worms, rats at the 30th day of infection were treated with either mebendazole or ivermectin.""?",True, -8294379,mebendazole treats helminthiasis,12,The findings suggest that only a course of mebendazol had a minor effect on the control of helminth infections.,"Is the triple ""mebendazole treats helminthiasis"" supported by the sentence: ""The findings suggest that only a course of mebendazol had a minor effect on the control of helminth infections.""?",True, -25435961,mebendazole treats hepatitis,13,"We report the case of a 47-year-old female patient, suffering from multiple hydatid cysts of the liver, in whom hepatitis developed after mebendazole treatment.","Is the triple ""mebendazole treats hepatitis"" supported by the sentence: ""We report the case of a 47-year-old female patient, suffering from multiple hydatid cysts of the liver, in whom hepatitis developed after mebendazole treatment.""?",True, -9391596,mebendazole treats Morphologically altered structure,14,Morphological changes in cysticerci of Taenia taeniaeformis after mebendazole treatment.,"Is the triple ""mebendazole treats Morphologically altered structure"" supported by the sentence: ""Morphological changes in cysticerci of Taenia taeniaeformis after mebendazole treatment.""?",True, -12017349,mebendazole treats Fetal anomaly,15,"Of 22,843 women who had newborns or fetuses with congenital abnormalities, 14 were found to have been treated with mebendazole for intestinal nematoda infections/diseases during pregnancy (crude POR: 1.8 with 95% CI: 0.7-4.2).","Is the triple ""mebendazole treats Fetal anomaly"" supported by the sentence: ""Of 22,843 women who had newborns or fetuses with congenital abnormalities, 14 were found to have been treated with mebendazole for intestinal nematoda infections/diseases during pregnancy (crude POR: 1.8 with 95% CI: 0.7-4.2).""?",True, -24628044,mebendazole treats poisoning,16,"In conclusion, our study showed that this broad-spectrum anthelminthic could be repurposed as a novel therapy for ulcerative colitis without any observed side effects, however, regarding the concerns about the potential toxicity of MBZ in UC patients, future experiments on MBZ therapy in other models of UC is needed to completely address the toxicity concerns.","Is the triple ""mebendazole treats poisoning"" supported by the sentence: ""In conclusion, our study showed that this broad-spectrum anthelminthic could be repurposed as a novel therapy for ulcerative colitis without any observed side effects, however, regarding the concerns about the potential toxicity of MBZ in UC patients, future experiments on MBZ therapy in other models of UC is needed to completely address the toxicity concerns.""?",True, -9364624,Thiabendazole treats injury,17,"The effectiveness of TBZ was much higher with the treatment at 150 mg/L TBZ at 52 degrees C, providing 91% control of severe CI and approximately 89% suppression of decay; no treatment damage occurred during storage and SMP.","Is the triple ""Thiabendazole treats injury"" supported by the sentence: ""The effectiveness of TBZ was much higher with the treatment at 150 mg/L TBZ at 52 degrees C, providing 91% control of severe CI and approximately 89% suppression of decay; no treatment damage occurred during storage and SMP.""?",True, -25717445,Thiabendazole treats Increased body weight,18,"The mean weight gain for the MSRB treated steers showed a significant advantage (70.9 lb) over the untreated animals, but was not significantly different from those which received thiabendazole.","Is the triple ""Thiabendazole treats Increased body weight"" supported by the sentence: ""The mean weight gain for the MSRB treated steers showed a significant advantage (70.9 lb) over the untreated animals, but was not significantly different from those which received thiabendazole.""?",True, -11359096,Thiabendazole treats infectious disease,19,"Ivermectin appears to be the drug of choice in Strongyloides stercoralis infections, a single dose is highly effective with less frequent side effects than thiabendazole.","Is the triple ""Thiabendazole treats infectious disease"" supported by the sentence: ""Ivermectin appears to be the drug of choice in Strongyloides stercoralis infections, a single dose is highly effective with less frequent side effects than thiabendazole.""?",True, -26299545,Thiabendazole treats Jaundice,20,A 55-yr-old man developed prolonged jaundice and sicca complex after a course of thiabendazole therapy.,"Is the triple ""Thiabendazole treats Jaundice"" supported by the sentence: ""A 55-yr-old man developed prolonged jaundice and sicca complex after a course of thiabendazole therapy.""?",True, -19004721,Thiabendazole treats intrahepatic cholestasis,21,We report the second case of a patient with intrahepatic cholestasis that developed after treatment with thiabendazole and progressed to severe micronodular cirrhosis.,"Is the triple ""Thiabendazole treats intrahepatic cholestasis"" supported by the sentence: ""We report the second case of a patient with intrahepatic cholestasis that developed after treatment with thiabendazole and progressed to severe micronodular cirrhosis.""?",True, -16484657,Thiabendazole treats Vomiting,22,Two subjects experienced severe nausea and vomiting during thiabendazole therapy.,"Is the triple ""Thiabendazole treats Vomiting"" supported by the sentence: ""Two subjects experienced severe nausea and vomiting during thiabendazole therapy.""?",True, -16484656,Thiabendazole treats Nausea,23,Two subjects experienced severe nausea and vomiting during thiabendazole therapy.,"Is the triple ""Thiabendazole treats Nausea"" supported by the sentence: ""Two subjects experienced severe nausea and vomiting during thiabendazole therapy.""?",True, -27186232,Albendazole treats aplastic anemia,24,Aplastic anemia during treatment with albendazole.,"Is the triple ""Albendazole treats aplastic anemia"" supported by the sentence: ""Aplastic anemia during treatment with albendazole.""?",True, -25154403,Albendazole treats Responsive Disease,25,"Demographic data, organs of involvement, clinical presentations and investigations, response to oral albendazole therapy, surgical procedures, operative findings, perioperative clinical courses, and surgical outcomes were recorded.","Is the triple ""Albendazole treats Responsive Disease"" supported by the sentence: ""Demographic data, organs of involvement, clinical presentations and investigations, response to oral albendazole therapy, surgical procedures, operative findings, perioperative clinical courses, and surgical outcomes were recorded.""?",True, -24851755,Albendazole treats Complete Recovery,26,"Notably, this child had a remarkably positive outcome with near complete recovery of neurologic function after treatment with albendazole and steroids.","Is the triple ""Albendazole treats Complete Recovery"" supported by the sentence: ""Notably, this child had a remarkably positive outcome with near complete recovery of neurologic function after treatment with albendazole and steroids.""?",True, -14427357,Albendazole treats fascioliasis,27,A recombinant-based ELISA evaluating the efficacy of netobimin and albendazole in ruminants with naturally acquired fascioliasis.,"Is the triple ""Albendazole treats fascioliasis"" supported by the sentence: ""A recombinant-based ELISA evaluating the efficacy of netobimin and albendazole in ruminants with naturally acquired fascioliasis.""?",True, -15517653,Albendazole treats Inflammation,28,The natural history of ocular neurocysticercosis or enhanced sub-retinal inflammation due to Albendazole therapy could have resulted in the retinal detachment in this case.,"Is the triple ""Albendazole treats Inflammation"" supported by the sentence: ""The natural history of ocular neurocysticercosis or enhanced sub-retinal inflammation due to Albendazole therapy could have resulted in the retinal detachment in this case.""?",True, -8712067,Albendazole treats helminthiasis,29,The study population was assessed for helminthic infection and those found to be positive were randomly assigned to either an albendazole treatment group or a control group who received a placebo.,"Is the triple ""Albendazole treats helminthiasis"" supported by the sentence: ""The study population was assessed for helminthic infection and those found to be positive were randomly assigned to either an albendazole treatment group or a control group who received a placebo.""?",True, -21367251,Albendazole treats brain disorder,30,DISCUSSION: Our case confirms that Loa loa treatment-related encephalopathy may occur even during albendazole treatment.,"Is the triple ""Albendazole treats brain disorder"" supported by the sentence: ""DISCUSSION: Our case confirms that Loa loa treatment-related encephalopathy may occur even during albendazole treatment.""?",True, -9352190,Albendazole treats hypereosinophilic syndrome,31,To reduce migration of Toxocara larvae a single course of albendazole is suggested in cases where eosinophilia and serology are at least moderately positive.,"Is the triple ""Albendazole treats hypereosinophilic syndrome"" supported by the sentence: ""To reduce migration of Toxocara larvae a single course of albendazole is suggested in cases where eosinophilia and serology are at least moderately positive.""?",True, -10233798,Albendazole treats Jaundice,32,"In patients with jaundice due to hilar invasion, biliary diversion from segment 3 or 5 is effective for palliation of the jaundice and facilitates albendazole treatment.","Is the triple ""Albendazole treats Jaundice"" supported by the sentence: ""In patients with jaundice due to hilar invasion, biliary diversion from segment 3 or 5 is effective for palliation of the jaundice and facilitates albendazole treatment.""?",True, -19990943,Albendazole treats Abnormal degeneration,33,"Those without LMD or PDCs can be effectively managed with long-term albendazole, artificially inducing larval involution.","Is the triple ""Albendazole treats Abnormal degeneration"" supported by the sentence: ""Those without LMD or PDCs can be effectively managed with long-term albendazole, artificially inducing larval involution.""?",True, -19251948,Albendazole treats Sjogren syndrome,34,Thrombocytopenia caused by albendazole in a patient with Sjogren's syndrome: A case report.,"Is the triple ""Albendazole treats Sjogren syndrome"" supported by the sentence: ""Thrombocytopenia caused by albendazole in a patient with Sjogren's syndrome: A case report.""?",True, -24655682,Albendazole treats Inflammatory Response,35,CONCLUSION: Single dose pretreatment with Albendazole could ameliorate inflammatory response and enhance ischemia threshold following induction of MIR injury.,"Is the triple ""Albendazole treats Inflammatory Response"" supported by the sentence: ""CONCLUSION: Single dose pretreatment with Albendazole could ameliorate inflammatory response and enhance ischemia threshold following induction of MIR injury.""?",True, -10829796,Albendazole treats poisoning,36,Signs of toxicosis were not observed in calves treated with albendazole.,"Is the triple ""Albendazole treats poisoning"" supported by the sentence: ""Signs of toxicosis were not observed in calves treated with albendazole.""?",True, -7667169,Albendazole treats Cyst,37,These were more frequent in albendazole-treated than in mebendazole-treated cysts (82.2% vs. 56.1%; P < .001).,"Is the triple ""Albendazole treats Cyst"" supported by the sentence: ""These were more frequent in albendazole-treated than in mebendazole-treated cysts (82.2% vs. 56.1%; P < .001).""?",True, -20420369,Albendazole treats pancytopenia,38,"One of the 7 patients, with underlying IgG4 sclerosing cholangitis and secondary biliary cirrhosis was on immunosuppressives and developed severe pancytopenia 15 days after albendazole treatment.","Is the triple ""Albendazole treats pancytopenia"" supported by the sentence: ""One of the 7 patients, with underlying IgG4 sclerosing cholangitis and secondary biliary cirrhosis was on immunosuppressives and developed severe pancytopenia 15 days after albendazole treatment.""?",True, -7132662,Albendazole treats echinococcosis,39,Albendazole was used in four patients with multiple hydatid cyst due to probable recurrence in the postoperative period.,"Is the triple ""Albendazole treats echinococcosis"" supported by the sentence: ""Albendazole was used in four patients with multiple hydatid cyst due to probable recurrence in the postoperative period.""?",True, -25977174,Latamoxef treats Superinfection,40,"For instance, there are more published reports of enterococcal superinfection in patients treated with moxalactam than in patients receiving the other third-generation cephalosporins.","Is the triple ""Latamoxef treats Superinfection"" supported by the sentence: ""For instance, there are more published reports of enterococcal superinfection in patients treated with moxalactam than in patients receiving the other third-generation cephalosporins.""?",True, -26169628,Latamoxef treats Pulmonary hemorrhage,41,Fatal pulmonary hemorrhage occurred on the eighth day of moxalactam therapy.,"Is the triple ""Latamoxef treats Pulmonary hemorrhage"" supported by the sentence: ""Fatal pulmonary hemorrhage occurred on the eighth day of moxalactam therapy.""?",True, -7703186,Latamoxef treats infectious disease,42,"Due to increasing multidrug resistance, choosing appropriate antimicrobial agents such as moxalactam, imipenem, and ciprofloxacin should be highly recommended for the treatment of S. marcescens infections.","Is the triple ""Latamoxef treats infectious disease"" supported by the sentence: ""Due to increasing multidrug resistance, choosing appropriate antimicrobial agents such as moxalactam, imipenem, and ciprofloxacin should be highly recommended for the treatment of S. marcescens infections.""?",True, -25699167,Latamoxef treats blood coagulation disease,43,The most severe coagulopathies occurred prior to moxalactam therapy and were seen only in those patients who had shock requiring 10 or more units of blood.,"Is the triple ""Latamoxef treats blood coagulation disease"" supported by the sentence: ""The most severe coagulopathies occurred prior to moxalactam therapy and were seen only in those patients who had shock requiring 10 or more units of blood.""?",True, -26216440,Latamoxef treats congenital prothrombin deficiency,44,"Previous clinical studies have emphasized that hypoprothrombinemia may occur during treatment with moxalactam disodium, a new broad-spectrum cephalosporin.","Is the triple ""Latamoxef treats congenital prothrombin deficiency"" supported by the sentence: ""Previous clinical studies have emphasized that hypoprothrombinemia may occur during treatment with moxalactam disodium, a new broad-spectrum cephalosporin.""?",True, -14104596,Ibuprofen treats Abdominal pain,45,"PATIENTS: Patients with osteoarthritis receiving treatment with ibuprofen, piroxicam, or naproxen and experiencing abdominal pain were eligible.","Is the triple ""Ibuprofen treats Abdominal pain"" supported by the sentence: ""PATIENTS: Patients with osteoarthritis receiving treatment with ibuprofen, piroxicam, or naproxen and experiencing abdominal pain were eligible.""?",True, -14738368,Ibuprofen treats thrombocytopenia,46,"Treatment with ibuprofen is safer, decreasing the risk of renal failure, thrombocytopenia, and hyponatremia.","Is the triple ""Ibuprofen treats thrombocytopenia"" supported by the sentence: ""Treatment with ibuprofen is safer, decreasing the risk of renal failure, thrombocytopenia, and hyponatremia.""?",True, -10868694,Ibuprofen treats Shock,47,We conclude that ibuprofen reversed the IL-1beta-induced shock by restoring the systemic vascular resistance to normal and thereby normalized the VO2/DO2 relation in the supply-independent range of DO2.,"Is the triple ""Ibuprofen treats Shock"" supported by the sentence: ""We conclude that ibuprofen reversed the IL-1beta-induced shock by restoring the systemic vascular resistance to normal and thereby normalized the VO2/DO2 relation in the supply-independent range of DO2.""?",True, -14738366,Ibuprofen treats Hyponatremia,48,"Treatment with ibuprofen is safer, decreasing the risk of renal failure, thrombocytopenia, and hyponatremia.","Is the triple ""Ibuprofen treats Hyponatremia"" supported by the sentence: ""Treatment with ibuprofen is safer, decreasing the risk of renal failure, thrombocytopenia, and hyponatremia.""?",True, -14738367,Ibuprofen treats kidney failure,49,"Treatment with ibuprofen is safer, decreasing the risk of renal failure, thrombocytopenia, and hyponatremia.","Is the triple ""Ibuprofen treats kidney failure"" supported by the sentence: ""Treatment with ibuprofen is safer, decreasing the risk of renal failure, thrombocytopenia, and hyponatremia.""?",True, diff --git a/data/true_false_chembl_labeled_sentense.csv b/data/true_false_chembl_labeled_sentense.csv deleted file mode 100644 index bded10e..0000000 --- a/data/true_false_chembl_labeled_sentense.csv +++ /dev/null @@ -1,98 +0,0 @@ -1001,,,,,Evaluation of granulated fenbendazole (22.2%) against induced and naturally occurring helminth infections in cats.,,,, -1002,,,,,"This study investigated worm control practices by free-range egg farmers and the efficacy of the commercial anthelmintics levamisole (LEV), piperazine (PIP), flubendazole (FLBZ) and fenbendazole (FBZ) against gastrointestinal nematodes on two free-range layer farms in Australia.",,,, -1003,,,,,Fenbendazole resistance in O. ostertagi was confirmed with a total treatment failure in reducing worm burden: efficacy of 0%.,,,, -1004,,,,,[The treatment of helminthiasis with thiabendazole].,,,, -1005,,,,,Symptoms of perianal itching and visualization of visible motile worms persisted for 6 months despite being treated with multiple courses of albendazole causing a lot of frustration and distress to the caregivers.,,,, -1006,,,,,"Ovicidal effects of albendazole in human ascariasis, ancylostomiasis and trichuriasis.",,,, -1007,,,,,"A combination of drugs Ivermectin, Diethylcarbamazine citrate and Albendazole is recommended by WHO to accelerate the Global Programme to Eliminate Lymphatic Filariasis (GPELF).",,,, -1008,,,,,Effect of albendazole in experimental toxocariasis of mice.,,,, -1009,,,,,"Given the low helminth prevalence in our children, the effect of albendazole on malaria is likely to be direct.",,,, -1010,,,,,"Mass co-administration of ivermectin and albendazole by the LFEP had a significant effect on STH, which was further amplified by treatment with praziquantel and albendazole 4 months later.",,,, -1011,,,,,The effect of single dose ivermectin alone or in combination with albendazole on Wuchereria bancrofti infection in primary school children in Tanzania.,,,, -1012,,,,,The control of STH infections is based on preventive chemotherapy using either albendazole or mebendazole.,,,, -1013,,,,,"A double-blind clinical trial was conducted in Monagas State, Venezuela to assess the tolerance and efficacy of albendazole in the therapy of Onchocerca volvulus infection.",,,, -1014,,,,,"The treatment of cutaneous larva migrans and Toxocara infection relies on antihelminthic agents such as thiabendazole, albendazole and ivermectin.",,,, -1015,,,,,"Three randomized clinical studies were conducted in 2000 to evaluate the efficacy of nitazoxanide paediatric suspension compared to albendazole in the treatment of ascariasis and trichuriasis and praziquantel in the treatment of hymenolepiasis in children from Cajamarca, Peru.",,,, -1016,,,,,"Today, the only way is the prophylactic control of Onchocerca vovulus infections and treating lymphatic filariosis with ivermectin, diethylcarbamacine, ivermectin/diethylcarbamazine. or ivermectin/albendazole combinations.",,,, -1017,,,,,The study population was assessed for helminthic infection and those found to be positive were randomly assigned to either an albendazole treatment group or a control group who received a placebo.,,,, -1018,,,,,"To determine the host factors involved in response to treatment, 46 patients with strongyloidiasis were treated with albendazole, followed-up for 1 year, and separated into two groups: cured and non-cured.",,,, -1019,,,,,The role of albendazole in programmes to eliminate lymphatic filariasis.,,,, -1020,,,,,On the basis of our results the single 400 mg dose of albendazole is the treatment of choice for hookworm infections in this region of Mali.,,,, -1021,,,,,The efficacy of albendazole (15 mg/kg/d for 1 week) was compared with praziquantel (100 mg/kg in three divided doses at 2-hour intervals) for therapy of parenchymal brain cysticercosis.,,,, -1022,,,,,"Additionally, compared with albendazole, it resulted in a significant reduction in adult worm and total larval counts; moreover, it caused a decrease in the number of larvae deposited in muscles, with a highly significant decrease in the inflammatory cell infiltrate around the larvae and a considerable decrease in the expression of the angiogenic marker vascular endothelial growth factor in muscles.",,,, -1023,,,,,"Quarterly albendazole during childhood was associated with reduced incidence of clinical malaria (HR 0.85 (95% CI 0.73-0.98), p = 0.03).",,,, -1024,,,,,CONCLUSIONS: Mebendazole and albendazole showed reduced efficacy against Ascaris lumbricoides and hookworm infections at the recommended doses.,,,, -1025,,,,,Evaluation of effectiveness of diethylcarbamazine/albendazole combination in reduction of Wuchereria bancrofti infection using multiple infection parameters.,,,, -1026,,,,,"Our evaluation suggests that although additional studies are needed to determine optimal treatment regimens for intestinal parasites, especially among young children and pregnant women, a five-day course of pre-departure albendazole was effective in reducing helminthic infection in treated refugees.",,,, -1027,,,,,"Clinical efficacy and safety of a new oxacephem, moxalactam, in serious bacterial infections.",,,, -1028,,,,,"The purpose of this study was the development and validation of an LC-MS-MS method for simultaneous analysis of ibuprofen (IBP), 2-hydroxyibuprofen (2-OH-IBP) enantiomers, and carboxyibuprofen (COOH-IBP) stereoisomers in fungi culture medium, to investigate the ability of some endophytic fungi to biotransform the chiral drug IBP into its metabolites.",,,, -1029,,,,,"AIMS: To carry out a randomized clinical trial to compare the effect of palmitoylethanolamide (PEA) versus ibuprofen, a nonsteroidal anti-inflammatory drug (NSAID), for pain relief in temporomandibular joint (TMJ) osteoarthritis or arthralgia.",,,, -1030,,,,,"We investigated the analgesic efficacy of single doses of ibuprofen, tramadol and pregabalin in menthol-evoked cold pain in a randomized, placebo-controlled four-way cross-over study in 20 healthy volunteers.",,,, -1031,,,,,Double blind study on emorfazone and ibuprofen in dental pain and inflammation.,,,, -1032,,,,,Glucosamine sulfate compared to ibuprofen in osteoarthritis of the knee.,,,, -1033,,,,,INTRODUCTION: The anti-inflammatory and anticoagulant effects of ibuprofen and heparin may enhance skin perfusion in cutaneous scald burns.,,,, -1034,,,,,"CONCLUSIONS: Ibuprofen-induced patent ductus arteriosus closure improved pulmonary mechanics, decreased total lung water, increased epithelial sodium channel expression, and decreased the detrimental effects of preterm birth on alveolarization.",,,, -1035,,,,,Protein profile in neuroblastoma cells incubated with S- and R-enantiomers of ibuprofen by iTRAQ-coupled 2-D LC-MS/MS analysis: possible action of induced proteins on Alzheimer's disease.,,,, -1036,,,,,Protective effect of glucosamine against ibuprofen-induced peptic ulcer in rats.,,,, -1037,,,,,Ibuprofen-induced fever in Sjogren's syndrome.,,,, -1038,,,,,There have been no prior definite cases reported of ibuprofen-induced pancreatitis.,,,, -1039,,,,,"RESULTS: None of the studies established any of the COX-2 inhibitors as clearly better than ibuprofen, the current gold standard for the treatment of surgically induced dental pain.",,,, -1040,,,,,Noncardiogenic pulmonary edema due to ibuprofen.,,,, -1041,,,,,"In a double-blind cross-over study on 22 healthy subjects the analgesic efficacies of the antipyretic analgesic drugs ibuprofen, dipyrone and paracetamol were tested against placebo using a model of experimentally induced pain.",,,, -1042,,,,,Unaltered ibuprofen-induced faecal blood loss upon coadministration of moclobemide.,,,, -1043,,,,,The C5a antagonist (1 or 3 mg/kg/day) and/or ibuprofen (30 mg/kg/day) were administered orally on a daily basis either before or after arthritis induction.,,,, -1044,,,,,RESULTS: Ketoprofen 50 mg t.d.s. suppressed prostaglandin synthesis to a significantly greater extent than ibuprofen and caused significantly more gastroduodenal injury.,,,, -1045,,,,,The duration of action of sustained-release ibuprofen ('Brufen Retard') was investigated in a 14-day double-blind study involving 14 osteoarthritis and 10 rheumatoid arthritis patients.,,,, -1046,,,,,This study attempts to investigate the effect of ibuprofen on reducing eye pain and migraine headaches caused by trochleitis.,,,, -1047,,,,,"Ibuprofen suppresses the production of various pro-inflammatory cytokines that are implicated in the ""cytokine storm"" and subsequent ARDS in COVID-19 disease.",,,, -1048,,,,,"After adjusting for covariates, the risk of BPD was associated independently with ibuprofen exposure (odds ratios (OR) 2.296, 95% confidence interval (CI): 1.166-4.522, p = 0.016).",,,, -1049,,,,,The opposite effect of ibuprofen on ethanol-induced cognitive impairment as measured by two lateralized functions is consistent with the reports in tissue and animal models that central nervous system effects of ethanol may be mediated at least in part by prostaglandins.,,,, -1,,,,,METHOD: These findings are extracted from a wider research study exploring congruence between service providers from a range of professional groups and service users regarding their endorsement of treatments for chronic pain.,,,, -2,,,,,Recognition by the American Heart Association that obesity is a major modifiable risk factor for coronary heart disease has prompted health providers to take a more active role in obesity management.,,,, -3,,,,,"Descriptive analyses and qualitative constant comparison methodology revealed individuals use local recreational facilities, senior centers, shopping centers, religious organizations, medical providers, pharmacies and their social network for OA management.",,,, -4,,,,,"Partnerships between researchers, policy makers, service providers, and families must be developed to address system barriers and build capacity in youth with CP and their communities.",,,, -5,,,,,We report findings from a qualitative interview study with stroke service providers undertaken during an investigation of inequalities in stroke care.,,,, -6,,,,,"Mental health providers who just several years ago sought carve outs for their services now say psychological issues are critical factors in the treatment of diseases such as cancer and heart disease, and must be integrated with other clinical services to achieve optimum outcomes and financial savings.",,,, -7,,,,,The percentages of respondents who reported having visited a medical provider for asthma-like symptoms in the previous year did not differ.,,,, -8,,,,,Patients of trained providers had a significant reduction in usual pain over the 4 months of data collection compared with patients of untrained providers (t = 2.0; p = .05).,,,, -9,,,,,"Treatment with fenbendazole at a dose of 10mg/kg for 3 consecutive days, successfully cleared the infection.",,,, -10,,,,,"This study investigated worm control practices by free-range egg farmers and the efficacy of the commercial anthelmintics levamisole (LEV), piperazine (PIP), flubendazole (FLBZ) and fenbendazole (FBZ) against gastrointestinal nematodes on two free-range layer farms in Australia.",,,, -11,,,,,"To investigate the pathogenetic contribution of the several parasitic factors involved, the following procedures were performed in rats: a) regarding the role of eggs, these were isolated and injected either into the peritoneal cavity or directly into the liver parenchyma; b) for worms alone, 15-day-old infection was treated with mebendazole, killing the parasites before oviposition started; c) for both eggs and worms, rats at the 30th day of infection were treated with either mebendazole or ivermectin.",,,, -12,,,,,The findings suggest that only a course of mebendazol had a minor effect on the control of helminth infections.,,,, -13,,,,,"We report the case of a 47-year-old female patient, suffering from multiple hydatid cysts of the liver, in whom hepatitis developed after mebendazole treatment.",,,, -14,,,,,Morphological changes in cysticerci of Taenia taeniaeformis after mebendazole treatment.,,,, -15,,,,,"Of 22,843 women who had newborns or fetuses with congenital abnormalities, 14 were found to have been treated with mebendazole for intestinal nematoda infections/diseases during pregnancy (crude POR: 1.8 with 95% CI: 0.7-4.2).",,,, -16,,,,,"In conclusion, our study showed that this broad-spectrum anthelminthic could be repurposed as a novel therapy for ulcerative colitis without any observed side effects, however, regarding the concerns about the potential toxicity of MBZ in UC patients, future experiments on MBZ therapy in other models of UC is needed to completely address the toxicity concerns.",,,, -17,,,,,"The effectiveness of TBZ was much higher with the treatment at 150 mg/L TBZ at 52 degrees C, providing 91% control of severe CI and approximately 89% suppression of decay; no treatment damage occurred during storage and SMP.",,,, -18,,,,,"The mean weight gain for the MSRB treated steers showed a significant advantage (70.9 lb) over the untreated animals, but was not significantly different from those which received thiabendazole.",,,, -19,,,,,"Ivermectin appears to be the drug of choice in Strongyloides stercoralis infections, a single dose is highly effective with less frequent side effects than thiabendazole.",,,, -20,,,,,A 55-yr-old man developed prolonged jaundice and sicca complex after a course of thiabendazole therapy.,,,, -21,,,,,We report the second case of a patient with intrahepatic cholestasis that developed after treatment with thiabendazole and progressed to severe micronodular cirrhosis.,,,, -22,,,,,Two subjects experienced severe nausea and vomiting during thiabendazole therapy.,,,, -23,,,,,Two subjects experienced severe nausea and vomiting during thiabendazole therapy.,,,, -24,,,,,Aplastic anemia during treatment with albendazole.,,,, -25,,,,,"Demographic data, organs of involvement, clinical presentations and investigations, response to oral albendazole therapy, surgical procedures, operative findings, perioperative clinical courses, and surgical outcomes were recorded.",,,, -26,,,,,"Notably, this child had a remarkably positive outcome with near complete recovery of neurologic function after treatment with albendazole and steroids.",,,, -27,,,,,A recombinant-based ELISA evaluating the efficacy of netobimin and albendazole in ruminants with naturally acquired fascioliasis.,,,, -28,,,,,The natural history of ocular neurocysticercosis or enhanced sub-retinal inflammation due to Albendazole therapy could have resulted in the retinal detachment in this case.,,,, -29,,,,,The study population was assessed for helminthic infection and those found to be positive were randomly assigned to either an albendazole treatment group or a control group who received a placebo.,,,, -30,,,,,DISCUSSION: Our case confirms that Loa loa treatment-related encephalopathy may occur even during albendazole treatment.,,,, -31,,,,,To reduce migration of Toxocara larvae a single course of albendazole is suggested in cases where eosinophilia and serology are at least moderately positive.,,,, -32,,,,,"In patients with jaundice due to hilar invasion, biliary diversion from segment 3 or 5 is effective for palliation of the jaundice and facilitates albendazole treatment.",,,, -33,,,,,"Those without LMD or PDCs can be effectively managed with long-term albendazole, artificially inducing larval involution.",,,, -34,,,,,Thrombocytopenia caused by albendazole in a patient with Sjogren's syndrome: A case report.,,,, -35,,,,,CONCLUSION: Single dose pretreatment with Albendazole could ameliorate inflammatory response and enhance ischemia threshold following induction of MIR injury.,,,, -36,,,,,Signs of toxicosis were not observed in calves treated with albendazole.,,,, -37,,,,,These were more frequent in albendazole-treated than in mebendazole-treated cysts (82.2% vs. 56.1%; P < .001).,,,, -38,,,,,"One of the 7 patients, with underlying IgG4 sclerosing cholangitis and secondary biliary cirrhosis was on immunosuppressives and developed severe pancytopenia 15 days after albendazole treatment.",,,, -39,,,,,Albendazole was used in four patients with multiple hydatid cyst due to probable recurrence in the postoperative period.,,,, -40,,,,,"For instance, there are more published reports of enterococcal superinfection in patients treated with moxalactam than in patients receiving the other third-generation cephalosporins.",,,, -41,,,,,Fatal pulmonary hemorrhage occurred on the eighth day of moxalactam therapy.,,,, -42,,,,,"Due to increasing multidrug resistance, choosing appropriate antimicrobial agents such as moxalactam, imipenem, and ciprofloxacin should be highly recommended for the treatment of S. marcescens infections.",,,, -43,,,,,The most severe coagulopathies occurred prior to moxalactam therapy and were seen only in those patients who had shock requiring 10 or more units of blood.,,,, -44,,,,,"Previous clinical studies have emphasized that hypoprothrombinemia may occur during treatment with moxalactam disodium, a new broad-spectrum cephalosporin.",,,, -45,,,,,"PATIENTS: Patients with osteoarthritis receiving treatment with ibuprofen, piroxicam, or naproxen and experiencing abdominal pain were eligible.",,,, -46,,,,,"Treatment with ibuprofen is safer, decreasing the risk of renal failure, thrombocytopenia, and hyponatremia.",,,, -47,,,,,We conclude that ibuprofen reversed the IL-1beta-induced shock by restoring the systemic vascular resistance to normal and thereby normalized the VO2/DO2 relation in the supply-independent range of DO2.,,,, -48,,,,,"Treatment with ibuprofen is safer, decreasing the risk of renal failure, thrombocytopenia, and hyponatremia.",,,, -49,,,,,"Treatment with ibuprofen is safer, decreasing the risk of renal failure, thrombocytopenia, and hyponatremia.",,,, diff --git a/data/true_false_chembl_labeled_triple.csv b/data/true_false_chembl_labeled_triple.csv deleted file mode 100644 index 381f3fa..0000000 --- a/data/true_false_chembl_labeled_triple.csv +++ /dev/null @@ -1,98 +0,0 @@ -26452786,1001,,causes,,Fenbendazole,,,,helminthiasis,,,,, -24413653,1002,,treats,,Fenbendazole,,,,helminthiasis,,,,, -22762728,1003,,prevents,,Fenbendazole,,,,helminthiasis,,,,, -9783282,1004,,treats,,Thiabendazole,,,,helminthiasis,,,,, -21848143,1005,,causes,,Albendazole,,,,helminthiasis,,,,, -25735916,1006,,affects,,Albendazole,,,,trichuriasis,,,,, -24685635,1007,,affects,,Albendazole,,,,filarial elephantiasis,,,,, -18452252,1008,,affects,,Albendazole,,,,toxocariasis,,,,, -16658505,1009,,affects,,Albendazole,,,,malaria,,,,, -13946207,1010,,affects,,Albendazole,,,,helminthiasis,,,,, -11239060,1011,,affects,,Albendazole,,,,filariasis,,,,, -22678969,1012,,treats,,Albendazole,,,,Infection,,,,, -10750815,1013,,treats,,Albendazole,,,,onchocerciasis,,,,, -10114050,1014,,treats,,Albendazole,,,,toxocariasis,,,,, -9588560,1015,,treats,,Albendazole,,,,trichuriasis,,,,, -9492446,1016,,treats,,Albendazole,,,,filariasis,,,,, -8712067,1017,,treats,,Albendazole,,,,helminthiasis,,,,, -7789677,1018,,treats,,Albendazole,,,,strongyloidiasis,,,,, -7640018,1019,,treats,,Albendazole,,,,filarial elephantiasis,,,,, -7620262,1020,,treats,,Albendazole,,,,Hookworm Infections,,,,, -7226097,1021,,treats,,Albendazole,,,,cysticercosis,,,,, -24729219,1022,,disrupts,,Albendazole,,,,helminthiasis,,,,, -16658503,1023,,disrupts,,Albendazole,,,,malaria,,,,, -13637338,1024,,disrupts,,Albendazole,,,,Hookworm Infections,,,,, -15248433,1025,,prevents,,Albendazole,,,,filariasis,,,,, -13732336,1026,,prevents,,Albendazole,,,,helminthiasis,,,,, -25678577,1027,,treats,,Latamoxef,,,,bacterial infectious disease,,,,, -15316470,1028,,subclass of,,Ibuprofen,,,,2-Hydroxyibuprofen,,,,, -16265626,1029,,related to,,Ibuprofen,,,,Arthralgia,,,,, -14582794,1030,,related to,,Ibuprofen,,,,Pain,,,,, -11440746,1031,,related to,,Ibuprofen,,,,Toothache,,,,, -9106384,1032,,related to,,Ibuprofen,,,,osteoarthritis,,,,, -8106985,1033,,related to,,Ibuprofen,,,,burn,,,,, -13726345,1034,,causes,,Ibuprofen,,,,patent ductus arteriosus,,,,, -13653982,1035,,causes,,Ibuprofen,,,,Alzheimer disease,,,,, -13133316,1036,,causes,,Ibuprofen,,,,peptic ulcer disease,,,,, -12641386,1037,,causes,,Ibuprofen,,,,Fever,,,,, -12482174,1038,,causes,,Ibuprofen,,,,pancreatitis,,,,, -12438812,1039,,causes,,Ibuprofen,,,,Toothache,,,,, -12079834,1040,,causes,,Ibuprofen,,,,adult acute respiratory distress syndrome,,,,, -11157616,1041,,causes,,Ibuprofen,,,,Pain,,,,, -10429873,1042,,causes,,Ibuprofen,,,,Hemorrhage,,,,, -9800201,1043,,causes,,Ibuprofen,,,,arthritic joint disease,,,,, -8163776,1044,,causes,,Ibuprofen,,,,injury,,,,, -26701175,1045,,affects,,Ibuprofen,,,,rheumatoid arthritis,,,,, -24384432,1046,,affects,,Ibuprofen,,,,migraine disorder,,,,, -23500890,1047,,affects,,Ibuprofen,,,,adult acute respiratory distress syndrome,,,,, -21214366,1048,,affects,,Ibuprofen,,,,bronchopulmonary dysplasia,,,,, -20886939,1049,,affects,,Ibuprofen,,,,Cognitive impairment,,,,, -10385921,1,,treats,,Provider,,,,Chronic pain,,,,, -9014061,2,,treats,,Provider,,,,obesity disorder,,,,, -16543798,3,,treats,,Provider,,,,osteoarthritis,,,,, -16923720,4,,treats,,Provider,,,,cerebral palsy,,,,, -12558657,5,,treats,,Provider,,,,stroke disorder,,,,, -7248329,6,,treats,,Provider,,,,heart disorder,,,,, -9133778,7,,treats,,Provider,,,,asthma,,,,, -9228776,8,,treats,,Provider,,,,Pain,,,,, -12643140,9,,treats,,Fenbendazole,,,,infectious disease,,,,, -24413653,10,,treats,,Fenbendazole,,,,helminthiasis,,,,, -9347430,11,,treats,,mebendazole,,,,infectious disease,,,,, -8294379,12,,treats,,mebendazole,,,,helminthiasis,,,,, -25435961,13,,treats,,mebendazole,,,,hepatitis,,,,, -9391596,14,,treats,,mebendazole,,,,Morphologically altered structure,,,,, -12017349,15,,treats,,mebendazole,,,,Fetal anomaly,,,,, -24628044,16,,treats,,mebendazole,,,,poisoning,,,,, -9364624,17,,treats,,Thiabendazole,,,,injury,,,,, -25717445,18,,treats,,Thiabendazole,,,,Increased body weight,,,,, -11359096,19,,treats,,Thiabendazole,,,,infectious disease,,,,, -26299545,20,,treats,,Thiabendazole,,,,Jaundice,,,,, -19004721,21,,treats,,Thiabendazole,,,,intrahepatic cholestasis,,,,, -16484657,22,,treats,,Thiabendazole,,,,Vomiting,,,,, -16484656,23,,treats,,Thiabendazole,,,,Nausea,,,,, -27186232,24,,treats,,Albendazole,,,,aplastic anemia,,,,, -25154403,25,,treats,,Albendazole,,,,Responsive Disease,,,,, -24851755,26,,treats,,Albendazole,,,,Complete Recovery,,,,, -14427357,27,,treats,,Albendazole,,,,fascioliasis,,,,, -15517653,28,,treats,,Albendazole,,,,Inflammation,,,,, -8712067,29,,treats,,Albendazole,,,,helminthiasis,,,,, -21367251,30,,treats,,Albendazole,,,,brain disorder,,,,, -9352190,31,,treats,,Albendazole,,,,hypereosinophilic syndrome,,,,, -10233798,32,,treats,,Albendazole,,,,Jaundice,,,,, -19990943,33,,treats,,Albendazole,,,,Abnormal degeneration,,,,, -19251948,34,,treats,,Albendazole,,,,Sjogren syndrome,,,,, -24655682,35,,treats,,Albendazole,,,,Inflammatory Response,,,,, -10829796,36,,treats,,Albendazole,,,,poisoning,,,,, -7667169,37,,treats,,Albendazole,,,,Cyst,,,,, -20420369,38,,treats,,Albendazole,,,,pancytopenia,,,,, -7132662,39,,treats,,Albendazole,,,,echinococcosis,,,,, -25977174,40,,treats,,Latamoxef,,,,Superinfection,,,,, -26169628,41,,treats,,Latamoxef,,,,Pulmonary hemorrhage,,,,, -7703186,42,,treats,,Latamoxef,,,,infectious disease,,,,, -25699167,43,,treats,,Latamoxef,,,,blood coagulation disease,,,,, -26216440,44,,treats,,Latamoxef,,,,congenital prothrombin deficiency,,,,, -14104596,45,,treats,,Ibuprofen,,,,Abdominal pain,,,,, -14738368,46,,treats,,Ibuprofen,,,,thrombocytopenia,,,,, -10868694,47,,treats,,Ibuprofen,,,,Shock,,,,, -14738366,48,,treats,,Ibuprofen,,,,Hyponatremia,,,,, -14738367,49,,treats,,Ibuprofen,,,,kidney failure,,,,, diff --git a/data/updated_neo4j_sentence_data.csv b/data/updated_neo4j_sentence_data.csv deleted file mode 100644 index c9b87fa..0000000 --- a/data/updated_neo4j_sentence_data.csv +++ /dev/null @@ -1,103 +0,0 @@ -546,,,,,"Veterinary anthelmintic. Fenbendazole is a fda approved for use in cattle, pigs and goats Fenbendazole (Hoechst brand names Panacur and Safe-Guard, Intervet Panacur and Panacur Rabbit) is a broad spectrum benzimidazole anthelmintic used against gastrointestinal parasites including roundworms, hookworms, whipworms, the taenia species of tapeworms, pinworms, aelurostrongylus, paragonimiasis, strongyles and strongyloides and can be administered to sheep, cattle, horses, fish, dogs, cats, rabbits and seals. Drug interactions may occur if using bromsalan flukicides (Dibromsalan, Tribromsalan). Abortions in cattle and death in sheep have been reported after using these medications together. (Plumb's Veterinary Drug Handbook, Fifth Edition. 2005",,,, -549,,,,,"A benzimidazole derivative with anthelminthic property. Although the mechanism of action has not been fully elucidated, thiabendazole inhibits the helminth-specific mitochondrial enzyme fumarate reductase, thereby inhibiting the citric acid cycle, mitochondrial respiration and subsequent production of ATP, ultimately leading to helminth's death. In addition, it has been suggested that thiabendazole may lead to inhibition of microtubule polymerization by binding to beta-tubulin and has an overt ovicidal effect with regard to some trichostrongylids. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C873"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C873"" NCI Thesaurus); A benzimidazole derivative with anthelminthic property. Although the mechanism of action has not been fully elucidated, thiabendazole inhibits the helminth-specific mitochondrial enzyme fumarate reductase, thereby inhibiting the citric acid cycle, mitochondrial respiration and subsequent production of ATP, ultimately leading to helminth's death. In addition, it has been suggested that thiabendazole may lead to inhibition of microtubule polymerization by binding to beta-tubulin and has an overt ovicidal effect with regard to some trichostrongylids.; 2-Substituted benzimidazole first introduced in 1962. It is active against a variety of nematodes and is the drug of choice for STRONGYLOIDIASIS. It has CENTRAL NERVOUS SYSTEM side effects and hepatototoxic potential. (From Smith and Reynard, Textbook of Pharmacology, 1992, p919); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -551,,,,,"A broad-spectrum, synthetic benzimidazole-derivative anthelmintic. Albendazole interferes with the reproduction and survival of helminths by inhibiting the formation of microtubules from tubulin. This leads to an impaired uptake of glucose, a depletion of glycogen stores, and results in the worm's death. Albendazole is used in the treatment of dog and pork tapeworm-causing diseases, including hydatid disease and neurocysticercosis. Albendazole may also be used to treat a variety of other roundworm infections. (NCI05); A benzimidazole broad-spectrum anthelmintic structurally related to MEBENDAZOLE that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -553,,,,,"A semisynthetic oxa-beta-lactam antibiotic, with antibacterial activity used mainly against gram-negative aerobic bacteria. Replacing the beta-lactam sulfur atom for an oxygen atom and the presence of the methyltetrazolethio moiety and the para-hydroxyphenylmalonyl group, increases the antibacterial activity of moxalactam. The 7-alpha-methoxy group and the para-hydroxyphenylmalonyl group increases the stability of this agent against beta-lactamases. The use of this agent has been associated with fatal bleeding events.; A parenteral oxacephem antibiotic with an oxygen molecule substituted for the sulfur atom in the beta-lactam nucleus. Moxalactam is a thrid-generation cephalosporin that has broad-spectrum antibiotic activity and high resistance to beta-lactameses. This agent is active against gram-negative enteric bacilli, including multiple drug-resistant strains.; Broad- spectrum beta-lactam antibiotic similar in structure to the CEPHALOSPORINS except for the substitution of an oxaazabicyclo moiety for the thiaazabicyclo moiety of certain CEPHALOSPORINS. It has been proposed especially for the meningitides because it passes the blood-brain barrier and for anaerobic infections.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",,,, -554,,,,,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]",,,, -556,,,,,"A third-generation, semi-synthetic, beta-lactam cephalosporin antibiotic with antibacterial activity. Cefmenoxime binds to penicillin-binding proteins (PBPs), transpeptidases that are responsible for crosslinking of peptidoglycan. By preventing crosslinking of peptidoglycan, cell wall integrity is lost and cell wall synthesis is halted.; A cephalosporin antibiotic that is administered intravenously or intramuscularly. It is active against most common gram-positive and gram-negative microorganisms, is a potent inhibitor of Enterobacteriaceae, and is highly resistant to hydrolysis by beta-lactamases. The drug has a high rate of efficacy in many types of infection and to date no severe side effects have been noted.",,,, -557,,,,,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age[Label]. Ivabradine acts by selectively inhibiting the ""funny"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a ""pure"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects.",,,, -558,,,,,"A broad-spectrum, third-generation cephalosporin antibiotic derived semisynthetically from the marine fungus Cephalosporium acremonium with antibacterial activity. As does penicillin, the beta-lactam antibiotic cefixime inhibits bacterial cell wall synthesis by disrupting peptidoglycan synthesis, resulting in a reduction in bacterial cell wall stability and bacterial cell lysis. Stable in the presence of a variety of beta-lactamases, this agent is more active against gram-negative bacteria and less active against gram-positive bacteria compared to second-generation cephalosporins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1100"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1100"" NCI Thesaurus); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",,,, -559,,,,,"A semisynthetic, broad-spectrum, beta-lactamase-resistant, third-generation cephalosporin with antibacterial activity. Ceftizoxime binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",,,, -560,,,,,"An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C76590"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C76590"" NCI Thesaurus); An orally available small molecule compound with anti-ischemic, and potential immunomodulating and antineoplastic properties. Although its exact mechanism is not yet fully elucidated, it is postulated that upon administration, trimetazidine selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT), the final enzyme in the free fatty acid (FFA) beta-oxidation pathway. This stimulates glucose oxidation, which requires less oxygen usage and cellular energy than in the beta-oxidation process. This optimizes myocardial energy metabolism and cardiac functioning in an ischemic condition. In cancer cells, the inhibition of fatty acid oxidation (FAO) alters the metabolic processes needed for tumor cell function and proliferation, thereby inducing tumor cell apoptosis. In addition, inhibition of FAO may potentially block the immunosuppressive functions of myeloid-derived suppressor cells (MSDCs), which are thought to promote malignant cell proliferation and migration by inhibiting T-cell function.; A vasodilator used in angina of effort or ischemic heart disease.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -561,,,,,"A cephalosporin compound having 5-(carboxymethyl)-4-methyl-1,3-thiazol-2-yl]sulfanyl}methyl and [2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetyl]amino side groups located at positions 3 and 7 respectively.",,,, -562,,,,,"A 5-aminoimidazole-4-carboxamide (AICA) riboside, a purine nucleoside analog, and a nucleotide biosynthesis precursor with B cell pro-apoptotic activity. Following cellular uptake, acadesine is phosphorylated to AICA ribotide (ZMP), which mimics 5'-adenosine monophosphate (AMP). Both AMP-activated protein kinase (AMPK) and AMPK kinase (AMPKK) are activated by ZMP, which appears to be necessary for the induction of apoptosis. Acadesine-induced apoptosis also appears to require cytochrome c release from mitochondria and caspase activation and is p53-independent. However, the exact mechanism of acadesine-induced apoptosis is unknown. T cells are significantly less susceptible than B cells to acadesine-induced apoptosis. AMPK regulates several cellular systems including the cellular uptake of glucose, the beta-oxidation of fatty acids, protein synthesis, and the biogenesis of glucose transporter 4 (GLUT4) and mitochondria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C71537"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C71537"" NCI Thesaurus); A 5-aminoimidazole-4-carboxamide (AICA) riboside, a ribnucleoside analog, and a nucleotide biosynthesis precursor with B cell pro-apoptotic activity. Following cellular uptake, acadesine is phosphorylated to AICA ribotide (ZMP), which mimics 5'-adenosine monophosphate (AMP). Both AMP-activated protein kinase (AMPK) and AMPK kinase (AMPKK) are activated by ZMP, which appears to be necessary for the induction of apoptosis. Acadesine-induced apoptosis also appears to require cytochrome c release from mitochondria and caspase activation and is p53-independent. However, the exact mechanism of acadesine-induced apoptosis is unknown. T cells are significantly less susceptible than B cells to acadesine-induced apoptosis. AMPK regulates several cellular systems including the cellular uptake of glucose, the beta-oxidation of fatty acids, protein synthesis, and the biogenesis of glucose transporter 4 (GLUT4) and mitochondria.",,,, -567,,,,,"Ranolazine is only found in individuals that have used or taken this drug. It is an antianginal medication. On January 31, 2006, ranolazine was approved for use in the United States by the FDA for the treatment of chronic angina. [Wikipedia]The mechanism of action of ranolazine is unknown. It does not increase the rate-pressure product, a measure of myocardial work, at maximal exercise. In vitro studies suggest that ranolazine is a P-gp inhibitor. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.",,,, -568,,,,,"Prednisolone is only found in individuals that have used or taken this drug. It is a glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",,,, -569,,,,,"Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",,,, -570,,,,,"Methylprednisolone is only found in individuals that have used or taken this drug. It is a prednisolone derivative with similar anti-inflammatory action. [PubChem]Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors, modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.",,,, -576,,,,,"A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C354"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C354"" NCI Thesaurus); A third generation semisynthetic cephalosporin antibiotic with bactericidal activity. Cefotaxime inhibits mucopeptide synthesis by binding to and inactivating penicillin binding proteins thereby interfering with the final transpeptidation step required for cross-linking of peptidoglycan units which are a component of bacterial cell walls. This results in a reduction of cell wall stability and causes cell lysis.; Semisynthetic broad-spectrum cephalosporin.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",,,, -578,,,,,"The sodium salt form of ceftriaxone, a beta-lactam, third-generation cephalosporin antibiotic with bactericidal activity. Ceftriaxone binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to the second and first generation cephalosporins, ceftriaxone is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftriaxone also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS). Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C817"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C817"" NCI Thesaurus); The sodium salt form of ceftriaxone, a beta-lactam, third-generation cephalosporin antibiotic with bactericidal activity. Ceftriaxone binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Compared to the second and first generation cephalosporins, ceftriaxone is more active against gram-negative bacteria and less active against gram-positive bacteria. Ceftriaxone also crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system (CNS).; A broad-spectrum cephalosporin antibiotic and cefotaxime derivative with a very long half-life and high penetrability to meninges, eyes and inner ears.",,,, -589,,,,,A water insoluble terpene fatty acid used in the treatment of gastrointestinal ulcers; it facilitates the healing and function of mucosal tissue.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109,,,, -590,,,,,"An adenosine derivative and selective A2A adenosine receptor agonist with coronary vasodilating activity. Upon administration, regadenoson selectively binds to and activates the A2A adenosine receptor, which induces coronary vasodilation. This leads to an increase in coronary blood flow and enhances myocardial perfusion. Compared to adenosine, regadenoson has a longer half-life and shows higher selectivity towards the A2A adenosine receptor. This agent is a very weak agonist for the A1 adenosine receptor and has negligible affinity for the A2B and A3 adenosine receptors. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C74420"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C74420"" NCI Thesaurus); An adenosine derivative and selective A2A adenosine receptor agonist with coronary vasodilating activity. Upon administration, regadenoson selectively binds to and activates the A2A adenosine receptor, which induces coronary vasodilation. This leads to an increase in coronary blood flow and enhances myocardial perfusion. Compared to adenosine, regadenoson has a longer half-life and shows higher selectivity towards the A2A adenosine receptor. This agent is a very weak agonist for the A1 adenosine receptor and has negligible affinity for the A2B and A3 adenosine receptors.",,,, -593,,,,,"An ammonium betaine that is beta-alaninate in which one of the amino hydrogens is replaced by a trimethylamino group. A clinically used cardioprotective drug that is used for treatment of heart failure, myocardial infarction, arrhythmia, atherosclerosis and diabetes.",,,, -603,,,,,"A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C683"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C683"" NCI Thesaurus); A broad spectrum aminoglycoside antibiotic derived from Streptomyces fradiae with antibacterial activity. Neomycin is an antibiotic complex consisting of 3 components: the two isomeric components B and C are the active components, and neomycin A is the minor component. Neomycin irreversibly binds to the 16S rRNA and S12 protein of the bacterial 30S ribosomal subunit. As a result, this agent interferes with the assembly of initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. In addition, neomycin induces misreading of the mRNA template and causes translational frameshift, thereby results in premature termination. This eventually leads to bacterial cell death.; Aminoglycoside antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C, and acts by inhibiting translation during protein synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",,,, -612,,,,,"A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab posesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C62528"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C62528"" NCI Thesaurus); A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab possesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116",,,, -616,,,,,"A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C375"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C375"" NCI Thesaurus); A synthetic broad spectrum fluoroquinolone antibiotic. Ciprofloxacin binds to and inhibits bacterial DNA gyrase, an enzyme essential for DNA replication. This agent is more active against Gram-negative bacteria than Gram-positive bacteria. (NCI04); A broad-spectrum antimicrobial carboxyfluoroquinoline.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -617,,,,,"A semisynthetic, broad-spectrum antibiotic derived from Streptomyces venequelae with primarily bacteriostatic activity. Chloramphenicol diffuses through the bacterial cell wall and reversibly binds to the bacterial 50S ribosomal subunit. The binding interferes with peptidyl transferase activity, thereby prevents transfer of amino acids to the growing peptide chains and blocks peptide bond formation. As a result bacterial protein synthesis is blocked and impede bacterial cell proliferation.; An antibiotic first isolated from cultures of Streptomyces venequelae in 1947 but now produced synthetically. It has a relatively simple structure and was the first broad-spectrum antibiotic to be discovered. It acts by interfering with bacterial protein synthesis and is mainly bacteriostatic. (From Martindale, The Extra Pharmacopoeia, 29th ed, p106); UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",,,, -618,,,,,"A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29852"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29852"" NCI Thesaurus); A quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.",,,, -619,,,,,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. It is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse.",,,, -622,,,,,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T116; Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment [L1737]. The U.S. Food and Drug Administration approved Adcetris in March 2018 to treat adult patients with previously untreated stage III or IV classical Hodgkin lymphoma (cHL) in combination with chemotherapy [L1737]. Adcetris has also been previously approved by the FDA to treat Hodgkin's lymphoma after relapse, Hodgkin's lymphoma after stem cell transplantation when a patient has a high risk of relapse or progression, systemic anaplastic large cell lymphoma (ALCL) after the failure of other treatment regimens, and primary cutaneous ALCL after failure of other treatment regimens [L1737]. Lymphoma is a malignancy that begins in the lymphatic system, which helps to combat infection and disease. Lymphoma may begin anywhere in the body and can spread to nearby lymph nodes. The two main types of lymphoma are Hodgkin lymphoma (also called Hodgkin disease) and non-Hodgkin lymphoma. Most individuals with Hodgkin's lymphoma have the classical type. In this type of lymphoma, large, abnormal lymphocytes (a type of white blood cell) are found in the lymph nodes called Reed-Sternberg cells. With early diagnosis and intervention, patients with Hodgkin lymphoma normally experience long-term remission [L1737]. The ECHELON-1 study results demonstrated superior efficacy of the drug combined with a chemotherapy regimen when it is compared to the previous standard of care. Importantly, removing the drug bleomycin, a highly toxic agent, was completely removed from the regimen. This demonstrates meaningful progress in treatment for patients affected by this disease [L1739].",,,, -628,,,,,UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. The FDA withdrew its approval for the use of all liquid oral drug products formulated for pediatric use containing tetracycline in a concentration greater than 25 mg/ml.[L43942] Other formulations of tetracycline continue to be used.,,,, -629,,,,,"UMLS Semantic Type: STY:T122; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Alginic acid, also referred to as algin or alginate, is a hydrophilic or anionic polysaccharide isolated from certain brown seaweed (_Phacophycae_) via alkaline extraction. It is present in cell walls of brown algae where it forms a viscous gel when binding with water. Alginic acid is a linear polymer consisted of L-glucuronic acid and D-mannuronic acid residues connected via 1,4-glycosidic linkages [A32961]. Available in different types of salt, alginic acid has been used in a variety of uses in food, cosmetics and pharmaceu-tical products for over 100 years [A32961]. Alginic acid is an FDA-approved food ingredient in soup and soup mixes as an emulsifier, thickener, and stabilizer [L2693]. It is also available in oral dietary supplements and is found in antacids such as Gaviscon to inhibit gastroesophageal reflux by creating a physical barrier in presence of gastric acid [F46]. Alginate-based raft-forming formulations in the management of heartburn and gastric acid reflux have been used worldwide for over 30 years [A32961].",,,, -635,,,,,ZOLIMIDINE; FULL_MW:272.33; MAX_FDA_APPROVAL_PHASE: -1.0,,,, -638,,,,,"A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C364"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C364"" NCI Thesaurus); A biguanide compound used as an antiseptic agent with topical antibacterial activity. Chlorhexidine is positively charged and reacts with the negatively charged microbial cell surface, thereby destroying the integrity of the cell membrane. Subsequently, chlorhexidine penetrates into the cell and causes leakage of intracellular components leading to cell death. Since gram positive bacteria are more negatively charged, they are more sensitive to this agent.; A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -630,,,,,"A mixture of the polypeptides polymyxins B1 and B2, both obtained from Bacillus polymyxa strains, with antimicrobial activity. Polymyxin B exerts its antimicrobial effect through its cationic detergent action on cell membranes. Specifically, this antibiotic binds to the negatively charged site in the lipopolysaccharide layer of the bacterial cell membrane via electrostatic affinity with the positively charged amino groups in the cyclic peptide portion. Subsequently, the fatty acid portion of polymyxin B dissolves in the hydrophobic region of the bacterial cell membrane. This results in an alteration in cell membrane structure, disruption of cell wall integrity and an increase in permeability for water and molecules. This will eventually lead to bacterial cell death. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C61894"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C61894"" NCI Thesaurus); A mixture of the polypeptides polymyxins B1 and B2, both obtained from Bacillus polymyxa strains, with antimicrobial activity. Polymyxin B exerts its antimicrobial effect through its cationic detergent action on cell membranes. Specifically, this antibiotic binds to the negatively charged site in the lipopolysaccharide layer of the bacterial cell membrane via electrostatic affinity with the positively charged amino groups in the cyclic peptide portion. Subsequently, the fatty acid portion of polymyxin B dissolves in the hydrophobic region of the bacterial cell membrane. This results in an alteration in cell membrane structure, disruption of cell wall integrity and an increase in permeability for water and molecules. This will eventually lead to bacterial cell death.; A mixture of polymyxins B1 and B2, obtained from BACILLUS POLYMYXA strains. They are basic polypeptides of about eight amino acids and have cationic detergent action on cell membranes. Polymyxin B is used for treatment of infections with gram-negative bacteria, but may be neurotoxic and nephrotoxic.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T116",,,, -706,,,,,"Benzoyl peroxide is found in cereals and cereal products. Added to bread and cheese as bleaching agent Benzoyl peroxide is an organic compound in the organic peroxide family. It consists of two benzoyl groups joined by a peroxide group. Its structural formula is [C6H5-C(O)]2O2. It is one of the most important organic peroxides in terms of applications and the scale of its production. Benzoyl peroxide is used as an acne treatment, for improving flour, for bleaching hair and teeth, for polymerising polyester and many other uses. In the U. S., the typical concentration for benzoyl peroxide is 2.5% to 10% for both prescription and over the counter preparations that are used in treatment for acne. Higher concentrations are used for hair bleach and teeth whitening. Benzoyl peroxide, like most peroxides, is a powerful bleaching agent. Contact with fabrics or hair can cause permanent color dampening almost immediately. Even secondary contact can cause bleaching. For example, contact with a towel that has been used to wash off benzoyl peroxide-containing hygiene products.[citation needed",,,, -710,,,,,"An antimuscarinic agent that inhibits gastric secretion at lower doses than are required to affect gastrointestinal motility, salivary, central nervous system, cardiovascular, ocular, and urinary function. It promotes the healing of duodenal ulcers and due to its cytoprotective action is beneficial in the prevention of duodenal ulcer recurrence. It also potentiates the effect of other antiulcer agents such as CIMETIDINE and RANITIDINE. It is generally well tolerated by patients.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -767,,,,,"A difluorophenyl derivate of salicylic acid and a nonsteroidal anti-inflammatory drug (NSAID) with antipyretic, analgesic and anti-inflammatory properties. Diflunisal competitively inhibits both cyclooxygenase (COX) -1 and -2, with higher affinity for COX-1, and subsequently blocks the conversion of arachidonic acid to prostaglandin precursors. This leads to an inhibition of the formation of prostaglandins that are involved in pain, inflammation and fever. Diflunisal differs from other salicylates, in that it is not metabolized to salicylic acid, hence it has a longer half-life. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C47489"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C47489"" NCI Thesaurus); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -774,,,,,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Salsalate is a nonsteroidal anti-inflammatory agent for oral administration. Salsalate's mode of action as an anti-inflammatory and antirheumatic agent may be due to inhibition of synthesis and release of prostaglandins. The usefulness of salicylic acid, the active in vivo product of salsalate, in the treatment of arthritic disorders has been established. In contrast to aspirin, salsalate causes no greater fecal gastrointestinal blood loss than placebo. Salsalate is readily soluble in the small intestine where it is partially hydrolyzed to two molecules of salicylic acid. A significant portion of the parent compound is absorbed unchanged and undergoes rapid esterase hydrolysis in the body. The parent compound has an elimination half-life of about 1 hour. Salicylic acid (the active metabolite) biotransformation is saturated at anti-inflammatory doses of salsalate. Such capacity limited biotransformation results in an increase in the half-life of salicylic acid from 3.5 to 16 or more hours.",,,, -797,,,,,"An orally administered, semi-synthetic, nonsystemic antibiotic derived from rifamycin SV with antibacterial activity. Rifaximin binds to the beta-subunit of bacterial DNA-dependent RNA polymerase, inhibiting bacterial RNA synthesis and bacterial cell growth. As rifaximin is not well absorbed, its antibacterial activity is largely localized to the gastrointestinal tract. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C61926"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C61926"" NCI Thesaurus); An orally administered, semi-synthetic, nonsystemic antibiotic derived from rifamycin SV with antibacterial activity. Rifaximin binds to the beta-subunit of bacterial DNA-dependent RNA polymerase, inhibiting bacterial RNA synthesis and bacterial cell growth. As rifaximin is not well absorbed, its antibacterial activity is largely localized to the gastrointestinal tract.; A synthetic rifamycin derivative and anti-bacterial agent that is used for the treatment of GASTROENTERITIS caused by ESCHERICHIA COLI INFECTIONS. It may also be used in the treatment of HEPATIC ENCEPHALOPATHY.",,,, -839,,,,,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Atropine is an alkaloid originally synthesized from Atropa belladonna. It is a racemic mixture of d-and l-hyoscyamine, of which only l-hyoscyamine is pharmacologically active.[A251670,L42835] Atropine is generally available as a sulfate salt and can be administered by intravenous, subcutaneous, intramuscular, intraosseous, endotracheal and ophthalmic methods. Oral atropine is only available in combination products.[A251660,L42840] Atropine is a competitive, reversible antagonist of muscarinic receptors that blocks the effects of acetylcholine and other choline esters.[A251660,L42815,L42825,L42835] It has a variety of therapeutic applications, including pupil dilation and the treatment of anticholinergic poisoning and symptomatic bradycardia in the absence of reversible causes.[A251660] Atropine is a relatively inexpensive drug and is included in the World Health Organization List of Essential Medicines.[A251675]",,,, -880,,,,,"A small molecule inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) with potential chemosensitizing, radiosensitizing, and antineoplastic activities. Olaparib selectively binds to and inhibits PARP, inhibiting PARP-mediated repair of single strand DNA breaks; PARP inhibition may enhance the cytotoxicity of DNA-damaging agents and may reverse tumor cell chemoresistance and radioresistance.PARP catalyzes post-translational ADP-ribosylation of nuclear proteins and can be activated by single-stranded DNA breaks. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C71721"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C71721"" NCI Thesaurus); A small molecule inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) with potential chemosensitizing, radiosensitizing, and antineoplastic activities. Olaparib selectively binds to and inhibits PARP, inhibiting PARP-mediated repair of single strand DNA breaks; PARP inhibition may enhance the cytotoxicity of DNA-damaging agents and may reverse tumor cell chemoresistance and radioresistance. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins and can be activated by single-stranded DNA breaks.",,,, -1066,,,,,"A naturally-occurring retinoic acid with potential antineoplastic activity. Isotretinoin binds to and activates nuclear retinoic acid receptors (RARs); activated RARs serve as transcription factors that promote cell differentiation and apoptosis. This agent also exhibits immunomodulatory and anti-inflammatory responses and inhibits ornithine decarboxylase, thereby decreasing polyamine synthesis and keratinization. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C603"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C603"" NCI Thesaurus); An orally- and topically-active naturally-occurring retinoic acid with antineoplastic, chemopreventive, teratogenic, and embryotoxic activities. Alitretinoin binds to and activates nuclear retinoic acid receptors (RAR) and retinoid X receptors (RXR); these activated receptors act as transcription factors, regulating gene expression that results in the inhibition of cell proliferation, induction of cell differentiation, and apoptosis of both normal cells and tumor cells. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1574"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1574"" NCI Thesaurus); An orally- and topically-active naturally-occurring retinoic acid with antineoplastic, chemopreventive, teratogenic, and embryotoxic activities. Alitretinoin binds to and activates nuclear retinoic acid receptors (RAR) and retinoid X receptors (RXR); these activated receptors act as transcription factors, regulating gene expression that results in the inhibition of cell proliferation, induction of cell differentiation, and apoptosis of both normal cells and tumor cells.; A naturally-occurring retinoic acid with potential antineoplastic activity. Isotretinoin binds to and activates nuclear retinoic acid receptors (RARs); activated RARs serve as transcription factors that promote cell differentiation and apoptosis. This agent also exhibits immunomodulatory and anti-inflammatory responses and inhibits ornithine decarboxylase, thereby decreasing polyamine synthesis and keratinization.; A topical dermatologic agent that is used in the treatment of ACNE VULGARIS and several other skin diseases. The drug has teratogenic and other adverse effects.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -1090,,,,,"Nelfinavir is only found in individuals that have used or taken this drug. It is a potent HIV-1 protease inhibitor. It is used in combination with other antiviral drugs in the treatment of HIV in both adults and children. [PubChem]Nelfinavir inhibits the HIV viral proteinase enzyme which prevents cleavage of the gag-pol polyprotein, resulting in noninfectious, immature viral particles.",,,, -1179,,,,,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Moxisylyte, denominated as thymoxamine in the UK, is a specific and orally active α1-adrenergic antagonist.[T45] According to the WHO, moxisylyte is approved since 1987[T91] and in the same year, it acquired the denomination of orphan product by the FDA.[L1172] This drug was developed by the Japanese company Fujirebio and also by the American company Iolab in the late 80s.",,,, -1261,,,,,"An organic nitrate with vasodilator activity. Nitroglycerin is converted into nitric oxide (NO) in smooth muscle and activates guanylyl cyclase, thereby increasing cGMP concentration, and resulting in smooth muscle relaxation. Dilatation of the veins results in decreased venous return to the heart, thereby decreasing left ventricular volume (reduced preload) and decreasing myocardial oxygen requirements. Arteriolar relaxation reduces arteriolar resistance (reduced afterload), thereby decreasing myocardial oxygen demands. In addition, nitroglycerin causes coronary artery dilatation, thereby improving myocardial blood distribution. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C29294"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C29294"" NCI Thesaurus); An organic nitrate with vasodilator activity. Nitroglycerin is converted into nitric oxide (NO) in smooth muscle and activates guanylyl cyclase, thereby increasing cGMP concentration, and resulting in smooth muscle relaxation. Dilatation of the veins results in decreased venous return to the heart, thereby decreasing left ventricular volume (reduced preload) and decreasing myocardial oxygen requirements. Arteriolar relaxation reduces arteriolar resistance (reduced afterload), thereby decreasing myocardial oxygen demands. In addition, nitroglycerine causes coronary artery dilatation, thereby improving myocardial blood distribution.; A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -1362,,,,,"Cefazolin is only found in individuals that have used or taken this drug. It is a semisynthetic cephalosporin analog with broad-spectrum antibiotic action due to inhibition of bacterial cell wall synthesis. It attains high serum levels and is excreted quickly via the urine. [PubChem]In vitro tests demonstrate that the bactericidal action of cephalosporins results from inhibition of cell wall synthesis. By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, it inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins.",,,, -1363,,,,,"A semisynthetic, beta-lactam, first-generation cephalosporin antibiotic with bactericidal activity. Cephalothin binds to and inactivates penicillin-binding proteins (PBP) located on the inner membrane of the bacterial cell wall. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.; A cephalosporin antibiotic.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",,,, -1394,,,,,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Valaciclovir (valacyclovir), also known as _Valtrex_, is an antiviral drug that has been used to manage and treat various herpes infections for more than 2 decades. It was initially approved by the FDA in 1995 [FDA label] and marketed by GlaxoSmithKline [L5671]. Valacyclovir is the L-valine ester of aciclovir. It is a member of the purine (guanine) nucleoside analog drug class [F3949]. This class of drugs forms an important part of hepatitis, HIV, and cytomegalovirus drug regimens [A175900]. One major use of valacyclovir is the treatment of genital herpes episodes or outbreaks. Genital herpes is a frequently diagnosed sexually transmitted disease which currently affects more than 400 million individuals worldwide. It is caused by infection with the herpes simplex virus (HSV). Infection with this virus is lifelong with periodic episodes of reactivation [A175903].",,,, -1417,,,,,"A fluorinated isopropyl ether with general anesthetic activity. Although the mechanism of action has not been fully elucidated, sevoflurane may interfere with the release and re-uptake of neurotransmitters at post-synaptic terminals, and/or alter ionic conductance following receptor activation by a neurotransmitter. This agent may also interact directly with the lipid matrix of neuronal membranes, thereby affecting gating properties of ion channels. In addition, sevoflurane may activate gamma-aminobutyric acid (GABA) receptors, hyperpolarizing cell membranes and resulting in a general anesthetic effect, a decrease in myocardial contractility and mean arterial pressure, and an increased respiratory rate. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C47717"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C47717"" NCI Thesaurus); A fluorinated isopropyl ether with general anesthetic property. Although the mechanism of action has not been fully elucidated, sevoflurane may act by interfering with the release and re-uptake of neurotransmitters at post-synaptic terminals, and/or alter ionic conductance following receptor activation by a neurotransmitter. Sevoflurane may also interact directly with lipid matrix of neuronal membranes, thereby affecting gating properties of ion channels. In addition, this agent may activate gamma-aminobutyric acid (GABA) receptors hyperpolarizing cell membranes. This results in a general anesthetic effect, a decrease in myocardial contractility and mean arterial pressure as well as an increased respiratory rate.; A non-explosive inhalation anesthetic used in the induction and maintenance of general anesthesia. It does not cause respiratory irritation and may also prevent PLATELET AGGREGATION.",,,, -1430,,,,,"An inorganic compound containing aluminum. Used in various immunologic preparations to improve immunogenicity, aluminum hydroxide adjuvant consists of aluminum hydroxide gel in a saline solution. In vaccines, this agent binds to the protein conjugate, resulting in improved antigen processing by the immune system. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C39707"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C39707"" NCI Thesaurus); An inorganic compound containing aluminum. Used in various immunologic preparations to improve immunogenicity, aluminum hydroxide adjuvant consists of aluminum hydroxide gel in a saline solution. In vaccines, this agent binds to the protein conjugate, resulting in improved antigen processing by the immune system. (NCI04); A compound with many biomedical applications: as a gastric antacid, an antiperspirant, in dentifrices, as an emulsifier, as an adjuvant in bacterins and vaccines, in water purification, etc.; UMLS Semantic Type: STY:T197; UMLS Semantic Type: STY:T121",,,, -1457,,,,,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T129; UMLS Semantic Type: STY:T125; UMLS Semantic Type: STY:T116; Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously.",,,, -1500,,,,,"An orally available competitive inhibitor of sodium-glucose co-transporter 2 (SGLT2; SLC5A2) with antihyperglycemic activity. Upon oral administration, empagliflozin selectively and potently inhibits SGLT2 in the kidneys, thereby suppressing the reabsorption of glucose in the proximal tubule. Inhibition of SGLT2 increases urinary glucose excretion by the kidneys, resulting in a reduction of plasma glucose levels in an insulin-independent manner. Inhibition of SGLT2 in the kidneys also suppresses the renal reabsorption of 1,5-anhydroglucitol (1,5AG). This lowers serum 1,5AG and neutrophil 1,5-anhydroglucitol-6-phosphate (1,5AG6P) levels, which may improve neutropenia and neutrophil dysfunction in patients with glycogen storage disease type Ib (GSD Ib). SGLT2, a transport protein exclusively expressed in the proximal renal tubules, mediates approximately 90% of renal glucose reabsorption from tubular fluid.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -1505,,,,,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Dapagliflozin is a sodium-glucose cotransporter 2 inhibitor indicated for managing diabetes mellitus type 2.[A6757] When combined with diet and exercise in adults, dapagliflozin helps to improve glycemic control by inhibiting glucose reabsorption in the proximal tubule of the nephron and causing glycosuria.[A6757] Dapagliflozin was approved by the FDA on Jan 08, 2014.[L6034]",,,, -1506,,,,,"Methyldopa or alpha-methyldopa (brand names Aldomet, Apo-Methyldopa, Dopamet, Novomedopa) is a centrally-acting adrenergic antihypertensive medication. Its use is now deprecated following introduction of alternative safer classes of agents. However it continues to have a role in otherwise difficult to treat hypertension and gestational hypertension (formerly known as pregnancy-induced hypertension). Methyldopa is an aromatic-amino-acid decarboxylase inhibitor in animals and in man. Only methyldopa, the L-isomer of alpha-methyldopa, has the ability to inhibit dopa decarboxylase and to deplete animal tissues of norepinephrine. In man the antihypertensive activity appears to be due solely to the L-isomer. About twice the dose of the racemate (DL-alpha-methyldopa) is required for equal antihypertensive effect. Methyldopa has no direct effect on cardiac function and usually does not reduce glomerular filtration rate, renal blood flow, or filtration fraction. Cardiac output usually is maintained without cardiac acceleration. In some patients the heart rate is slowed. Normal or elevated plasma renin activity may decrease in the course of methyldopa therapy. Methyldopa reduces both supine and standing blood pressure. Methyldopa usually produces highly effective lowering of the supine pressure with infrequent symptomatic postural hypotension. Exercise hypotension and diurnal blood pressure variations rarely occur. Methyldopa, in its active metabolite form, is a central alpha-2 receptor agonist. Using methyldopa leads to alpha-2 receptor-negative feedback to sympathetic nervous system (SNS) (centrally and peripherally), allowing peripheral sympathetic nervous system tone to decrease. Such activity leads to a decrease in total peripheral resistance (TPR) and cardiac output. When introduced it was a mainstay of antihypertensive therapy, but its use has declined, with increased use of other safer classes of agents. One of its important present-day uses is in the management of pregnancy-induced hypertension, as it is relatively safe in pregnancy compared to other antihypertensive drugs (Wikipedia).",,,, -1538,,,,,"A synthetic 4-azasteroid compound. Finasteride competitively binds to and inhibits steroid type II 5-alpha-reductase in the prostate gland, liver, and skin, thereby interfering with the enzymatic conversion of testosterone to 5-dihydrotestosterone (DHT) and reducing serum DHT levels. The reduction in serum DHT levels results in diminished stimulation of androgen receptors in the nuclei of prostate cells and, so, diminished prostate cell proliferation. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1099"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1099"" NCI Thesaurus); A synthetic 4-azasteroid compound. Finasteride competitively binds to and inhibits steroid type II 5-alpha-reductase in the prostate gland, liver, and skin, thereby interfering with the enzymatic conversion of testosterone to 5-dihydrotestosterone (DHT) and reducing serum DHT levels. The reduction in serum DHT levels results in diminished stimulation of androgen receptors in the nuclei of prostate cells and, so, diminished prostate cell proliferation.; An orally active 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE inhibitor. It is used as a surgical alternative for treatment of benign PROSTATIC HYPERPLASIA.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T125; UMLS Semantic Type: STY:T109",,,, -1659,,,,,"In the United States, glucosamine is not approved by the Food and Drug Administration for medical use in humans. Since glucosamine is classified as a dietary supplement, evidence of safety and efficacy is not required as long as it is not advertised as a treatment for a medical condition. Nevertheless, glucosamine is a popular alternative medicine used by consumers for the treatment of osteoarthritis. Glucosamine is also extensively used in veterinary medicine as an unregulated but widely accepted supplement (Nolen RS, 2002). Treatment with oral glucosamine is commonly used for the treatment of osteoarthritis. Since glucosamine is a precursor for glycosaminoglycans, and glycosaminoglycans are a major component of joint cartilage, supplemental glucosamine may help to rebuild cartilage and treat arthritis. However, there is little evidence that any clinical effect of glucosamine works this way (Laverty et al., 2005; Biggee et al., 2005). Its use as a therapy for osteoarthritis appears safe but there is conflicting evidence as to its effectiveness. Glucosamine (C6H14NO5) is an amino sugar that is an important precursor in the biochemical synthesis of glycosylated proteins and lipids.",,,, -1715,,,,,"Candesartan is an angiotensin-receptor blocker (ARB) that may be used alone or with other agents to treat hypertension. It is administered orally as the prodrug, candesartan cilexetil, which is rapidly converted to its active metabolite, candesartan, during absorption in the gastrointestinal tract. Candesartan lowers blood pressure by antagonizing the renin-angiotensin-aldosterone system (RAAS); it competes with angiotensin II for binding to the type-1 angiotensin II receptor (AT1) subtype and prevents the blood pressure increasing effects of angiotensin II. Unlike angiotensin-converting enzyme (ACE) inhibitors, ARBs do not have the adverse effect of dry cough. Candesartan may be used to treat hypertension, isolated systolic hypertension, left ventricular hypertrophy and diabetic nephropathy. It may also be used as an alternative agent for the treatment of heart failure, systolic dysfunction, myocardial infarction and coronary artery disease.",,,, -1721,,,,,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Losartan is an angiotensin II receptor blocker (ARB) used to treat hypertension.[L7423] Angiotensin-converting enzyme (ACE) inhibitors are used for a similar indication but are associated with a cough.[L7423] When patients with ACE inhibitor associated coughs are switched to ARBs like losartan, they have an incidence of cough similar to placebo or [hydrochlorothiazide].[L7423] Losartan is available as losartan potassium oral tablets as well as a combination tablet of losartan potassium and hydrochlorothiazide.[L7423,L7426] Patients taking losartan should have their renal function and potassium levels monitored.[L7423] Losartan was granted FDA approval on 14 April 1995.[L7423]",,,, -1728,,,,,"An isomer of tetrahydrocannabinol (THC) that is the main and most active isomer found in the cannabis sativa L. plant, with potential anti-emetic, analgesic and appetite stimulating activities. Upon administration, dronabinol, also called delta-9-THC, targets and binds to cannabinoid receptors (CBRs) located in the central nervous system (CNS). Dronabinol acts directly on the appetite and vomiting control centers in the brain to stimulate appetite and prevent emesis. In addition, this agent induces analgesia. Urine levels may be used as a marker to determine the exposure to certain preparations containing parts of the cannabis plant, such as marijuana. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C867"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C867"" NCI Thesaurus); An isomer of tetrahydrocannabinol (THC) that is the main and most active isomer found in the Cannabis sativa L. plant, with potential anti-emetic, analgesic and appetite stimulating activities. Upon administration, dronabinol, also called delta-9-THC, targets and binds to cannabinoid receptors (CBRs) located in the central nervous system (CNS). Dronabinol acts directly on the appetite and vomiting control centers in the brain to stimulate appetite and prevent emesis. In addition, this agent induces analgesia. Urine levels may be used as a marker to determine the exposure to certain preparations containing parts of the cannabis plant, such as marijuana.; A psychoactive compound extracted from the resin of Cannabis sativa (marihuana, hashish). The isomer delta-9-tetrahydrocannabinol (THC) is considered the most active form, producing characteristic mood and perceptual changes associated with this compound.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -1768,,,,,"A synthetic pyrrolizine carboxylic acid derivative with anti-inflammatory, analgesic, and antipyretic activities. Ketorolac non-selective inhibits the enzymes cyclooxygenase 1 (COX-1) and COX-2. The inhibition of COX-2, up-regulated at sites of inflammation, prevents conversion of arachidonic acid to pro-inflammatory prostaglandins. The inhibition of COX-1 by this agent prevents the normal steady-state production of prostaglandins that play housekeeping roles in the protection of the gastrointestinal tract, the regulation of renal blood flow, and platelet aggregation. As a result, the inhibition of COX-1 may be associated with gastrointestinal toxicity, nephrotoxicity, and the inhibition of platelet aggregation. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1219"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1219"" NCI Thesaurus); A synthetic pyrrolizine carboxylic acid derivative with anti-inflammatory, analgesic, and antipyretic activities. Ketorolac non-selective inhibits the enzymes cyclooxygenase 1 (COX-1) and COX-2. The inhibition of COX-2, up-regulated at sites of inflammation, prevents conversion of arachidonic acid to pro-inflammatory prostaglandins. The inhibition of COX-1 by this agent prevents the normal steady-state production of prostaglandins that play housekeeping roles in the protection of the gastrointestinal tract, the regulation of renal blood flow, and platelet aggregation. As a result, the inhibition of COX-1 may be associated with gastrointestinal toxicity, nephrotoxicity, and the inhibition of platelet aggregation.; A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is an NSAID and is used principally for its analgesic activity. (From Martindale The Extra Pharmacopoeia, 31st ed); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -1797,,,,,"A nonhalogenated, synthetic, inhaled corticosteroid (ICS) with anti-inflammatory and potential antiviral activities. Upon administration by oral inhalation into the lungs, ciclesonide (CIC) is converted by local esterases to its active metabolite desisobutyryl-ciclesonide (des-CIC), which binds to intracellular glucocorticoid receptors (GRs). The ligand-bound GRs regulate gene expressions, which lead to inhibitory activities against multiple cell types, such as mast cells, eosinophils, basophils, lymphocytes, macrophages and neutrophils, and various mediators associated with inflammation, such as histamine, eicosanoids, leukotrienes and cytokines. In addition, ciclesonide may suppress the replication of human coronavirus by targeting viral nonstructural protein 15 (NSP15).; UMLS Semantic Type: STY:T123; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -1845,,,,,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T125; UMLS Semantic Type: STY:T116; Human chorionic gonadotropin (HCG), a polypeptide hormone produced by the human placenta. Endogenously produced HCG interacts with the LHCG receptor of the ovary and promotes the maintenance of the corpus luteum during the beginning of pregnancy. This allows the corpus luteum to continuously secrete the hormone progesterone during the first trimester, which is required for maintenance of the uterus and prevents menstruation. In males, HCG also stimulates the production of gonadal steroid hormones by stimulating the interstitial cells (Leydig cells) of the testis to produce androgens. HCG is composed of an alpha and a beta sub-unit. The alpha sub-unit is essentially identical to the alpha sub­ units of the human pituitary gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), as well as to the alpha sub-unit of human thyroid-stimulating hormone (TSH), while the beta sub­ units of these hormones differ in amino acid sequence. As a drug product, chorionic gonadotropin is a highly purified pyrogen-free preparation obtained from the urine of pregnant females.",,,, -1868,,,,,"A benzothiadiazine derivate with antihypertensive and hyperglycemic activities. Diazoxide increases membrane permeability to potassium ions in vascular smooth muscle, thereby stabilizing the membrane action potential and preventing vascular smooth muscle contraction; this results in peripheral vasodilatation and decreases in peripheral vascular resistance. This agent also inhibits insulin release by interacting with ATP-sensitive potassium channels of pancreatic islet beta-cells. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C428"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C428"" NCI Thesaurus); A benzothiadiazine derivate with antihypertensive and hyperglycemic activities. Diazoxide increases membrane permeability to potassium ions in vascular smooth muscle, thereby stabilizing the membrane action potential and preventing vascular smooth muscle contraction; this results in peripheral vasodilatation and decreases in peripheral vascular resistance. This agent also inhibits insulin release by interacting with ATP-sensitive potassium channels of pancreatic islet beta-cells.; A benzothiadiazine derivative that is a peripheral vasodilator used for hypertensive emergencies. It lacks diuretic effect, apparently because it lacks a sulfonamide group.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -1893,,,,,"A substituted benzimidazole prodrug with selective and irreversible proton pump inhibitor activity. Lansoprazole prodrug is converted to an active sulfonamide derivative in the acidic environment of the gastric parietal cell; the sulfonamide derivative binds to the gastric proton pump H+/K+ ATPase and forms a stable disulfide bond with the sulfhydryl group near the potassium-binding site on the luminal side, resulting in inactivation of the ATPase and a reduction in gastric acid secretion. This agent does not have anticholinergic or histamine H2 -receptor antagonistic properties.; A 2,2,2-trifluoroethoxypyridyl derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS. Lansoprazole is a racemic mixture of (R)- and (S)-isomers.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -1903,,,,,"Esomeprazole is only found in individuals that have used or taken this drug. It is a highly effective inhibitor of gastric acid secretion used in the therapy of stomach ulcers and Zollinger-Ellison syndrome. The drug inhibits the H(+)-K(+)-ATPase (H(+)-K(+)-exchanging ATPase) in the proton pump of gastric parietal cells. [PubChem]Esomeprazole is a proton pump inhibitor that suppresses gastric acid secretion by specific inhibition of the H+/K+-ATPase in the gastric parietal cell. By acting specifically on the proton pump, Esomeprazole blocks the final step in acid production, thus reducing gastric acidity.",,,, -2038,,,,,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; The most significant modifiable risk factor for cardiovascular disease and the most prominent contributor to all-cause mortality is hypertension.[A204155] Characterized by an office blood pressure of ≥140/90, hypertension is pervasive and impacts an estimated 25% of adults globally.[A204155] Treatment for hypertension should include a number of lifestyle changes (ie. reduced sodium intake) along with pharmacotherapy - it should be noted that treatment with several antihypertensive agents may be required in order to achieve blood pressure targets.[A204155] Thiazide-like diuretics such as indapamide are a valuable tool for the treatment of hypertension and continue to grow in popularity, falling behind only ACE inhibitors in terms of prescription frequency.[A204134] When compared to [hydrochlorothiazide] (another commonly prescribed diuretic), indapamide has been shown to be superior at lowering systolic blood pressure, reducing left ventricular mass index, lowering oxidative stress, inhibiting platelet aggregation, and reducing microalbuminuria associated with diabetes.[A204134] Interestingly, unlike thiazide diuretics, several sources suggest that indapamide is not associated with glucose or lipid disturbances.[A204134,A204161] Indapamide is characterized by both a methylindoline and a sulfamoyl chlorobenzamide functional group, with the former being largely responsible for the molecule’s lipid solubility.[A204158]",,,, -2086,,,,,"Labetalol is only found in individuals that have used or taken this drug. It is a blocker of both alpha- and beta-adrenergic receptors that is used as an antihypertensive (PubChem). Labetalol HCl combines both selective, competitive, alpha-1-adrenergic blocking and nonselective, competitive, beta-adrenergic blocking activity in a single substance. In man, the ratios of alpha- to beta- blockade have been estimated to be approximately 1:3 and 1:7 following oral and intravenous (IV) administration, respectively. The principal physiologic action of labetalol is to competitively block adrenergic stimulation of β-receptors within the myocardium (β1-receptors) and within bronchial and vascular smooth muscle (β2-receptors), and α1-receptors within vascular smooth muscle. This causes a decrease in systemic arterial blood pressure and systemic vascular resistance without a substantial reduction in resting heart rate, cardiac output, or stroke volume, apparently because of its combined α- and β-adrenergic blocking activity.",,,, -2195,,,,,"Vitamin D3, also called cholecalciferol, is one of the forms of vitamin D. Vitamin D3 is a steroid hormone that has long been known for its important role in regulating body levels of calcium and phosphorus, in mineralization of bone, and for the assimilation of Vitamin A. It is structurally similar to steroids such as testosterone, cholesterol, and cortisol (although vitamin D3, itself, is a secosteroid). Vitamin D3 is a derivative of 7-dehydroxycholesterol formed by ultraviolet rays breaking the C9-C10 bond. It differs from ergocalciferol in having a single bond between C22 and C23 and lacking a methyl group at C24. Vitamin D3 can also come from dietary sources, such as beef liver, cheese, egg yolks, and fatty fish (PubChem). The first step involved in the activation of vitamin D3 is a 25-hydroxylation catalyzed by 25-hydroxylase in the liver and then by other enzymes. The mitochondrial sterol 27-hydroxylase catalyzes the first reaction in the oxidation of the side chain of sterol intermediates. The active form of vitamin D3 (calcitriol) binds to intracellular receptors that then function as transcription factors to modulate gene expression. Like the receptors for other steroid hormones and thyroid hormones, the vitamin D receptor has hormone-binding and DNA-binding domains. The vitamin D receptor forms a complex with another intracellular receptor, the retinoid-X receptor, and that heterodimer is what binds to DNA. In most cases studied, the effect is to activate transcription, but situations are also known in which vitamin D suppresses transcription. Calcitriol increases the serum calcium concentrations by (1) increasing GI absorption of phosphorus and calcium, (2) increasing osteoclastic resorption, and (3) increasing distal renal tubular reabsorption of calcium. Calcitriol appears to promote intestinal absorption of calcium through binding to the vitamin D receptor in the mucosal cytoplasm of the intestine. Subsequently, calcium is absorbed through the formation of a calcium-binding protein.",,,, -686,,,,,Ampicillin is found in common pea. It is also a potential contaminant of cow's milk arising from its veterinary use. Ampicillin is a semi-synthetic derivative of penicillin that functions as an orally active broad-spectrum antibiotic. It has been used extensively to treat bacterial infections since 1961. It is considered part of the aminopenicillin family and is roughly equivalent to amoxicillin in terms of spectrum and level of activity,,,, -724,,,,,"Mannitol is a diuretic and renal diagnostic aid related to sorbitol. It has little significant energy value as it is largely eliminated from the body before any metabolism can take place. It can be used to treat oliguria associated with kidney failure or other manifestations of inadequate renal function and has been used for determination of glomerular filtration rate. Mannitol is also commonly used as a research tool in cell biological studies, usually to control osmolarity. Chemically, mannitol is an alcohol and a sugar, or a polyol; it is similar to xylitol or sorbitol. However, mannitol has a tendency to lose a hydrogen ion in aqueous solutions, which causes the solution to become acidic. For this, it is not uncommon to add a substance to adjust its pH, such as sodium bicarbonate. Mannitol is a non-permeating molecule i.e. it cannot cross biological membranes. Mannitol or hexan-1,2,3,4,5,6-hexol (C6H8(OH)6) is an osmotic diuretic agent and a weak renal vasodilator. It is a sorbitol isomer.",,,, -779,,,,,"Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).",,,, -789,,,,,"A sulfur-rich glycosaminoglycan with anticoagulant property. Heparin binds to antithrombin III to form a heparin-antithrombin III complex. The complex binds to and irreversibly inactivates thrombin and other activated clotting factors, such as factors IX, X, XI, and XII, thereby preventing the polymerization of fibrinogen to fibrin and the subsequent formation of clots.; A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.",,,, -886,,,,,"Capsaicin is identified as the primary pungent principle in Capsicum fruits. Hot chili peppers that belong to the plant genus Capsicum (family Solanaceae) are among the most heavily consumed spices throughout the world. The capsaicin content of green and red peppers ranges from 0.1 to 1%. Capsaicin evokes numerous biological effects and thus has been the target of extensive., investigations since its initial identification in 1919. One of the most recognized physiological properties of capsaicin is its selective effects on the peripheral part of the sensory nervous system, particularly on the primary afferent neurons. The compound is known to deplete the neurotransmitter of painful impulses known as substance P from the sensory nerve terminals, which provides a rationale for its use as a versatile experimental tool for studying pain mechanisms and also for pharmacotherapy to treat some peripheral painful states, such as rheumatoid arthritis, post-herpetic neuralgia, post-mastectomy pain syndrome and diabetic neuropathy. Considering the frequent consumption of capsaicin as a food additive and its current therapeutic application, correct assessment of any harmful effects of this compound is important from the public health standpoint. Ingestion of large amounts of capsaicin has been reported to cause histopathological and biochemical changes, including erosion of gastric mucosa and hepatic necrosis. However, there are contradictory data on the mutagenicity of capsaicin. A recent epidemiological study conducted in Mexico revealed that consumers of chili pepper were at higher risk for gastric cancer than non-consumers. However, it remains unclear whether capsaicin present in hot chili pepper is a major causative factor in the aetiology of gastric cancer in humans. A growing number of recent studies have focused on anticarcinogenic or antimutagenic phytochemicals, particularly those included in human diet. In summary, capsaicin has dual effects on chemically induced carcinogenesis and mutagenesis. Although a minute amount of capsaicin displays few or no deleterious effects, heavy ingestion of the compound has been associated with necrosis, ulceration and even carcinogenesis. Capsaicin is considered to be metabolized by cytochrome P-450-dependent mixed-function oxidases to reactive species. (PMID: 8621114).",,,, -921,,,,,"A synthetic imidazole bisphosphonate analog of pyrophosphate with anti-bone-resorption activity. A third-generation bisphosphonate, zoledronic acid binds to hydroxyapatite crystals in the bone matrix, slowing their dissolution and inhibiting the formation and aggregation of these crystals. This agent also inhibits farnesyl pyrophosphate synthase, an enzyme involved in terpenoid biosynthesis. Inhibition of this enzyme prevents the biosynthesis of isoprenoid lipids, donor substrates of farnesylation and geranylgeranylation during the post-translational modification of small GTPase signalling proteins, which are important in the process of osteoclast turnover. Decreased bone turnover and stabilization of the bone matrix contribute to the analgesic effect of zoledronic acid with respect to painful osteoblastic lesions. The agent also reduces serum calcium concentrations associated with hypercalcemia. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1699"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1699"" NCI Thesaurus); A synthetic imidazole bisphosphonate analog of pyrophosphate with anti-bone-resorption activity. A third-generation bisphosphonate, zoledronic acid binds to hydroxyapatite crystals in the bone matrix, slowing their dissolution and inhibiting the formation and aggregation of these crystals. This agent also inhibits farnesyl pyrophosphate synthase, an enzyme involved in terpenoid biosynthesis. Inhibition of this enzyme prevents the biosynthesis of isoprenoid lipids, donor substrates of farnesylation and geranylgeranylation during the post-translational modification of small GTPase signalling proteins, which are important in the process of osteoclast turnover. Decreased bone turnover and stabilization of the bone matrix contribute to the analgesic effect of zoledronic acid with respect to painful osteoblastic lesions. The agent also reduces serum calcium concentrations associated with hypercalcemia.; An imidobisphosphonate inhibitor of BONE RESORPTION that is used for the treatment of malignancy-related HYPERCALCEMIA; OSTEITIS DEFORMANS; and OSTEOPOROSIS.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -953,,,,,"The hydrochloride salt of a short-acting benzodiazepine derivative with an imidazole structure and anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam binds to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS), resulting in increases in the opening of chloride channels, membrane hyperpolarization, and the inhibitory effect of GABA. This agent may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C654"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C654"" NCI Thesaurus); A short-acting benzodiazepine derivative with an imidazole structure and with anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam exerts its effect by binding to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS). This leads to an increase in the opening of chloride channels, membrane hyperpolarization and increases the inhibitory effect of GABA in the CNS. Midazolam may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft.; The hydrochloride salt of a short-acting benzodiazepine derivative with an imidazole structure and anxiolytic, amnestic, hypnotic, anticonvulsant and sedative properties. Midazolam binds to the benzodiazepine receptor at the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex in the central nervous system (CNS), resulting in increases in the opening of chloride channels, membrane hyperpolarization, and the inhibitory effect of GABA. This agent may also interfere with the reuptake of GABA, thereby causing accumulation of GABA in the synaptic cleft.; A short-acting hypnotic-sedative drug with anxiolytic and amnestic properties. It is used in dentistry, cardiac surgery, endoscopic procedures, as preanesthetic medication, and as an adjunct to local anesthesia. The short duration and cardiorespiratory stability makes it useful in poor-risk, elderly, and cardiac patients. It is water-soluble at pH less than 4 and lipid-soluble at physiological pH.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -1000,,,,,"A cardioselective competitive beta-1 adrenergic receptor antagonist with antihypertensive properties and devoid of intrinsic sympathomimetic activity. Metoprolol antagonizes beta 1-adrenergic receptors in the myocardium, thereby reducing the rate and force of myocardial contraction leading to a reduction in cardiac output. This agent may also reduce the secretion of renin with subsequent reduction in levels of angiotensin II thereby preventing vasoconstriction and aldosterone secretion. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C61845"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C61845"" NCI Thesaurus); A cardioselective competitive beta-1 adrenergic receptor antagonist with antihypertensive properties and devoid of intrinsic sympathomimetic activity. Metoprolol antagonizes beta 1-adrenergic receptors in the myocardium, thereby reducing the rate and force of myocardial contraction leading to a reduction in cardiac output. This agent may also reduce the secretion of renin with subsequent reduction in levels of angiotensin II thereby preventing vasoconstriction and aldosterone secretion.; A selective adrenergic beta-1 blocking agent that is commonly used to treat ANGINA PECTORIS; HYPERTENSION; and CARDIAC ARRHYTHMIAS.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -1213,,,,,"Clemastine is only found in individuals that have used or taken this drug. It is an ethanolamine-derivative, first generation histamine H1 antagonist used in hay fever, rhinitis, allergic skin conditions, and pruritus. It causes drowsiness. [PubChem]Clemastine is a selective histamine H1 antagonist and binds to the histamine H1 receptor. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine.",,,, -1300,,,,,"A metal halide composed of sodium and chloride with sodium and chloride replacement capabilities. When depleted in the body, sodium must be replaced in order to maintain intracellular osmolarity, nerve conduction, muscle contraction and normal renal function.; A ubiquitous sodium salt that is commonly used to season food.; UMLS Semantic Type: STY:T197",,,, -1357,,,,,"A methylazirinopyrroloindoledione antineoplastic antibiotic isolated from the bacterium Streptomyces caespitosus and other Streptomyces bacterial species. Bioreduced mitomycin C generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis. Preferentially toxic to hypoxic cells, mitomycin C also inhibits RNA and protein synthesis at high concentrations. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1820"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1820"" NCI Thesaurus); A methylazirinopyrroloindoledione antineoplastic antibiotic isolated from the bacterium Streptomyces caespitosus and other Streptomyces bacterial species. Bioreduced mitomycin C generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis. Preferentially toxic to hypoxic cells, mitomycin C also inhibits RNA and protein synthesis at high concentrations. (NCI04); An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",,,, -1379,,,,,"The hydrochloride salt of an anthracenedione antibiotic with antineoplastic activity. Mitoxantrone intercalates into and crosslinks DNA, thereby disrupting DNA and RNA replication. This agent also binds to topoisomerase II, resulting in DNA strand breaks and inhibition of DNA repair. Mitoxantrone is less cardiotoxic compared to doxorubicin. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C665"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C665"" NCI Thesaurus); An anthracenedione antibiotic with antineoplastic activity. Mitoxantrone intercalates into and crosslinks DNA, thereby disrupting DNA and RNA replication. This agent also binds to topoisomerase II, resulting in DNA strand breaks and inhibition of DNA repair. Mitoxantrone is less cardiotoxic compared to doxorubicin.; An anthracenedione-derived antineoplastic agent.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -1383,,,,,"The hydrochloride salt of doxorubicin, an anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1326"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1326"" NCI Thesaurus); The hydrochloride salt of doxorubicin, an anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.; An anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.; Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.; UMLS Semantic Type: STY:T195; UMLS Semantic Type: STY:T109",,,, -1478,,,,,"An essential nutrient and natural water-soluble vitamin of the B-complex family that must combine with an intrinsic factor for absorption by the intestine. Cyanocobalamin is necessary for hematopoiesis, neural metabolism, DNA and RNA production, and carbohydrate, fat, and protein metabolism. B12 improves iron functions in the metabolic cycle and assists folic acid in choline synthesis. B12 metabolism is interconnected with that of folic acid. Vitamin B12 deficiency causes pernicious anemia, megaloblastic anemia, and neurologic lesions. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C64333"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C64333"" NCI Thesaurus); A synthetic and active form of vitamin B12 that can cross the blood brain barrier without biotransformation, that may be used to treat or prevent vitamin B12 deficiency and its complications. Upon administration, mecobalamin is able to replace endogenous vitamin B12, increase vitamin B12 levels and improve vitamin B12 deficiency. Vitamin B12 is necessary for hematopoiesis, neural metabolism, DNA and RNA production, and carbohydrate, fat, and protein metabolism. It improves iron functions in the metabolic cycle and assists folic acid in choline synthesis. Its metabolism is interconnected with that of folic acid.; A cobalt-containing coordination compound generated by intestinal microbes, and a natural water-soluble vitamin of the B-complex family that must combine with Intrinsic Factor for absorption by the intestine. Cyanocobalamin is necessary for hematopoiesis, neural metabolism, DNA and RNA production, and carbohydrate, fat, and protein metabolism. B12 improves iron functions in the metabolic cycle and assists folic acid in choline synthesis. B12 metabolism is interconnected with that of folic acid. Vitamin B12 deficiency causes pernicious anemia, megaloblastic anemia, and neurologic lesions.; A cobalt-containing coordination compound produced by intestinal micro-organisms and found also in soil and water. Higher plants do not concentrate vitamin B 12 from the soil and so are a poor source of the substance as compared with animal tissues. INTRINSIC FACTOR is important for the assimilation of vitamin B 12.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T127; UMLS Semantic Type: STY:T109",,,, -1523,,,,,"A nonsteroidal inhibitor of estrogen synthesis with antineoplastic activity. As a third-generation aromatase inhibitor, letrozole selectively and reversibly inhibits aromatase, which may result in growth inhibition of estrogen-dependent breast cancer cells. Aromatase, a cytochrome P-450 enzyme localized to the endoplasmic reticulum of the cell and found in many tissues including those of the premenopausal ovary, liver, and breast, catalyzes the aromatization of androstenedione and testosterone into estrone and estradiol, the final step in estrogen biosynthesis. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1527"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1527"" NCI Thesaurus); A nonsteroidal inhibitor of estrogen synthesis with antineoplastic activity. As a third-generation aromatase inhibitor, letrozole selectively and reversibly inhibits aromatase, which may result in growth inhibition of estrogen-dependent breast cancer cells. Aromatase, a cytochrome P-450 enzyme localized to the endoplasmic reticulum of the cell and found in many tissues including those of the premenopausal ovary, liver, and breast, catalyzes the aromatization of androstenedione and testosterone into estrone and estradiol, the final step in estrogen biosynthesis.; A triazole and benzonitrile derivative that is a selective non-steroidal aromatase inhibitor, similar to ANASTROZOLE. It is used in the treatment of metastatic or locally advanced breast cancer in postmenopausal women.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -1540,,,,,"Celecoxib (INN) is a non-steroidal anti-inflammatory drug (NSAID) used in the treatment of osteoarthritis, rheumatoid arthritis, acute pain, painful menstruation and menstrual symptoms, and to reduce numbers of colon and rectum polyps in patients with familial adenomatous polyposis. It is marketed by Pfizer under the brand name Celebrex. In some countries, it is branded Celebra. Celecoxib is a non-steroidal anti-inflammatory drug (NSAID) used in the treatment of osteoarthritis, rheumatoid arthritis, acute pain, painful menstruation and menstrual symptoms, and to reduce numbers of colon and rectum polyps in patients with familial adenomatous polyposis. Celecoxib is a highly selective COX-2 inhibitor and primarily inhibits this isoform of cyclooxygenase, whereas traditional NSAIDs inhibit both COX-1 and COX-2. Celecoxib is approximately 10-20 times more selective for COX-2 inhibition over COX-1. In theory, this specificity allows celecoxib and other COX-2 inhibitors to reduce inflammation (and pain) while minimizing gastrointestinal adverse drug reactions (e.g. stomach ulcers) that are common with non-selective NSAIDs. It also means that it has a reduced effect on platelet aggregation compared to traditional NSAIDs; Celecoxib is a highly selective COX-2 inhibitor and primarily inhibits this isoform of cyclooxygenase, whereas traditional NSAIDs inhibit both COX-1 and COX-2. Celecoxib is approximately 10-20 times more selective for COX-2 inhibition over COX-1. In theory, this specificity allows celecoxib and other COX-2 inhibitors to reduce inflammation (and pain) while minimizing gastrointestinal adverse drug reactions (e.g. stomach ulcers) that are common with non-selective NSAIDs. It also means that it has a reduced effect on platelet aggregation compared to traditional NSAIDs.",,,, -1541,,,,,"A synthetic, nonsteroidal derivative of phenyl-furanone with antiinflammatory, antipyretic and analgesic properties and potential antineoplastic properties. Rofecoxib binds to and inhibits the enzyme cyclooxygenase-2 (COX-2), resulting in an inhibition of the conversion of arachidonic acid to prostaglandins. COX-related metabolic pathways may represent key regulators of cell proliferation and neo-angiogenesis. Some epithelial tumor cell types overexpress pro-angiogenic COX-2. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1832"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1832"" NCI Thesaurus); A synthetic, nonsteroidal derivative of phenyl-furanone with antiinflammatory, antipyretic and analgesic properties and potential antineoplastic properties. Rofecoxib binds to and inhibits the enzyme cyclooxygenase-2 (COX-2), resulting in an inhibition of the conversion of arachidonic acid to prostaglandins. COX-related metabolic pathways may represent key regulators of cell proliferation and neo-angiogenesis. Some epithelial tumor cell types overexpress pro-angiogenic COX-2. (NCI04)",,,, -1579,,,,,"A synthetic ergoline derivative and a long-acting dopamine receptor agonist with high affinity for the dopamine D2 receptor. Cabergoline exerts an inhibitory effect on prolactin secretion by acting on dopamine receptors present in pituitary lactotrophs. This drug also binds to dopamine D2 receptors in the corpus striatum, thereby mimicking the actions of dopamine on motor control. Cabergoline also possesses antioxidant and neuroprotective properties due to its free radical scavenging activity. Cabergoline is used in the treatment of Parkinson's disease and in the treatment of hyperprolactinemia. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C47428"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C47428"" NCI Thesaurus); A synthetic ergoline derivative and a long-acting dopamine receptor agonist with high affinity for the dopamine D2 receptor. Cabergoline exerts an inhibitory effect on prolactin secretion by acting on dopamine receptors present in pituitary lactotrophs. This drug also binds to dopamine D2 receptors in the corpus striatum, thereby mimicking the actions of dopamine on motor control. Cabergoline also possesses antioxidant and neuroprotective properties due to its free radical scavenging activity. Cabergoline is used in the treatment of Parkinson's disease and in the treatment of hyperprolactinemia.; An ergoline derivative and dopamine D2-agonist that inhibits PROLACTIN secretion. It is used in the management of HYPERPROLACTINEMIA, and to suppress lactation following childbirth for medical reasons. Cabergoline is also used in the management of PARKINSON DISEASE.",,,, -1580,,,,,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; Pramipexole is a drug used to treat the symptoms of Parkinson's Disease (PD). It is a _non-ergot dopamine agonist_ drug that is efficacious in treating various Parkinson's symptoms such as tremor, rigidity, and bradykinesia (slow movement) [A176867]. It was first approved by the FDA in 1997 [L5882]. Parkinson's Disease is one of the most common neurodegenerative disorders and causes a high level of disability in patients [A176855], leading to increased difficulty in performing activities of daily living due to symptoms that progress over time [A176858]. The prevalence of Parkinson's Disease worldwide has increased from approximately 2.5 million in 1990 to about 6.1 million in 2016 [A176861]. This increase may be attributed to an aging population along with other contributing factors [A176861]. In addition to the above FDA approval for Parkinson's Disease, pramipexole was also approved by the FDA in 2006 for the treatment of Restless Legs Syndrome (RLS) [A176873]. RLS is a sleep-related disorder characterized by unpleasant sensations in the lower extremities, often accompanied by an uncontrollable urge to move the legs [A176876].",,,, -1619,,,,,"Folic acid or folate, is a vitamin that belongs to the class of compounds known as pterins. Chemically, folate consists of three distinct chemical moieties linked together. A pterin (2-amino-4-hydroxy-pteridine) linked by a methylene bridge to a p-aminobenzoyl group that in turn is linked through an amide linkage to glutamic acid. It is a member of the vitamin B family and is primarily known as vitamin B9. Folate is required for the body to make DNA and RNA and metabolize amino acids necessary for cell division for the hematopoietic system. As humans cannot make folate, it is required in the diet, making it an essential nutrient (i.e. a vitamin). Folate occurs naturally in many foods including mushrooms, spinach, yeast, green leaves, and grasses (poaceae). Folic acid, being biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by the enzyme known as dihydrofolate reductase. Tetrahydrofolate and methyltetrahydrofolate are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids and generate formic acid. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in babies. Low levels in early pregnancy are believed to be the cause of more than half of babies born with NTDs (PMID: 28097362). Folic acid is also a microbial metabolite produced by Bifidobacterium and Lactobacillus (PMID: 22254078).",,,, -1652,,,,,"An anthranilic derivative and loop diuretic with antihypertensive effect. Furosemide blocks the Na-K-Cl cotransporter (NKCC) in the luminal membrane of the thick ascending limb of the loop of Henle in the kidney, by binding to the Cl-binding site located in the cotransporter's transmembrane domain, thereby inhibiting reabsorption of sodium, chloride, potassium ions and water. This agent reduces plasma and extracellular fluid volume resulting in decreased blood pressure and cardiac output. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C515"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C515"" NCI Thesaurus); A sulfamoylanthranilic acid derivative, also known as frusemide, and potent loop diuretic. Furosemide is widely used to treat hypertension and edema. This agent is highly bound to albumin and is largely excreted unchanged in the urine.; A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -1660,,,,,"An anilinopyridine sulfonylurea belonging to the class of loop diuretics. Torsemide has a prolonged duration of action compared to other loop diuretics, is extensively protein bound in plasma and has a relatively long half-life.; A pyridine and sulfonamide derivative that acts as a sodium-potassium chloride symporter inhibitor (loop diuretic). It is used for the treatment of EDEMA associated with CONGESTIVE HEART FAILURE; CHRONIC RENAL INSUFFICIENCY; and LIVER DISEASES. It is also used for the management of HYPERTENSION.",,,, -1678,,,,,"The acetate salt of a synthetic nonapeptide analogue of gonadotropin-releasing hormone. Leuprolide binds to and activates gonadotropin-releasing hormone (GnRH) receptors. Continuous, prolonged administration of leuprolide in males results in pituitary GnRH receptor desensitization and inhibition of pituitary secretion of follicle stimulating hormone (FSH) and luteinizing hormone (LH), leading to a significant decline in testosterone production; in females, prolonged administration results in a decrease in estradiol production. This agent reduces testosterone production to castration levels and may inhibit androgen receptor-positive tumor progression. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C1319"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C1319"" NCI Thesaurus); A synthetic nonapeptide analogue of gonadotropin-releasing hormone. Leuprolide binds to and activates gonadotropin-releasing hormone (GnRH) receptors. Continuous, prolonged administration of leuprolide in males results in pituitary GnRH receptor desensitization and inhibition of pituitary secretion of follicle stimulating hormone (FSH) and luteinizing hormone (LH), leading to a significant decline in testosterone production; in females, prolonged administration results in a decrease in estradiol production. This agent reduces testosterone production to castration levels and may inhibit androgen receptor-positive tumor progression.; A potent synthetic long-acting agonist of GONADOTROPIN-RELEASING HORMONE that regulates the synthesis and release of pituitary gonadotropins, LUTEINIZING HORMONE and FOLLICLE STIMULATING HORMONE.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T125; UMLS Semantic Type: STY:T116",,,, -1822,,,,,"Etoposide, also known as vepesid or VP-16, belongs to the class of organic compounds known as podophyllotoxins. These are tetralin lignans in which the benzene moiety of the tetralin skeleton is fused to a 1,3-dioxolane and the cyclohexane is fused to a butyrolactone (pyrrolidin-2-one). Etoposide is a drug. Within humans, etoposide participates in a number of enzymatic reactions. In particular, etoposide can be converted into etoposide ortho-quinone; which is mediated by the enzymes prostaglandin g/h synthase 1 and prostaglandin g/h synthase 2. In addition, etoposide and uridine diphosphate glucuronic acid can be converted into etoposide glucuronide and uridine 5'-diphosphate; which is mediated by the enzyme UDP-glucuronosyltransferase 1-1. In humans, etoposide is involved in etoposide metabolism pathway. Etoposide is formally rated as a carcinogen (by IARC 1) and is also a potentially toxic compound. Etoposide is used as a form of chemotherapy for cancers such as Kaposi's sarcoma, Ewing's sarcoma, lung cancer, testicular cancer, lymphoma, nonlymphocytic leukemia, and glioblastoma multiforme. It is given intravenously (IV) or orally in capsule or tablet form. It is believed to work by damaging DNA. Etoposide was approved for medical use in the United States in 1983. They can include low blood cell counts, vomiting, loss of appetite, diarrhea, hair loss, and fever.",,,, -1826,,,,,"UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T125; UMLS Semantic Type: STY:T116; Urofollitropin is a urinary-derived follicle-stimulating hormone (FSH) that is extracted and purified from human urine samples. It consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Urofollitropin is typically used injected subcutaneously in combination with human chorionic gonadotropin (hCG) to induce ovulation. Urofollitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF).",,,, -1829,,,,,"The biologically active molecule nitric oxide (NO) is a simple, membrane-permeable gas with unique chemistry. It is formed by the conversion of L-arginine to L-citrulline, with the release of NO. The enzymatic oxidation of L-arginine to L-citrulline takes place in the presence of oxygen and NADPH using flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), heme, thiol, and tetrahydrobiopterin as cofactors. The enzyme responsible for the generation of NO is nitric oxide synthase (E.C. 1.7.99.7; NOS). Three NOS isoforms have been described and shown to be encoded on three distinct genes: neuronal NOS (nNOS, NOS type I), inducible NOS (NOS type II), and endothelial NOS (eNOS, NOS type III). Two of them are constitutively expressed and dependent on the presence of calcium ions and calmodulin to function (nNOS and eNOS), while iNOS is considered non-constitutive and calcium-independent. However, experience has shown that constitutive expression of nNOS and eNOS is not as rigid as previously thought (i.e. either present or absent), but can be dynamically controlled during development and in response to injury. Functionally, NO may act as a hormone, neurotransmitter, paracrine messenger, mediator, cytoprotective molecule, and cytotoxic molecule. NO has multiple cellular molecular targets. It influences the activity of transcription factors, modulates upstream signaling cascades, mRNA stability and translation, and processes the primary gene products. In the brain, many processes are linked to NO. NO activates its receptor, soluble guanylate cyclase by binding to it. The stimulation of this enzyme leads to increased synthesis of the second messenger, cGMP, which in turn activates cGMP-dependent kinases in target cells. NO exerts a strong influence on glutamatergic neurotransmission by directly interacting with the N-methyl-D-aspartate (NMDA) receptor. Neuronal NOS is connected to NMDA receptors (see below) and sharply increases NO production following activation of this receptor. Thus, the level of endogenously produced NO around NMDA synapses reflects the activity of glutamate-mediated neurotransmission. However, there is recent evidence showing that non-NMDA glutamate receptors (i.e. AMPA and type I metabotropic receptors) also contribute to NO generation. Besides its influence on glutamate, NO is known to have effects on the storage, uptake and/or release of most other neurotransmitters in the CNS (acetylcholine, dopamine, noradrenaline, GABA, taurine, and glycine) as well as of certain neuropeptides. Finally, since NO is a highly diffusible molecule, it may reach extrasynaptic receptors at target cell membranes that are some distance away from the place of NO synthesis. NO is thus capable of mediating both synaptic and nonsynaptic communication processes. NO is a potent vasodilator (a major endogenous regulator of vascular tone), and an important endothelium-dependent relaxing factor. NO is synthesized by NO synthases (NOS) and NOS are inhibited by asymmetrical dimethylarginine (ADMA). ADMA is metabolized by dimethylarginine dimethylaminohydrolase (DDAH) and excreted in the kidneys. Lower ADMA levels in pregnant women compared to non-pregnant controls suggest that ADMA has a role in vascular dilatation and blood pressure changes. Several studies show an increase in ADMA levels in pregnancies complicated with preeclampsia. Elevated ADMA levels in preeclampsia are seen before clinical symptoms have developed; these findings suggest that ADMA has a role in the pathogenesis of preeclampsia. In some pulmonary hypertensive states such as ARDS, the production of endogenous NO may be impaired. Nitric oxide inhalation selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because NO is inactivated by rapidly binding to hemoglobin. In an injured lung with pulmonary hypertension, inhaled NO produces local vasodilation of well-ventilated lung units and may ""steal"" blood flow away from unventilated regions. This reduces intrapulmonary shunting and may improve systemic arterial oxygenation. Nitric oxide is a chemical mediator fundamental in the maintenance of adequate tissue perfusion and effective cardiovascular function. The use of nitrates is well established as pharmacological agents but it is only recently that it has been recognized that they act as a source of nitric oxide (PMID: 16966108, 8752507, 17181668, 16005189). Nitric oxide is used as a food additive (EAFUS: Everything Added to Food in the United States).",,,, -1860,,,,,"A natural alkaloid isolated from the plant Vinca rosea Linn. Vincristine binds irreversibly to microtubules and spindle proteins in S phase of the cell cycle and interferes with the formation of the mitotic spindle, thereby arresting tumor cells in metaphase. This agent also depolymerizes microtubules and may also interfere with amino acid, cyclic AMP, and glutathione metabolism; calmodulin-dependent Ca++ -transport ATPase activity; cellular respiration; and nucleic acid and lipid biosynthesis. (NCI04); An antitumor alkaloid isolated from VINCA ROSEA. (Merck, 11th ed.); UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -1894,,,,,"A benzimidazole with selective and irreversible proton pump inhibition activity. Omeprazole forms a stable disulfide bond with the sulfhydryl group of the hydrogen-potassium (H+ - K+) ATPase found on the secretory surface of parietal cells, thereby inhibiting the final transport of hydrogen ions (via exchange with potassium ions) into the gastric lumen and suppressing gastric acid secretion. This agent exhibits no anticholinergic activities and does not antagonize histamine H2 receptors. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C716"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C716"" NCI Thesaurus); A benzimidazole with selective and irreversible proton pump inhibition activity. Omeprazole forms a stable disulfide bond with the sulfhydryl group of the hydrogen-potassium (H+ - K+) ATPase found on the secretory surface of parietal cells, thereby inhibiting the final transport of hydrogen ions (via exchange with potassium ions) into the gastric lumen and suppressing gastric acid secretion. This agent exhibits no anticholinergic activities and does not antagonize histamine H2 receptors.; A 4-methoxy-3,5-dimethylpyridyl, 5-methoxybenzimidazole derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits an H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -1939,,,,,"Melatonin is a biogenic amine that is found in animals, plants and microbes. Aaron B. Lerner of Yale University is credited for naming the hormone and for defining its chemical structure in 1958. In mammals, melatonin is produced by the pineal gland. The pineal gland is small endocrine gland, about the size of a rice grain and shaped like a pine cone (hence the name), that is located in the center of the brain (rostro-dorsal to the superior colliculus) but outside the blood-brain barrier. The secretion of melatonin increases in darkness and decreases during exposure to light, thereby regulating the circadian rhythms of several biological functions, including the sleep-wake cycle. In particular, melatonin regulates the sleep-wake cycle by chemically causing drowsiness and. lowering the body temperature. Melatonin is also implicated in the regulation of mood,learning and memory, immune activity, dreaming, fertility and reproduction. Melatonin is also an effective antioxidant. Most of the actions of melatonin are mediated through the binding and activation of melatonin receptors. Individuals with autism spectrum disorders(ASD) may have lower than normal levels of melatonin. A 2008 study found that unaffected parents of individuals with ASD also have lower melatonin levels, and that the deficits. were associated with low activity of the ASMT gene, which encodes the last enzyme of melatonin synthesis. Reduced melatonin production has also been proposed as a likely factor in the significantly higher cancer rates in night workers.",,,, -1955,,,,,UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T126; UMLS Semantic Type: STY:T116; Urokinase is an endogenous peptide that is cleaved in the presence of plasmin between lysine 158 and isoleucine 159 to yield active urokinase.[A191943] Urokinase remains connected between these 2 chains by a sulfhydryl bond.[A191943] Urokinase was granted FDA approval on 16 January 1978.[L12138],,,, -1980,,,,,"A p-aminophenol derivative with analgesic and antipyretic activities. Although the exact mechanism through which acetaminophen exert its effects has yet to be fully determined, acetaminophen may inhibit the nitric oxide (NO) pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate (NMDA) and substance P, resulting in elevation of the pain threshold. The antipyretic activity may result from inhibition of prostaglandin synthesis and release in the central nervous system (CNS) and prostaglandin-mediated effects on the heat-regulating center in the anterior hypothalamus. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C198"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C198"" NCI Thesaurus); A p-aminophenol derivative with analgesic and antipyretic activities. Although the exact mechanism through which acetaminophen exert its effects has yet to be fully determined, acetaminophen may inhibit the nitric oxide (NO) pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate (NMDA) and substance P, resulting in elevation of the pain threshold. The antipyretic activity may result from inhibition of prostaglandin synthesis and release in the central nervous system (CNS) and prostaglandin-mediated effects on the heat-regulating center in the anterior hypothalamus.; Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -2016,,,,,"A volatile liquid prepared by fermentation of certain carbohydrates. Alcohol acts as a central nervous system (CNS) depressant, a diuretic, and a disinfectant. Although the exact mechanism of CNS depression is unknown, alcohol may act by inhibiting the opening of calcium channels, mediated by the binding of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) to GABA-A receptors, or through inhibitory actions at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Alcohol inhibits the production of antidiuretic hormone, thereby producing diuresis that may lead to dehydration. This agent kills organisms by denaturing their proteins. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C2190"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C2190"" NCI Thesaurus); A volatile liquid prepared by fermentation of certain carbohydrates. Alcohol acts as a central nervous system (CNS) depressant, a diuretic, and a disinfectant. Although the exact mechanism of CNS depression is unknown, alcohol may act by inhibiting the opening of calcium channels, mediated by the binding of the inhibitory neurotransmitter gamma-amino butyric acid (GABA) to GABA-A receptors, or through inhibitory actions at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Alcohol inhibits the production of antidiuretic hormone, thereby producing diuresis that may lead to dehydration. This agent kills organisms by denaturing their proteins.; A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in ALCOHOLIC BEVERAGES.; If you are like many Americans, you drink alcohol at least occasionally. For many people, moderate drinking is probably safe. But drinking less is better for your health than drinking more. And there are some people who should not drink at all. Because drinking too much can be harmful, it's important to know how alcohol affects you and how much is too much. How does alcohol affect the body? Alcohol is a central nervous system depressant. This means that it is a drug that slows down brain activity. It can change your mood, behavior, and self-control. It can cause problems with memory and thinking clearly. Alcohol can also affect your coordination and physical control. Alcohol also has effects on the other organs in your body. For example, it can raise your blood pressure and heart rate. If you drink too much at once, it could make you throw up. Why are the effects of alcohol different from person to person? Alcohol's effects vary from person to person, depending on a variety of factors, including: How much you drank How quickly you drank it The amount of food you ate before drinking Your age Your sex Your race or ethnicity Your physical condition Whether or not you have a family history of alcohol problems What is moderate drinking? For most women, moderate drinking is no more than one standard drink a day For most men, moderate drinking is no more than two standard drinks a day Even though moderate drinking may be safe for many people, there are still risks. Moderate drinking can raise the risk of death from certain cancers and heart diseases. What is a standard drink? In the United States, a standard drink is one that contains about 14 grams of pure alcohol, which is found in: 12 ounces of beer (5% alcohol content) 5 ounces of wine (12% alcohol content) 1.5 ounces or a ""shot"" of distilled spirits or liquor (40% alcohol content) Who should not drink alcohol? Some people should not drink alcohol at all, including those who: Are recovering from an alcohol use disorder (AUD) or are unable to control the amount they drink Are under age 21 Are pregnant or trying to become pregnant Are taking medicines that can interact with alcohol Have medical conditions that get can worse if you drink alcohol Are planning on driving Will be operating machinery If you have questions about whether it is safe for you to drink, talk with your health care provider. What is excessive drinking? Excessive drinking includes binge drinking and heavy alcohol use: Binge drinking is drinking so much at once that your blood alcohol concentration (BAC) level is 0.08% or more. For a man, this usually happens after having 5 or more drinks within a few hours. For a woman, it is after about 4 or more drinks within a few hours. Heavy alcohol use is having having more than 4 drinks on any day for men or more than 3 drinks for women Binge drinking raises your risk of injuries, car crashes, and alcohol poisoning. It also puts you of becoming violent or being the victim of violence. Heavy alcohol use over a long period of time may cause health problems such as: Alcohol use disorder Liver diseases, including cirrhosis and fatty liver disease Heart diseases Increased risk for certain cancers Increased risk of injuries Heavy alcohol use can also cause problems at home, at work, and with friends. But treatment can help. NIH: National Institute on Alcohol Abuse and Alcoholism; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T109",,,, -2092,,,,,"A synthetic antihypertensive methoxyphenoxy- 2-propanol derivative with no intrinsic sympathomimetic activity, Carvedilol acts as a nonselective beta-adrenoceptor blocking agent (S(-) enantiomer) and as an alpha 1-adrenoceptor blocker (R(+) and S(-) enantiomers). Its acts more strongly on beta-receptors than on alpha 1-receptors, reduces peripheral vascular resistance by vasodilation, and prevents reflex tachycardia (beta-blockade) so that heart rate is either unchanged or decreased. Carvedilol also reduces renin release through beta-blockade.; A synthetic antihypertensive methoxyphenoxy- 2-propanol derivative with no intrinsic sympathomimetic activity, Carvedilol acts as a nonselective beta-adrenoceptor blocking agent (S(-) enantiomer) and as an alpha 1-adrenoceptor blocker (R(+) and S(-) enantiomers). Its acts more strongly on beta-receptors than on alpha 1-receptors, reduces peripheral vascular resistance by vasodilation, and prevents reflex tachycardia (beta-blockade) so that heart rate is either unchanged or decreased. Carvedilol also reduces renin release through beta-blockade. (NCI04); A carbazole and propanol derivative that acts as a non-cardioselective beta blocker and vasodilator. It has blocking activity for ALPHA 1 ADRENERGIC RECEPTORS and, at higher doses, may function as a blocker of CALCIUM CHANNELS; it also has antioxidant properties. Carvedilol is used in the treatment of HYPERTENSION; ANGINA PECTORIS; and HEART FAILURE. It can also reduce the risk of death following MYOCARDIAL INFARCTION.",,,, -2119,,,,,"Vancomycin is only found in individuals that have used or taken this drug. It is an antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to ristocetin that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear. [PubChem]The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Normally this is a five-point interaction. This binding of vancomycin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi.",,,, -2167,,,,,"A 20 amino acid long synthetic peptide with thrombin-specific anticoagulant properties. Bivalirudin reversibly binds thrombin, free as well as clot bound, at the catalytic site and the anion-binding exosite, thereby preventing the formation and activation of fibrin, factor XIIIa, and other coagulation factors. This drug is primarily used during coronary angioplasty procedures, in combination with aspirin, in patients with unstable angina.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T116",,,, -2193,,,,,"A synthetic physiologically-active analog of vitamin D, specifically the vitamin D3 form. Calcitriol regulates calcium in vivo by promoting absorption in the intestine, reabsorption in the kidneys, and, along with parathyroid hormone, regulation of bone growth. A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Calcitriol also induces cell cycle arrest at G0/G1 phase of the cell cycle, cell differentiation, and apoptosis, resulting in inhibition of proliferation of some tumor cell types. This agent may be chemopreventive for colon and prostate cancers. Check for ""https://www.cancer.gov/about-cancer/treatment/clinical-trials/intervention/C330"" active clinical trials using this agent. (""http://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI%20Thesaurus&code=C330"" NCI Thesaurus); A synthetic physiologically-active analog of vitamin D, specifically the vitamin D3 form. Calcitriol regulates calcium in vivo by promoting absorption in the intestine, reabsorption in the kidneys, and, along with parathyroid hormone, regulation of bone growth. A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Calcitriol also induces cell cycle arrest at G0/G1 phase of the cell cycle, cell differentiation, and apoptosis, resulting in inhibition of proliferation of some tumor cell types. This agent may be chemopreventive for colon and prostate cancers. (NCI04); The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (CALCIFEDIOL). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption.; UMLS Semantic Type: STY:T121; UMLS Semantic Type: STY:T127; UMLS Semantic Type: STY:T109",,,, diff --git a/data/updated_neo4j_triple_data.csv b/data/updated_neo4j_triple_data.csv deleted file mode 100644 index 57d91c0..0000000 --- a/data/updated_neo4j_triple_data.csv +++ /dev/null @@ -1,1000 +0,0 @@ -30347257,1417,,treats,,Sevoflurane,,,,Inflammation,,,,, -24413653,546,,treats,,Fenbendazole,,,,helminthiasis,,,,, -30376577,1300,,treats,,Sodium Chloride,,,,Ascites,,,,, -9783282,549,,treats,,Thiabendazole,,,,helminthiasis,,,,, -16658505,551,,affects,,Albendazole,,,,malaria,,,,, -16658503,551,,disrupts,,Albendazole,,,,malaria,,,,, -11239060,551,,affects,,Albendazole,,,,filariasis,,,,, -9492446,551,,treats,,Albendazole,,,,filariasis,,,,, -15248433,551,,prevents,,Albendazole,,,,filariasis,,,,, -25735916,551,,affects,,Albendazole,,,,trichuriasis,,,,, -9588560,551,,treats,,Albendazole,,,,trichuriasis,,,,, -21848143,551,,causes,,Albendazole,,,,helminthiasis,,,,, -13946207,551,,affects,,Albendazole,,,,helminthiasis,,,,, -8712067,551,,treats,,Albendazole,,,,helminthiasis,,,,, -24729219,551,,disrupts,,Albendazole,,,,helminthiasis,,,,, -13732336,551,,prevents,,Albendazole,,,,helminthiasis,,,,, -18452252,551,,affects,,Albendazole,,,,toxocariasis,,,,, -10114050,551,,treats,,Albendazole,,,,toxocariasis,,,,, -30355168,1300,,treats,,Sodium Chloride,,,,heart disorder,,,,, -10750815,551,,treats,,Albendazole,,,,onchocerciasis,,,,, -7620262,551,,treats,,Albendazole,,,,Hookworm Infections,,,,, -13637338,551,,disrupts,,Albendazole,,,,Hookworm Infections,,,,, -24685635,551,,affects,,Albendazole,,,,filarial elephantiasis,,,,, -7640018,551,,treats,,Albendazole,,,,filarial elephantiasis,,,,, -7226097,551,,treats,,Albendazole,,,,cysticercosis,,,,, -22678969,551,,treats,,Albendazole,,,,Infection,,,,, -25678577,553,,treats,,Latamoxef,,,,bacterial infectious disease,,,,, -21214366,554,,affects,,Ibuprofen,,,,bronchopulmonary dysplasia,,,,, -30645203,953,,treats,,Midazolam,,,,Agitation,,,,, -14332005,554,,predisposes,,Ibuprofen,,,,bronchopulmonary dysplasia,,,,, -24384432,554,,affects,,Ibuprofen,,,,migraine disorder,,,,, -8452594,554,,treats,,Ibuprofen,,,,migraine disorder,,,,, -30647282,1538,,treats,,Finasteride,,,,benign prostatic hyperplasia,,,,, -13826486,554,,affects,,Ibuprofen,,,,osteoarthritis,,,,, -8819538,554,,affects,,Ibuprofen,,,,osteoarthritis,,,,, -7887942,554,,treats,,Ibuprofen,,,,osteoarthritis,,,,, -19399624,554,,prevents,,Ibuprofen,,,,osteoarthritis,,,,, -13653982,554,,causes,,Ibuprofen,,,,Alzheimer disease,,,,, -9436288,554,,treats,,Ibuprofen,,,,Alzheimer disease,,,,, -8331095,554,,disrupts,,Ibuprofen,,,,Alzheimer disease,,,,, -7843138,554,,prevents,,Ibuprofen,,,,Alzheimer disease,,,,, -14294004,554,,predisposes,,Ibuprofen,,,,Alzheimer disease,,,,, -9800201,554,,causes,,Ibuprofen,,,,arthritic joint disease,,,,, -7686895,554,,treats,,Ibuprofen,,,,arthritic joint disease,,,,, -18599970,554,,disrupts,,Ibuprofen,,,,arthritic joint disease,,,,, -21268743,554,,treats,,Ibuprofen,,,,glioma,,,,, -30361649,1728,,treats,,Dronabinol,,,,cannabis dependence,,,,, -8397426,554,,treats,,Ibuprofen,,,,rheumatoid arthritis,,,,, -17292168,554,,treats,,Ibuprofen,,,,Chronic pain,,,,, -13710734,554,,prevents,,Ibuprofen,,,,Chronic pain,,,,, -8698382,554,,treats,,Ibuprofen,,,,Tension-type headache,,,,, -9536612,554,,treats,,Ibuprofen,,,,Low back pain,,,,, -12482174,554,,causes,,Ibuprofen,,,,pancreatitis,,,,, -21354514,554,,prevents,,Ibuprofen,,,,pancreatitis,,,,, -12079834,554,,causes,,Ibuprofen,,,,adult acute respiratory distress syndrome,,,,, -23500890,554,,affects,,Ibuprofen,,,,adult acute respiratory distress syndrome,,,,, -11440746,554,,related to,,Ibuprofen,,,,Toothache,,,,, -12438812,554,,causes,,Ibuprofen,,,,Toothache,,,,, -7210912,554,,treats,,Ibuprofen,,,,Toothache,,,,, -10195210,554,,treats,,Ibuprofen,,,,influenza,,,,, -30645465,724,,treats,,Mannitol,,,,Edema,,,,, -27630106,554,,disrupts,,Ibuprofen,,,,Acute Pain,,,,, -8748381,554,,treats,,Ibuprofen,,,,Dysmenorrhea,,,,, -15961024,554,,prevents,,Ibuprofen,,,,Dysmenorrhea,,,,, -30341165,779,,treats,,Aspirin,,,,preeclampsia,,,,, -11239637,554,,treats,,Ibuprofen,,,,Back pain,,,,, -13726345,554,,causes,,Ibuprofen,,,,patent ductus arteriosus,,,,, -10170540,554,,affects,,Ibuprofen,,,,patent ductus arteriosus,,,,, -7851777,554,,treats,,Ibuprofen,,,,patent ductus arteriosus,,,,, -8584177,554,,prevents,,Ibuprofen,,,,patent ductus arteriosus,,,,, -25518118,554,,treats,,Ibuprofen,,,,Fractured ankle,,,,, -26824955,554,,treats,,Ibuprofen,,,,spondylosis,,,,, -8106985,554,,related to,,Ibuprofen,,,,burn,,,,, -22125431,554,,treats,,Ibuprofen,,,,preeclampsia,,,,, -8163776,554,,causes,,Ibuprofen,,,,injury,,,,, -30381272,1659,,treats,,D-Glucosamine,,,,osteoarthritis,,,,, -9104501,554,,treats,,Ibuprofen,,,,injury,,,,, -9104502,554,,prevents,,Ibuprofen,,,,injury,,,,, -15342704,554,,exacerbates,,Ibuprofen,,,,injury,,,,, -14085648,554,,predisposes,,Ibuprofen,,,,injury,,,,, -20886939,554,,affects,,Ibuprofen,,,,Cognitive impairment,,,,, -30383678,1300,,treats,,Sodium Chloride,,,,cataract,,,,, -17621968,554,,treats,,Ibuprofen,,,,Cognitive impairment,,,,, -18977843,554,,affects,,Ibuprofen,,,,Headache,,,,, -7852264,554,,treats,,Ibuprofen,,,,Headache,,,,, -10201705,554,,prevents,,Ibuprofen,,,,Headache,,,,, -30643233,1619,,treats,,Folic Acid,,,,Reduced blood folate concentration,,,,, -25670779,554,,treats,,Ibuprofen,,,,sunburn,,,,, -17687542,554,,prevents,,Ibuprofen,,,,canker sore,,,,, -11381904,554,,treats,,Ibuprofen,,,,Premature birth,,,,, -20007370,554,,predisposes,,Ibuprofen,,,,cerebral palsy,,,,, -20285347,554,,treats,,Ibuprofen,,,,periodontitis,,,,, -13826476,554,,treats,,Ibuprofen,,,,"osteoarthritis, spine",,,,, -10429873,554,,causes,,Ibuprofen,,,,Hemorrhage,,,,, -11159990,554,,affects,,Ibuprofen,,,,Hemorrhage,,,,, -9889792,554,,affects,,Ibuprofen,,,,Hemorrhage,,,,, -45041718,2038,,treats,,Indapamide,,,,Edema,,,,, -22159382,554,,prevents,,Ibuprofen,,,,Hemorrhage,,,,, -9950431,554,,treats,,Ibuprofen,,,,rheumatic disorder,,,,, -20821983,554,,treats,,Ibuprofen,,,,common cold,,,,, -13133316,554,,causes,,Ibuprofen,,,,peptic ulcer disease,,,,, -45031985,2092,,treats,,Carvedilol,,,,congestive heart failure,,,,, -11790277,554,,treats,,Ibuprofen,,,,hypertensive disorder,,,,, -25657729,554,,prevents,,Ibuprofen,,,,hypertensive disorder,,,,, -30353057,570,,treats,,Methylprednisolone,,,,neoplasm,,,,, -30361615,569,,treats,,Hydrocortisone,,,,adrenal cortex neoplasm,,,,, -16265626,554,,related to,,Ibuprofen,,,,Arthralgia,,,,, -9444914,554,,treats,,Ibuprofen,,,,Arthralgia,,,,, -11536369,554,,treats,,Ibuprofen,,,,seasonal allergic rhinitis,,,,, -14582794,554,,related to,,Ibuprofen,,,,Pain,,,,, -11157616,554,,causes,,Ibuprofen,,,,Pain,,,,, -7732956,554,,treats,,Ibuprofen,,,,Pain,,,,, -30340030,1980,,treats,,Acetaminophen,,,,Pain,,,,, -9022792,554,,prevents,,Ibuprofen,,,,Pain,,,,, -10026104,554,,affects,,Ibuprofen,,,,Myalgia,,,,, -30359313,880,,treats,,Olaparib,,,,head and neck neoplasm,,,,, -23399675,554,,disrupts,,Ibuprofen,,,,Myalgia,,,,, -10026105,554,,prevents,,Ibuprofen,,,,Myalgia,,,,, -12641386,554,,causes,,Ibuprofen,,,,Fever,,,,, -12659717,554,,affects,,Ibuprofen,,,,Fever,,,,, -8421263,554,,affects,,Ibuprofen,,,,Fever,,,,, -7258310,554,,treats,,Ibuprofen,,,,Fever,,,,, -15072611,554,,disrupts,,Ibuprofen,,,,Fever,,,,, -22123299,554,,prevents,,Ibuprofen,,,,Fever,,,,, -15258520,554,,treats,,Ibuprofen,,,,cardiovascular disorder,,,,, -15316470,554,,subclass of,,Ibuprofen,,,,2-Hydroxyibuprofen,,,,, -25984950,556,,treats,,Cefmenoxime,,,,bacterial infectious disease,,,,, -21500374,557,,treats,,Ivabradine,,,,hypotensive disorder,,,,, -30370778,1300,,treats,,Sodium Chloride,,,,liver and intrahepatic bile duct neoplasm,,,,, -30341285,569,,treats,,Hydrocortisone,,,,toxic shock syndrome,,,,, -17909104,557,,disrupts,,Ivabradine,,,,coronary artery disorder,,,,, -13559450,557,,treats,,Ivabradine,,,,Tachycardia,,,,, -10817471,557,,prevents,,Ivabradine,,,,Tachycardia,,,,, -45058087,1478,,treats,,vitamin B12,,,,Methylmalonic acidemia,,,,, -30378782,886,,treats,,Capsaicin,,,,Vomiting,,,,, -20784958,557,,affects,,Ivabradine,,,,atrial fibrillation,,,,, -17604342,557,,treats,,Ivabradine,,,,atrial fibrillation,,,,, -19514713,557,,disrupts,,Ivabradine,,,,atrial fibrillation,,,,, -17822394,557,,prevents,,Ivabradine,,,,atrial fibrillation,,,,, -19153602,557,,predisposes,,Ivabradine,,,,atrial fibrillation,,,,, -15681673,557,,treats,,Ivabradine,,,,multiple organ dysfunction syndrome,,,,, -15641743,557,,treats,,Ivabradine,,,,systolic heart failure,,,,, -20520107,557,,affects,,Ivabradine,,,,mitral valve stenosis,,,,, -18126606,557,,treats,,Ivabradine,,,,mitral valve stenosis,,,,, -12164130,557,,treats,,Ivabradine,,,,Stable angina,,,,, -17604344,557,,related to,,Ivabradine,,,,diastolic heart failure,,,,, -20004006,557,,affects,,Ivabradine,,,,diastolic heart failure,,,,, -17604340,557,,treats,,Ivabradine,,,,diastolic heart failure,,,,, -30369142,724,,treats,,Mannitol,,,,brain injury,,,,, -11342280,557,,treats,,Ivabradine,,,,cardiovascular disorder,,,,, -15385004,558,,affects,,Cefixime,,,,chronic bronchitis,,,,, -15252860,558,,affects,,Cefixime,,,,gonorrhea,,,,, -8827692,558,,treats,,Cefixime,,,,gonorrhea,,,,, -30650079,1090,,treats,,Nelfinavir,,,,diarrheal disease,,,,, -20619094,558,,treats,,Cefixime,,,,bronchitis,,,,, -7594422,558,,treats,,Cefixime,,,,bacterial infectious disease,,,,, -26843374,558,,treats,,Cefixime,,,,tonsillitis,,,,, -22138225,558,,treats,,Cefixime,,,,syphilis,,,,, -23970374,558,,treats,,Cefixime,,,,Infection,,,,, -12941415,558,,treats,,Cefixime,,,,otitis media,,,,, -18811968,558,,prevents,,Cefixime,,,,otitis media,,,,, -26078551,559,,treats,,Ceftizoxime,,,,bacterial infectious disease,,,,, -25661332,559,,treats,,Ceftizoxime,,,,osteomyelitis,,,,, -17748395,560,,related to,,Trimetazidine,,,,diabetic kidney disease,,,,, -22426756,560,,affects,,Trimetazidine,,,,diabetic kidney disease,,,,, -23911647,560,,treats,,Trimetazidine,,,,diabetic kidney disease,,,,, -30376926,1500,,treats,,Empagliflozin,,,,myocardial infarction,,,,, -17755056,560,,treats,,Trimetazidine,,,,Cardiotoxicity,,,,, -18547788,560,,prevents,,Trimetazidine,,,,Cardiotoxicity,,,,, -19164679,560,,affects,,Trimetazidine,,,,cardiovascular disorder,,,,, -17682787,560,,treats,,Trimetazidine,,,,cardiovascular disorder,,,,, -19370408,561,,treats,,Cefodizime,,,,bacterial infectious disease,,,,, -9968932,562,,treats,,Acadesine,,,,B-cell chronic lymphocytic leukemia,,,,, -30379029,724,,treats,,Mannitol,,,,acute kidney failure,,,,, -16822044,567,,treats,,Ranolazine,,,,type 2 diabetes mellitus,,,,, -24441273,567,,treats,,Ranolazine,,,,amyotrophic lateral sclerosis,,,,, -12975239,567,,treats,,Ranolazine,,,,coronary artery disorder,,,,, -30341213,2195,,treats,,Cholecalciferol,,,,vitamin D deficiency,,,,, -17475563,567,,prevents,,Ranolazine,,,,Angina pectoris,,,,, -15243162,567,,treats,,Ranolazine,,,,diastolic heart failure,,,,, -15199166,567,,affects,,Ranolazine,,,,myocardial ischemia,,,,, -9302562,567,,treats,,Ranolazine,,,,myocardial ischemia,,,,, -14751648,567,,prevents,,Ranolazine,,,,myocardial ischemia,,,,, -30358501,953,,treats,,Midazolam,,,,epilepsy,,,,, -13317799,567,,causes,,Ranolazine,,,,atrial fibrillation,,,,, -19002641,567,,affects,,Ranolazine,,,,atrial fibrillation,,,,, -16599546,567,,affects,,Ranolazine,,,,atrial fibrillation,,,,, -13891593,567,,treats,,Ranolazine,,,,atrial fibrillation,,,,, -30341213,2195,,treats,,Cholecalciferol,,,,vitamin D deficiency,,,,, -14280230,567,,prevents,,Ranolazine,,,,atrial fibrillation,,,,, -17988674,567,,predisposes,,Ranolazine,,,,atrial fibrillation,,,,, -19314329,567,,affects,,Ranolazine,,,,cardiovascular disorder,,,,, -30362728,1300,,treats,,Sodium Chloride,,,,Hyperhidrosis,,,,, -19409335,568,,affects,,Prednisolone,,,,sarcoidosis,,,,, -9135976,568,,treats,,Prednisolone,,,,sarcoidosis,,,,, -14345678,568,,treats,,Prednisolone,,,,thrombotic thrombocytopenic purpura,,,,, -12061894,568,,related to,,Prednisolone,,,,West syndrome,,,,, -8752241,568,,treats,,Prednisolone,,,,West syndrome,,,,, -30644310,1363,,treats,,Cephalothin,,,,osteomyelitis,,,,, -30351529,1362,,treats,,Cefazolin,,,,bacterial infectious disease with sepsis,,,,, -24042094,568,,treats,,Prednisolone,,,,biliary atresia,,,,, -11810617,568,,treats,,Prednisolone,,,,congenital adrenal hyperplasia,,,,, -26862829,568,,related to,,Prednisolone,,,,multiple sclerosis,,,,, -7600829,568,,treats,,Prednisolone,,,,multiple sclerosis,,,,, -10531966,568,,related to,,Prednisolone,,,,allergic disease,,,,, -21556285,568,,causes,,Prednisolone,,,,allergic disease,,,,, -25790510,568,,affects,,Prednisolone,,,,allergic disease,,,,, -8906209,568,,treats,,Prednisolone,,,,allergic disease,,,,, -30643845,1894,,treats,,Omeprazole,,,,gastric ulcer,,,,, -27646185,568,,prevents,,Prednisolone,,,,allergic disease,,,,, -13988965,568,,related to,,Prednisolone,,,,osteoarthritis,,,,, -9361682,568,,affects,,Prednisolone,,,,osteoarthritis,,,,, -10565149,568,,treats,,Prednisolone,,,,osteoarthritis,,,,, -17312178,568,,treats,,Prednisolone,,,,type 2 diabetes mellitus,,,,, -30353114,1357,,treats,,mitomycin C,,,,sarcoma,,,,, -17604301,568,,treats,,Prednisolone,,,,cataract,,,,, -22130331,568,,treats,,Prednisolone,,,,schizophrenia,,,,, -30346212,1579,,treats,,Cabergoline,,,,endometriosis,,,,, -18736907,568,,affects,,Prednisolone,,,,asthma,,,,, -30352162,1383,,treats,,Doxorubicin,,,,leukemia,,,,, -30357414,1394,,treats,,Valacyclovir,,,,psychotic disorder,,,,, -10594561,568,,disrupts,,Prednisolone,,,,asthma,,,,, -11858005,568,,prevents,,Prednisolone,,,,asthma,,,,, -25959730,568,,related to,,Prednisolone,,,,sarcoma,,,,, -25621708,568,,related to,,Prednisolone,,,,uveitis,,,,, -26677891,568,,causes,,Prednisolone,,,,uveitis,,,,, -27658451,568,,affects,,Prednisolone,,,,uveitis,,,,, -7485161,568,,treats,,Prednisolone,,,,uveitis,,,,, -27206106,568,,disrupts,,Prednisolone,,,,uveitis,,,,, -7323744,568,,related to,,Prednisolone,,,,pemphigus,,,,, -45053590,1660,,treats,,Torsemide,,,,Edema,,,,, -30648958,1860,,treats,,Leurocristine,,,,leukemia,,,,, -30346114,2195,,treats,,Cholecalciferol,,,,"dermatitis, atopic",,,,, -26365803,568,,related to,,Prednisolone,,,,adrenocortical insufficiency,,,,, -21293782,568,,causes,,Prednisolone,,,,adrenocortical insufficiency,,,,, -10782301,568,,treats,,Prednisolone,,,,adrenocortical insufficiency,,,,, -27323391,568,,affects,,Prednisolone,,,,focal segmental glomerulosclerosis,,,,, -30342047,1894,,treats,,Omeprazole,,,,peptic ulcer disease,,,,, -9924521,568,,related to,,Prednisolone,,,,colitis,,,,, -10519611,568,,causes,,Prednisolone,,,,colitis,,,,, -19824794,568,,affects,,Prednisolone,,,,colitis,,,,, -30342356,1523,,treats,,Letrozole,,,,polycystic ovary syndrome,,,,, -15809068,568,,prevents,,Prednisolone,,,,colitis,,,,, -30351325,551,,treats,,Albendazole,,,,helminthiasis,,,,, -21634207,568,,treats,,Prednisolone,,,,chronic primary adrenal insufficiency,,,,, -20512112,568,,related to,,Prednisolone,,,,castration-resistant prostate carcinoma,,,,, -27410586,568,,affects,,Prednisolone,,,,castration-resistant prostate carcinoma,,,,, -12190701,568,,treats,,Prednisolone,,,,castration-resistant prostate carcinoma,,,,, -24523226,568,,related to,,Prednisolone,,,,glomerulonephritis,,,,, -25165576,568,,affects,,Prednisolone,,,,glomerulonephritis,,,,, -9729887,568,,treats,,Prednisolone,,,,glomerulonephritis,,,,, -9668241,568,,treats,,Prednisolone,,,,pure red-cell aplasia,,,,, -45032669,617,,treats,,Chloramphenicol,,,,typhoid fever,,,,, -10574409,568,,treats,,Prednisolone,,,,epicondylitis,,,,, -20612701,568,,treats,,Prednisolone,,,,myocarditis,,,,, -14373522,568,,causes,,Prednisolone,,,,exfoliative dermatitis,,,,, -24297743,568,,treats,,Prednisolone,,,,exfoliative dermatitis,,,,, -10715297,568,,related to,,Prednisolone,,,,keratitis,,,,, -11808057,568,,treats,,Prednisolone,,,,keratitis,,,,, -26194122,568,,related to,,Prednisolone,,,,synovitis,,,,, -10574410,568,,treats,,Prednisolone,,,,synovitis,,,,, -26227245,568,,prevents,,Prednisolone,,,,synovitis,,,,, -10736101,568,,related to,,Prednisolone,,,,Graves disease,,,,, -9538921,568,,treats,,Prednisolone,,,,Graves disease,,,,, -22194722,568,,related to,,Prednisolone,,,,pulmonary eosinophilia,,,,, -27042309,568,,affects,,Prednisolone,,,,pulmonary eosinophilia,,,,, -15104714,568,,treats,,Prednisolone,,,,pulmonary eosinophilia,,,,, -17143213,568,,related to,,Prednisolone,,,,temporal arteritis,,,,, -30355172,1300,,treats,,Sodium Chloride,,,,bone fracture,,,,, -30645957,767,,treats,,Diflunisal,,,,Pain,,,,, -30355232,1300,,treats,,Sodium Chloride,,,,Sepsis,,,,, -10949449,568,,related to,,Prednisolone,,,,polymyalgia rheumatica,,,,, -7900659,568,,treats,,Prednisolone,,,,polymyalgia rheumatica,,,,, -24291326,568,,treats,,Prednisolone,,,,Anti-neutrophil cytoplasmic antibody-associated vasculitis,,,,, -12510603,568,,related to,,Prednisolone,,,,membranous glomerulonephritis,,,,, -30372878,1768,,treats,,Ketorolac,,,,Miosis,,,,, -30355181,1300,,treats,,Sodium Chloride,,,,cardiac rhythm disease,,,,, -27055840,568,,causes,,Prednisolone,,,,glaucoma,,,,, -12496746,568,,related to,,Prednisolone,,,,neoplasm,,,,, -45040554,789,,treats,,Sodium heparin,,,,myocardial infarction,,,,, -13311736,568,,treats,,Prednisolone,,,,neoplasm,,,,, -26515767,568,,disrupts,,Prednisolone,,,,neoplasm,,,,, -16706850,568,,prevents,,Prednisolone,,,,neoplasm,,,,, -25753407,568,,predisposes,,Prednisolone,,,,neoplasm,,,,, -10496403,568,,related to,,Prednisolone,,,,Inflammation,,,,, -30376517,568,,treats,,Prednisolone,,,,colitis,,,,, -9848677,568,,treats,,Prednisolone,,,,Inflammation,,,,, -8854473,568,,disrupts,,Prednisolone,,,,Inflammation,,,,, -30644574,1860,,treats,,Leurocristine,,,,diffuse large B-cell lymphoma,,,,, -17230021,568,,causes,,Prednisolone,,,,Headache,,,,, -11166436,568,,affects,,Prednisolone,,,,Headache,,,,, -10671990,568,,treats,,Prednisolone,,,,Headache,,,,, -10757066,568,,treats,,Prednisolone,,,,atopic eczema,,,,, -30340353,1538,,treats,,Finasteride,,,,prostate cancer,,,,, -12949384,568,,affects,,Prednisolone,,,,hypereosinophilic syndrome,,,,, -8755027,568,,treats,,Prednisolone,,,,hypereosinophilic syndrome,,,,, -30375875,886,,treats,,Capsaicin,,,,stroke disorder,,,,, -19453072,568,,prevents,,Prednisolone,,,,hypereosinophilic syndrome,,,,, -21254689,568,,treats,,Prednisolone,,,,hypersensitivity pneumonitis,,,,, -8540122,568,,treats,,Prednisolone,,,,autoimmune hemolytic anemia,,,,, -27475554,568,,treats,,Prednisolone,,,,microscopic polyangiitis,,,,, -12428137,568,,related to,,Prednisolone,,,,croup,,,,, -17184322,568,,treats,,Prednisolone,,,,croup,,,,, -30346915,1580,,treats,,Pramipexole,,,,restless legs syndrome,,,,, -7800931,568,,treats,,Prednisolone,,,,autoimmune thrombocytopenic purpura,,,,, -30645606,630,,treats,,CID 49800004,,,,otitis externa,,,,, -22922261,568,,affects,,Prednisolone,,,,allergic bronchopulmonary aspergillosis,,,,, -13327146,568,,treats,,Prednisolone,,,,allergic bronchopulmonary aspergillosis,,,,, -9216084,568,,related to,,Prednisolone,,,,non-Hodgkin lymphoma,,,,, -7990669,568,,treats,,Prednisolone,,,,non-Hodgkin lymphoma,,,,, -11142916,568,,related to,,Prednisolone,,,,lupus nephritis,,,,, -8499057,568,,treats,,Prednisolone,,,,lupus nephritis,,,,, -11037266,568,,related to,,Prednisolone,,,,granulomatosis with polyangiitis,,,,, -7941298,568,,treats,,Prednisolone,,,,granulomatosis with polyangiitis,,,,, -16169223,568,,related to,,Prednisolone,,,,mucocutaneous lymph node syndrome,,,,, -11889996,568,,treats,,Prednisolone,,,,mucocutaneous lymph node syndrome,,,,, -10735679,568,,related to,,Prednisolone,,,,kidney disorder,,,,, -25953223,568,,causes,,Prednisolone,,,,kidney disorder,,,,, -10651502,568,,affects,,Prednisolone,,,,kidney disorder,,,,, -30359098,1829,,treats,,Nitric oxide,,,,Sepsis,,,,, -16371065,568,,related to,,Prednisolone,,,,celiac disease,,,,, -10513879,568,,treats,,Prednisolone,,,,celiac disease,,,,, -15441636,568,,treats,,Prednisolone,,,,lipoma,,,,, -12983495,568,,related to,,Prednisolone,,,,prostate cancer,,,,, -11373326,568,,treats,,Prednisolone,,,,prostate cancer,,,,, -30383695,1300,,treats,,Sodium Chloride,,,,pulmonary arterial hypertension,,,,, -15365269,568,,causes,,Prednisolone,,,,infertility disorder,,,,, -11497678,568,,treats,,Prednisolone,,,,infertility disorder,,,,, -13151963,568,,related to,,Prednisolone,,,,diffuse large B-cell lymphoma,,,,, -11988157,568,,treats,,Prednisolone,,,,diffuse large B-cell lymphoma,,,,, -26295217,568,,related to,,Prednisolone,,,,angioimmunoblastic T-cell lymphoma,,,,, -14012190,568,,treats,,Prednisolone,,,,angioimmunoblastic T-cell lymphoma,,,,, -10527508,568,,related to,,Prednisolone,,,,acute myeloid leukemia,,,,, -7866839,568,,treats,,Prednisolone,,,,acute myeloid leukemia,,,,, -14564343,568,,related to,,Prednisolone,,,,acute lymphoblastic leukemia,,,,, -26879702,568,,has part,,Prednisolone,,,,acute lymphoblastic leukemia,,,,, -30649989,1860,,treats,,Leurocristine,,,,plasma cell myeloma,,,,, -7985554,568,,treats,,Prednisolone,,,,acute lymphoblastic leukemia,,,,, -16852549,568,,treats,,Prednisolone,,,,mature T-cell and NK-cell non-Hodgkin lymphoma,,,,, -16983852,568,,related to,,Prednisolone,,,,Hodgkins lymphoma,,,,, -10020250,568,,treats,,Prednisolone,,,,Hodgkins lymphoma,,,,, -10687782,568,,related to,,Prednisolone,,,,hepatocellular carcinoma,,,,, -10509017,568,,treats,,Prednisolone,,,,hepatocellular carcinoma,,,,, -13151962,568,,related to,,Prednisolone,,,,follicular lymphoma,,,,, -13566191,568,,treats,,Prednisolone,,,,follicular lymphoma,,,,, -11179224,568,,related to,,Prednisolone,,,,alcoholic hepatitis,,,,, -8573433,568,,treats,,Prednisolone,,,,alcoholic hepatitis,,,,, -22580782,568,,treats,,Prednisolone,,,,interstitial lung disease 2,,,,, -13234063,568,,affects,,Prednisolone,,,,pericarditis,,,,, -15369817,568,,treats,,Prednisolone,,,,pericarditis,,,,, -7676165,568,,treats,,Prednisolone,,,,hypercalcemia disease,,,,, -9282196,568,,related to,,Prednisolone,,,,IgA glomerulonephritis,,,,, -7417999,568,,treats,,Prednisolone,,,,IgA glomerulonephritis,,,,, -8268574,568,,treats,,Prednisolone,,,,thrombocytopenia,,,,, -30340776,779,,treats,,Aspirin,,,,infertility disorder,,,,, -23496152,568,,related to,,Prednisolone,,,,subacute thyroiditis,,,,, -8865745,568,,treats,,Prednisolone,,,,subacute thyroiditis,,,,, -8819323,568,,treats,,Prednisolone,,,,meningeal tuberculosis,,,,, -12767794,568,,treats,,Prednisolone,,,,pneumonia,,,,, -25763558,568,,disrupts,,Prednisolone,,,,pneumonia,,,,, -16546227,568,,predisposes,,Prednisolone,,,,pneumonia,,,,, -11013570,568,,related to,,Prednisolone,,,,leukemia,,,,, -30351622,779,,treats,,Aspirin,,,,Hemorrhage,,,,, -10502737,568,,treats,,Prednisolone,,,,hemolytic anemia,,,,, -16960031,568,,related to,,Prednisolone,,,,psoriatic arthritis,,,,, -9109448,568,,treats,,Prednisolone,,,,psoriatic arthritis,,,,, -30649035,1540,,treats,,Celecoxib,,,,colorectal neoplasm,,,,, -22500116,568,,treats,,Prednisolone,,,,HIV infectious disease,,,,, -23374627,568,,treats,,Prednisolone,,,,trichinellosis,,,,, -13758030,568,,treats,,Prednisolone,,,,optic neuritis,,,,, -10503828,568,,related to,,Prednisolone,,,,seasonal allergic rhinitis,,,,, -16502712,568,,related to,,Prednisolone,,,,aplastic anemia,,,,, -14992803,568,,treats,,Prednisolone,,,,aplastic anemia,,,,, -10576837,568,,related to,,Prednisolone,,,,juvenile idiopathic arthritis,,,,, -20836940,568,,treats,,Prednisolone,,,,juvenile idiopathic arthritis,,,,, -19750187,568,,related to,,Prednisolone,,,,lymphoma,,,,, -11074135,568,,affects,,Prednisolone,,,,lymphoma,,,,, -9077262,568,,treats,,Prednisolone,,,,lymphoma,,,,, -16192798,568,,related to,,Prednisolone,,,,dermatomyositis,,,,, -24270725,568,,affects,,Prednisolone,,,,dermatomyositis,,,,, -9061500,568,,treats,,Prednisolone,,,,dermatomyositis,,,,, -11663099,568,,related to,,Prednisolone,,,,Crohn disease,,,,, -30362692,1300,,treats,,Sodium Chloride,,,,Nausea,,,,, -45055265,1860,,treats,,Leurocristine,,,,acute lymphoblastic leukemia,,,,, -10703266,568,,related to,,Prednisolone,,,,ulcerative colitis,,,,, -20789636,568,,causes,,Prednisolone,,,,ulcerative colitis,,,,, -10183156,568,,affects,,Prednisolone,,,,ulcerative colitis,,,,, -7586864,568,,treats,,Prednisolone,,,,ulcerative colitis,,,,, -18452194,568,,exacerbates,,Prednisolone,,,,ulcerative colitis,,,,, -7844202,568,,related to,,Prednisolone,,,,chronic obstructive pulmonary disease,,,,, -13029310,568,,affects,,Prednisolone,,,,chronic obstructive pulmonary disease,,,,, -8455402,568,,treats,,Prednisolone,,,,chronic obstructive pulmonary disease,,,,, -16360878,568,,treats,,Prednisolone,,,,ophthalmic herpes zoster,,,,, -10735861,568,,causes,,Prednisolone,,,,contact dermatitis,,,,, -26379811,568,,disrupts,,Prednisolone,,,,contact dermatitis,,,,, -10744705,568,,related to,,Prednisolone,,,,"dermatitis, atopic",,,,, -11527350,568,,treats,,Prednisolone,,,,"dermatitis, atopic",,,,, -9437304,568,,related to,,Prednisolone,,,,systemic lupus erythematosus,,,,, -8757881,568,,causes,,Prednisolone,,,,systemic lupus erythematosus,,,,, -7395227,568,,affects,,Prednisolone,,,,systemic lupus erythematosus,,,,, -7819165,568,,treats,,Prednisolone,,,,systemic lupus erythematosus,,,,, -16114172,568,,related to,,Prednisolone,,,,plasma cell myeloma,,,,, -26670577,568,,has part,,Prednisolone,,,,plasma cell myeloma,,,,, -11213963,568,,related to,,Prednisolone,,,,leprosy,,,,, -8583398,568,,treats,,Prednisolone,,,,leprosy,,,,, -10983909,568,,prevents,,Prednisolone,,,,leprosy,,,,, -7262473,568,,related to,,Prednisolone,,,,rheumatoid arthritis,,,,, -30363399,1903,,treats,,Esomeprazole,,,,gastric ulcer,,,,, -7158230,568,,treats,,Prednisolone,,,,rheumatoid arthritis,,,,, -10565620,568,,related to,,Prednisolone,,,,nephrotic syndrome,,,,, -16304261,568,,causes,,Prednisolone,,,,nephrotic syndrome,,,,, -7927983,568,,treats,,Prednisolone,,,,nephrotic syndrome,,,,, -30372622,1678,,treats,,Leuprorelin,,,,hypogonadism,,,,, -23981131,568,,treats,,Prednisolone,,,,mycosis fungoides,,,,, -11166361,568,,treats,,Prednisolone,,,,erythema multiforme,,,,, -10555139,568,,affects,,Prednisolone,,,,peptic ulcer disease,,,,, -10557390,568,,treats,,Prednisolone,,,,peptic ulcer disease,,,,, -25942811,568,,treats,,Prednisolone,,,,sympathetic ophthalmia,,,,, -7206314,568,,related to,,Prednisolone,,,,pulmonary tuberculosis,,,,, -10545904,568,,causes,,Prednisolone,,,,pulmonary tuberculosis,,,,, -8647269,568,,treats,,Prednisolone,,,,pulmonary tuberculosis,,,,, -11166363,568,,treats,,Prednisolone,,,,canker sore,,,,, -30646900,1868,,treats,,Diazoxide,,,,hyperinsulinism,,,,, -8856354,568,,related to,,Prednisolone,,,,Prednisone,,,,, -30353606,1417,,treats,,Sevoflurane,,,,Pain,,,,, -30351325,551,,treats,,Albendazole,,,,helminthiasis,,,,, -26415442,568,,derives from,,Prednisolone,,,,Prednisone,,,,, -14808035,568,,physically interacts with,,Prednisolone,,,,Prednisone,,,,, -9296682,568,,physically interacts with,,Prednisolone,,,,Prednisone,,,,, -30649726,1379,,treats,,Mitoxantrone,,,,leukemia,,,,, -21722189,568,,affects,,Prednisolone,,,,Prednisone,,,,, -9655099,568,,has input,,Prednisolone,,,,Prednisone,,,,, -14483328,569,,related to,,Hydrocortisone,,,,bronchopulmonary dysplasia,,,,, -8632826,569,,treats,,Hydrocortisone,,,,bronchopulmonary dysplasia,,,,, -14020540,569,,prevents,,Hydrocortisone,,,,bronchopulmonary dysplasia,,,,, -11888652,569,,related to,,Hydrocortisone,,,,congenital adrenal hyperplasia,,,,, -18446972,569,,causes,,Hydrocortisone,,,,congenital adrenal hyperplasia,,,,, -26997315,569,,affects,,Hydrocortisone,,,,congenital adrenal hyperplasia,,,,, -13999195,569,,affects,,Hydrocortisone,,,,congenital adrenal hyperplasia,,,,, -8061437,569,,treats,,Hydrocortisone,,,,congenital adrenal hyperplasia,,,,, -23738730,569,,produces,,Hydrocortisone,,,,congenital adrenal hyperplasia,,,,, -19793698,569,,related to,,Hydrocortisone,,,,alcohol abuse,,,,, -10522181,569,,related to,,Hydrocortisone,,,,osteoarthritis,,,,, -21274202,569,,affects,,Hydrocortisone,,,,osteoarthritis,,,,, -30342362,1506,,treats,,Methyldopa,,,,preeclampsia,,,,, -9235597,569,,related to,,Hydrocortisone,,,,type 1 diabetes mellitus,,,,, -9175521,569,,treats,,Hydrocortisone,,,,type 1 diabetes mellitus,,,,, -16473285,569,,produces,,Hydrocortisone,,,,type 1 diabetes mellitus,,,,, -8615164,569,,related to,,Hydrocortisone,,,,asthma,,,,, -13347553,569,,affects,,Hydrocortisone,,,,asthma,,,,, -30381740,1980,,treats,,Acetaminophen,,,,type 1 diabetes mellitus,,,,, -7363431,569,,treats,,Hydrocortisone,,,,asthma,,,,, -13669597,569,,produces,,Hydrocortisone,,,,asthma,,,,, -8552834,569,,predisposes,,Hydrocortisone,,,,asthma,,,,, -11089023,569,,related to,,Hydrocortisone,,,,pancreatitis,,,,, -30346592,1457,,treats,,Erythropoietin,,,,injury,,,,, -7432481,569,,treats,,Hydrocortisone,,,,pancreatitis,,,,, -13724762,569,,treats,,Hydrocortisone,,,,severe acute respiratory syndrome,,,,, -45059666,1505,,treats,,Dapagliflozin,,,,congestive heart failure,,,,, -9318796,569,,causes,,Hydrocortisone,,,,adrenocortical insufficiency,,,,, -9535781,569,,treats,,Hydrocortisone,,,,adrenocortical insufficiency,,,,, -13783969,569,,produces,,Hydrocortisone,,,,adrenocortical insufficiency,,,,, -27711985,569,,disrupts,,Hydrocortisone,,,,adrenocortical insufficiency,,,,, -16963888,569,,prevents,,Hydrocortisone,,,,adrenocortical insufficiency,,,,, -7573954,569,,related to,,Hydrocortisone,,,,neoplasm,,,,, -30360418,1652,,treats,,Furosemide,,,,nephrotic syndrome,,,,, -9610203,569,,affects,,Hydrocortisone,,,,neoplasm,,,,, -12524121,569,,treats,,Hydrocortisone,,,,neoplasm,,,,, -8077250,569,,produces,,Hydrocortisone,,,,neoplasm,,,,, -26389045,569,,disrupts,,Hydrocortisone,,,,neoplasm,,,,, -45053023,628,,treats,,Tetracycline,,,,enterocolitis,,,,, -30344072,1955,,treats,,UROKINASE,,,,pulmonary embolism,,,,, -7378370,569,,treats,,Hydrocortisone,,,,chronic primary adrenal insufficiency,,,,, -15330155,569,,produces,,Hydrocortisone,,,,chronic primary adrenal insufficiency,,,,, -7882717,569,,treats,,Hydrocortisone,,,,castration-resistant prostate carcinoma,,,,, -14360687,569,,related to,,Hydrocortisone,,,,dermatitis,,,,, -20336537,569,,affects,,Hydrocortisone,,,,dermatitis,,,,, -17499762,569,,treats,,Hydrocortisone,,,,dermatitis,,,,, -12576998,569,,related to,,Hydrocortisone,,,,Hypoxemia,,,,, -24030854,569,,related to,,Hydrocortisone,,,,Hypoxemia,,,,, -20591759,569,,causes,,Hydrocortisone,,,,Hypoxemia,,,,, -11695335,569,,affects,,Hydrocortisone,,,,Hypoxemia,,,,, -30340776,779,,treats,,Aspirin,,,,infertility disorder,,,,, -15602187,569,,treats,,Hydrocortisone,,,,Hypoxemia,,,,, -11989948,569,,produces,,Hydrocortisone,,,,Hypoxemia,,,,, -30347184,1845,,treats,,CHORIONIC GONADOTROPIN,,,,Pregnancy,,,,, -15155784,569,,related to,,Hydrocortisone,,,,psoriasis,,,,, -20701310,569,,affects,,Hydrocortisone,,,,psoriasis,,,,, -15325707,569,,treats,,Hydrocortisone,,,,psoriasis,,,,, -14450267,569,,related to,,Hydrocortisone,,,,adrenal cortex neoplasm,,,,, -30649058,1829,,treats,,Nitric oxide,,,,Hypoxemia,,,,, -16946872,569,,treats,,Hydrocortisone,,,,adrenal cortex neoplasm,,,,, -13796050,569,,produces,,Hydrocortisone,,,,adrenal cortex neoplasm,,,,, -10518203,569,,related to,,Hydrocortisone,,,,otitis externa,,,,, -9145908,569,,causes,,Hydrocortisone,,,,otitis externa,,,,, -45033357,1797,,treats,,Ciclesonide,,,,asthma,,,,, -25927636,569,,related to,,Hydrocortisone,,,,cardiac arrest,,,,, -26940919,569,,affects,,Hydrocortisone,,,,cardiac arrest,,,,, -19834754,569,,treats,,Hydrocortisone,,,,cardiac arrest,,,,, -11866289,569,,related to,,Hydrocortisone,,,,nicotine dependence,,,,, -30645269,1652,,treats,,Furosemide,,,,hypertensive disorder,,,,, -9850315,569,,causes,,Hydrocortisone,,,,dissociative amnesia,,,,, -7266667,569,,affects,,Hydrocortisone,,,,dissociative amnesia,,,,, -15753359,569,,treats,,Hydrocortisone,,,,dissociative amnesia,,,,, -8615556,569,,predisposes,,Hydrocortisone,,,,dissociative amnesia,,,,, -30381236,2119,,treats,,Vancomycin,,,,nosocomial infection,,,,, -30343321,1523,,treats,,Letrozole,,,,neoplasm,,,,, -19531872,569,,related to,,Hydrocortisone,,,,atrial fibrillation,,,,, -19531871,569,,affects,,Hydrocortisone,,,,atrial fibrillation,,,,, -13075196,569,,prevents,,Hydrocortisone,,,,atrial fibrillation,,,,, -25411585,569,,predisposes,,Hydrocortisone,,,,atrial fibrillation,,,,, -14891361,569,,related to,,Hydrocortisone,,,,"dermatitis, atopic",,,,, -13585273,569,,causes,,Hydrocortisone,,,,"dermatitis, atopic",,,,, -8540090,569,,treats,,Hydrocortisone,,,,"dermatitis, atopic",,,,, -20514012,569,,produces,,Hydrocortisone,,,,"dermatitis, atopic",,,,, -8778414,569,,related to,,Hydrocortisone,,,,Inflammation,,,,, -24445107,569,,related to,,Hydrocortisone,,,,Inflammation,,,,, -10068843,569,,causes,,Hydrocortisone,,,,Inflammation,,,,, -15925719,569,,affects,,Hydrocortisone,,,,Inflammation,,,,, -10431364,569,,affects,,Hydrocortisone,,,,Inflammation,,,,, -8776300,569,,treats,,Hydrocortisone,,,,Inflammation,,,,, -18924640,569,,produces,,Hydrocortisone,,,,Inflammation,,,,, -8865955,569,,disrupts,,Hydrocortisone,,,,Inflammation,,,,, -15550113,569,,prevents,,Hydrocortisone,,,,Inflammation,,,,, -11782928,569,,predisposes,,Hydrocortisone,,,,Inflammation,,,,, -9238280,569,,related to,,Hydrocortisone,,,,Sepsis,,,,, -27747115,569,,causes,,Hydrocortisone,,,,Sepsis,,,,, -24701128,569,,affects,,Hydrocortisone,,,,Sepsis,,,,, -8248241,569,,treats,,Hydrocortisone,,,,Sepsis,,,,, -12147996,569,,produces,,Hydrocortisone,,,,Sepsis,,,,, -17956690,569,,prevents,,Hydrocortisone,,,,Sepsis,,,,, -14643692,569,,exacerbates,,Hydrocortisone,,,,Sepsis,,,,, -19755964,569,,predisposes,,Hydrocortisone,,,,Sepsis,,,,, -30343847,1000,,treats,,Metoprolol,,,,hypertensive disorder,,,,, -8054429,569,,treats,,Hydrocortisone,,,,borderline personality disorder,,,,, -9718673,569,,related to,,Hydrocortisone,,,,atopic eczema,,,,, -27073884,569,,causes,,Hydrocortisone,,,,atopic eczema,,,,, -17910566,569,,affects,,Hydrocortisone,,,,atopic eczema,,,,, -30381224,1066,,treats,,Isotretinoin,,,,breast neoplasm,,,,, -18705900,569,,related to,,Hydrocortisone,,,,phobic disorder,,,,, -22345112,569,,treats,,Hydrocortisone,,,,oral submucous fibrosis,,,,, -15213238,569,,treats,,Hydrocortisone,,,,herpes labialis,,,,, -8570630,569,,related to,,Hydrocortisone,,,,fibromyalgia,,,,, -25383174,569,,causes,,Hydrocortisone,,,,fibromyalgia,,,,, -20137862,569,,affects,,Hydrocortisone,,,,fibromyalgia,,,,, -7402054,569,,treats,,Hydrocortisone,,,,fibromyalgia,,,,, -9492934,569,,related to,,Hydrocortisone,,,,opiate dependence,,,,, -25205462,569,,causes,,Hydrocortisone,,,,hypotensive disorder,,,,, -14533429,569,,affects,,Hydrocortisone,,,,hypotensive disorder,,,,, -13180935,569,,affects,,Hydrocortisone,,,,hypotensive disorder,,,,, -9459897,569,,treats,,Hydrocortisone,,,,hypotensive disorder,,,,, -12533519,569,,related to,,Hydrocortisone,,,,Insulin resistance,,,,, -8017438,569,,related to,,Hydrocortisone,,,,Insulin resistance,,,,, -7929803,569,,causes,,Hydrocortisone,,,,Insulin resistance,,,,, -14970164,569,,affects,,Hydrocortisone,,,,Insulin resistance,,,,, -7974249,569,,affects,,Hydrocortisone,,,,Insulin resistance,,,,, -13691671,569,,treats,,Hydrocortisone,,,,Insulin resistance,,,,, -14100936,569,,produces,,Hydrocortisone,,,,Insulin resistance,,,,, -12187318,569,,prevents,,Hydrocortisone,,,,Insulin resistance,,,,, -30376934,1478,,treats,,vitamin B12,,,,depressive disorder,,,,, -27027571,569,,related to,,Hydrocortisone,,,,HIV infectious disease,,,,, -10074536,569,,affects,,Hydrocortisone,,,,HIV infectious disease,,,,, -13951019,569,,treats,,Hydrocortisone,,,,HIV infectious disease,,,,, -27426083,569,,produces,,Hydrocortisone,,,,HIV infectious disease,,,,, -10280121,569,,treats,,Hydrocortisone,,,,melanoma,,,,, -26128287,569,,disrupts,,Hydrocortisone,,,,melanoma,,,,, -30340084,779,,treats,,Aspirin,,,,hypertensive disorder,,,,, -10518308,569,,treats,,Hydrocortisone,,,,ulcerative colitis,,,,, -11442939,569,,related to,,Hydrocortisone,,,,prostate cancer,,,,, -9665107,569,,treats,,Hydrocortisone,,,,prostate cancer,,,,, -8328567,569,,produces,,Hydrocortisone,,,,prostate cancer,,,,, -45028270,779,,treats,,Aspirin,,,,migraine disorder,,,,, -26840479,569,,affects,,Hydrocortisone,,,,myocardial infarction,,,,, -12881395,569,,treats,,Hydrocortisone,,,,myocardial infarction,,,,, -25797574,569,,related to,,Hydrocortisone,,,,lymphoma,,,,, -18495054,569,,affects,,Hydrocortisone,,,,lymphoma,,,,, -21368080,569,,treats,,Hydrocortisone,,,,lymphoma,,,,, -18495053,569,,affects,,Hydrocortisone,,,,leukemia,,,,, -23769275,569,,treats,,Hydrocortisone,,,,leukemia,,,,, -26428860,569,,disrupts,,Hydrocortisone,,,,leukemia,,,,, -13844584,569,,related to,,Hydrocortisone,,,,acute myeloid leukemia,,,,, -10480635,569,,treats,,Hydrocortisone,,,,atopic conjunctivitis,,,,, -11530989,569,,related to,,Hydrocortisone,,,,pneumonia,,,,, -19555227,569,,affects,,Hydrocortisone,,,,pneumonia,,,,, -9971730,569,,treats,,Hydrocortisone,,,,pneumonia,,,,, -11730055,569,,produces,,Hydrocortisone,,,,pneumonia,,,,, -21020907,569,,disrupts,,Hydrocortisone,,,,pneumonia,,,,, -15540854,569,,prevents,,Hydrocortisone,,,,pneumonia,,,,, -30648642,706,,treats,,Benzoyl Peroxide,,,,contact dermatitis,,,,, -7182905,569,,related to,,Hydrocortisone,,,,obesity disorder,,,,, -12645476,569,,causes,,Hydrocortisone,,,,obesity disorder,,,,, -11304252,569,,affects,,Hydrocortisone,,,,obesity disorder,,,,, -8017440,569,,affects,,Hydrocortisone,,,,obesity disorder,,,,, -30341662,1826,,treats,,Urofollitropin,,,,azoospermia,,,,, -13891079,569,,produces,,Hydrocortisone,,,,obesity disorder,,,,, -15895489,569,,disrupts,,Hydrocortisone,,,,obesity disorder,,,,, -19342068,569,,prevents,,Hydrocortisone,,,,obesity disorder,,,,, -8122784,569,,exacerbates,,Hydrocortisone,,,,obesity disorder,,,,, -30648950,1383,,treats,,Doxorubicin,,,,Cardiotoxicity,,,,, -14075841,569,,treats,,Hydrocortisone,,,,acute lymphoblastic leukemia,,,,, -14387016,569,,related to,,Hydrocortisone,,,,cirrhosis of liver,,,,, -14532907,569,,treats,,Hydrocortisone,,,,cirrhosis of liver,,,,, -24427531,569,,produces,,Hydrocortisone,,,,cirrhosis of liver,,,,, -8977987,569,,related to,,Hydrocortisone,,,,injury,,,,, -18240145,569,,causes,,Hydrocortisone,,,,injury,,,,, -14804311,569,,affects,,Hydrocortisone,,,,injury,,,,, -10523644,569,,affects,,Hydrocortisone,,,,injury,,,,, -11965490,569,,treats,,Hydrocortisone,,,,injury,,,,, -30644075,686,,treats,,Ampicillin,,,,bacterial urinary tract infection,,,,, -45058827,1430,,treats,,Aluminum hydroxide,,,,gastric ulcer,,,,, -13712588,569,,predisposes,,Hydrocortisone,,,,injury,,,,, -22282269,569,,treats,,Hydrocortisone,,,,Infection,,,,, -30370494,1894,,treats,,Omeprazole,,,,ulcer disease,,,,, -11029944,569,,treats,,Hydrocortisone,,,,eye disorder,,,,, -8763179,569,,related to,,Hydrocortisone,,,,toxic shock syndrome,,,,, -27747116,569,,causes,,Hydrocortisone,,,,toxic shock syndrome,,,,, -18310128,569,,affects,,Hydrocortisone,,,,toxic shock syndrome,,,,, -9872405,569,,affects,,Hydrocortisone,,,,toxic shock syndrome,,,,, -7996696,569,,treats,,Hydrocortisone,,,,toxic shock syndrome,,,,, -15760263,569,,produces,,Hydrocortisone,,,,toxic shock syndrome,,,,, -19245686,569,,prevents,,Hydrocortisone,,,,toxic shock syndrome,,,,, -12555774,569,,predisposes,,Hydrocortisone,,,,toxic shock syndrome,,,,, -10516843,569,,treats,,Hydrocortisone,,,,diffuse alopecia areata,,,,, -30370758,1300,,treats,,Sodium Chloride,,,,hyperinsulinism,,,,, -11547088,570,,treats,,Methylprednisolone,,,,thrombotic thrombocytopenic purpura,,,,, -30352387,1523,,treats,,Letrozole,,,,endometriosis,,,,, -9744990,570,,prevents,,Methylprednisolone,,,,ovarian hyperstimulation syndrome,,,,, -7668599,570,,related to,,Methylprednisolone,,,,multiple sclerosis,,,,, -9646753,570,,affects,,Methylprednisolone,,,,multiple sclerosis,,,,, -7668594,570,,treats,,Methylprednisolone,,,,multiple sclerosis,,,,, -14876749,570,,related to,,Methylprednisolone,,,,osteoarthritis,,,,, -30343846,1715,,treats,,Candesartan,,,,hypertensive disorder,,,,, -7443745,570,,related to,,Methylprednisolone,,,,asthma,,,,, -8596544,570,,affects,,Methylprednisolone,,,,asthma,,,,, -8761529,570,,treats,,Methylprednisolone,,,,asthma,,,,, -14967074,570,,prevents,,Methylprednisolone,,,,asthma,,,,, -13533673,570,,treats,,Methylprednisolone,,,,macrophage activation syndrome,,,,, -22495910,570,,related to,,Methylprednisolone,,,,myocarditis,,,,, -22495912,570,,treats,,Methylprednisolone,,,,myocarditis,,,,, -30362692,1300,,treats,,Sodium Chloride,,,,Nausea,,,,, -30358013,1678,,treats,,Leuprorelin,,,,neoplasm,,,,, -19962298,570,,treats,,Methylprednisolone,,,,Hodgkins lymphoma,,,,, -8227578,570,,treats,,Methylprednisolone,,,,mucocutaneous lymph node syndrome,,,,, -24273559,570,,treats,,Methylprednisolone,,,,Abdominal pain,,,,, -18266414,570,,prevents,,Methylprednisolone,,,,Abdominal pain,,,,, -13679356,570,,treats,,Methylprednisolone,,,,hemophagocytic syndrome,,,,, -25845844,570,,related to,,Methylprednisolone,,,,breast neoplasm,,,,, -15407991,570,,treats,,Methylprednisolone,,,,radiculopathy,,,,, -17649050,570,,affects,,Methylprednisolone,,,,optic nerve disorder,,,,, -13096165,570,,treats,,Methylprednisolone,,,,optic nerve disorder,,,,, -23116362,570,,treats,,Methylprednisolone,,,,pneumocystosis,,,,, -7827490,570,,treats,,Methylprednisolone,,,,optic neuritis,,,,, -30368010,2016,,treats,,Ethanol,,,,alcohol abuse,,,,, -19340184,570,,related to,,Methylprednisolone,,,,chronic obstructive pulmonary disease,,,,, -9346353,570,,affects,,Methylprednisolone,,,,chronic obstructive pulmonary disease,,,,, -13619118,570,,treats,,Methylprednisolone,,,,chronic obstructive pulmonary disease,,,,, -14166179,570,,related to,,Methylprednisolone,,,,cardiac arrest,,,,, -23772707,570,,treats,,Methylprednisolone,,,,cardiac arrest,,,,, -15072844,570,,related to,,Methylprednisolone,,,,Edema,,,,, -24161886,570,,causes,,Methylprednisolone,,,,Edema,,,,, -30383695,1300,,treats,,Sodium Chloride,,,,pulmonary arterial hypertension,,,,, -30643177,1478,,treats,,vitamin B12,,,,vitamin B12 deficiency,,,,, -19744632,570,,disrupts,,Methylprednisolone,,,,Edema,,,,, -30353725,921,,treats,,Zoledronic acid,,,,hepatocellular carcinoma,,,,, -7944646,570,,related to,,Methylprednisolone,,,,myasthenia gravis,,,,, -16634377,570,,affects,,Methylprednisolone,,,,myasthenia gravis,,,,, -30381742,1980,,treats,,Acetaminophen,,,,osteoarthritis,,,,, -10221573,570,,treats,,Methylprednisolone,,,,myeloproliferative neoplasm,,,,, -22175056,570,,related to,,Methylprednisolone,,,,myopathy,,,,, -8525599,570,,causes,,Methylprednisolone,,,,myopathy,,,,, -25366540,570,,treats,,Methylprednisolone,,,,myopathy,,,,, -20879022,570,,related to,,Methylprednisolone,,,,Pain,,,,, -15906641,570,,causes,,Methylprednisolone,,,,Pain,,,,, -15906642,570,,affects,,Methylprednisolone,,,,Pain,,,,, -10845505,570,,affects,,Methylprednisolone,,,,Pain,,,,, -8018847,570,,treats,,Methylprednisolone,,,,Pain,,,,, -11106658,570,,disrupts,,Methylprednisolone,,,,Pain,,,,, -8345063,570,,prevents,,Methylprednisolone,,,,Pain,,,,, -30368757,1383,,treats,,Doxorubicin,,,,B-cell neoplasm,,,,, -14278238,570,,related to,,Methylprednisolone,,,,"dermatitis, atopic",,,,, -10049014,570,,treats,,Methylprednisolone,,,,"dermatitis, atopic",,,,, -17333962,570,,related to,,Methylprednisolone,,,,Inflammation,,,,, -18534953,570,,causes,,Methylprednisolone,,,,Inflammation,,,,, -24420470,570,,affects,,Methylprednisolone,,,,Inflammation,,,,, -30341844,568,,treats,,Prednisolone,,,,systemic lupus erythematosus,,,,, -7552935,570,,treats,,Methylprednisolone,,,,Inflammation,,,,, -30368410,839,,treats,,ATROPINE,,,,digestive system disorder,,,,, -9645180,570,,predisposes,,Methylprednisolone,,,,Inflammation,,,,, -30351417,1980,,treats,,Acetaminophen,,,,Postoperative Nausea and Vomiting,,,,, -10048898,570,,affects,,Methylprednisolone,,,,ulcerative colitis,,,,, -8503951,570,,treats,,Methylprednisolone,,,,ulcerative colitis,,,,, -23573980,570,,related to,,Methylprednisolone,,,,pneumonia,,,,, -17307095,570,,causes,,Methylprednisolone,,,,pneumonia,,,,, -8291810,570,,treats,,Methylprednisolone,,,,pneumonia,,,,, -30348579,1939,,treats,,Melatonin,,,,anxiety,,,,, -14399082,570,,related to,,Methylprednisolone,,,,aplastic anemia,,,,, -30376926,1500,,treats,,Empagliflozin,,,,myocardial infarction,,,,, -13166073,570,,causes,,Methylprednisolone,,,,thrombocytopenia,,,,, -8083160,570,,treats,,Methylprednisolone,,,,thrombocytopenia,,,,, -18407557,570,,disrupts,,Methylprednisolone,,,,thrombocytopenia,,,,, -30360429,1478,,treats,,vitamin B12,,,,osteoporosis,,,,, -11819955,570,,affects,,Methylprednisolone,,,,spinal cord injury,,,,, -7980138,570,,prevents,,Methylprednisolone,,,,spinal cord injury,,,,, -24691450,570,,related to,,Methylprednisolone,,,,plantar fasciitis,,,,, -18276332,570,,treats,,Methylprednisolone,,,,plantar fasciitis,,,,, -10812685,570,,related to,,Methylprednisolone,,,,immunoglobulin a vasculitis,,,,, -9980473,570,,treats,,Methylprednisolone,,,,immunoglobulin a vasculitis,,,,, -12672767,570,,causes,,Methylprednisolone,,,,drug-induced liver injury,,,,, -19674675,570,,treats,,Methylprednisolone,,,,microscopic polyangiitis,,,,, -10130342,570,,related to,,Methylprednisolone,,,,adult acute respiratory distress syndrome,,,,, -30378561,2016,,treats,,Ethanol,,,,burn,,,,, -7483648,570,,treats,,Methylprednisolone,,,,adult acute respiratory distress syndrome,,,,, -17478785,570,,treats,,Methylprednisolone,,,,nasal cavity polyp,,,,, -30340397,554,,treats,,Ibuprofen,,,,Fever,,,,, -11313619,570,,treats,,Methylprednisolone,,,,vestibular neuronitis,,,,, -8588816,570,,treats,,Methylprednisolone,,,,Bell's palsy,,,,, -24759961,570,,related to,,Methylprednisolone,,,,non-Hodgkin lymphoma,,,,, -25734987,570,,treats,,Methylprednisolone,,,,non-Hodgkin lymphoma,,,,, -10558884,570,,related to,,Methylprednisolone,,,,lupus nephritis,,,,, -24973247,570,,causes,,Methylprednisolone,,,,lupus nephritis,,,,, -9720542,570,,treats,,Methylprednisolone,,,,lupus nephritis,,,,, -8063034,570,,treats,,Methylprednisolone,,,,granulomatosis with polyangiitis,,,,, -20290784,570,,related to,,Methylprednisolone,,,,membranous glomerulonephritis,,,,, -14232595,570,,treats,,Methylprednisolone,,,,membranous glomerulonephritis,,,,, -14398237,570,,related to,,Methylprednisolone,,,,IgA glomerulonephritis,,,,, -14398238,570,,treats,,Methylprednisolone,,,,IgA glomerulonephritis,,,,, -25642231,570,,treats,,Methylprednisolone,,,,heart disorder,,,,, -9003326,570,,related to,,Methylprednisolone,,,,systemic sclerosis,,,,, -20530617,570,,affects,,Methylprednisolone,,,,systemic sclerosis,,,,, -13161419,570,,treats,,Methylprednisolone,,,,systemic sclerosis,,,,, -8447481,570,,related to,,Methylprednisolone,,,,rheumatoid arthritis,,,,, -15610554,570,,affects,,Methylprednisolone,,,,rheumatoid arthritis,,,,, -7853881,570,,treats,,Methylprednisolone,,,,rheumatoid arthritis,,,,, -20014108,570,,prevents,,Methylprednisolone,,,,rheumatoid arthritis,,,,, -26450412,570,,treats,,Methylprednisolone,,,,leukemia,,,,, -25642837,570,,related to,,Methylprednisolone,,,,dermatomyositis,,,,, -18008318,570,,treats,,Methylprednisolone,,,,dermatomyositis,,,,, -14027935,570,,treats,,Methylprednisolone,,,,diffuse large B-cell lymphoma,,,,, -27228384,570,,related to,,Methylprednisolone,,,,Crohn disease,,,,, -10634179,570,,treats,,Methylprednisolone,,,,Crohn disease,,,,, -18260665,570,,causes,,Methylprednisolone,,,,neoplasm,,,,, -27357949,570,,affects,,Methylprednisolone,,,,neoplasm,,,,, -14636779,570,,treats,,Methylprednisolone,,,,neoplasm,,,,, -26279366,570,,treats,,Methylprednisolone,,,,angioimmunoblastic T-cell lymphoma,,,,, -12183687,570,,related to,,Methylprednisolone,,,,acute lymphoblastic leukemia,,,,, -10136260,570,,treats,,Methylprednisolone,,,,acute lymphoblastic leukemia,,,,, -12975348,570,,treats,,Methylprednisolone,,,,mature T-cell and NK-cell non-Hodgkin lymphoma,,,,, -7432980,570,,treats,,Methylprednisolone,,,,myelodysplastic syndrome,,,,, -26513818,570,,related to,,Methylprednisolone,,,,B-cell chronic lymphocytic leukemia,,,,, -30644476,2119,,treats,,Vancomycin,,,,Clostridium difficile colitis,,,,, -19534575,570,,treats,,Methylprednisolone,,,,anterior ischemic optic neuropathy,,,,, -45033357,1797,,treats,,Ciclesonide,,,,asthma,,,,, -8095661,570,,treats,,Methylprednisolone,,,,carpal tunnel syndrome,,,,, -24559507,570,,related to,,Methylprednisolone,,,,respiratory system disorder,,,,, -23209303,570,,treats,,Methylprednisolone,,,,respiratory system disorder,,,,, -12755316,570,,related to,,Methylprednisolone,,,,plasma cell myeloma,,,,, -11895116,570,,treats,,Methylprednisolone,,,,plasma cell myeloma,,,,, -17288506,570,,related to,,Methylprednisolone,,,,autoimmune thrombocytopenic purpura,,,,, -7808987,570,,treats,,Methylprednisolone,,,,autoimmune thrombocytopenic purpura,,,,, -20286711,570,,related to,,Methylprednisolone,,,,neuromyelitis optica,,,,, -16277488,570,,affects,,Methylprednisolone,,,,neuromyelitis optica,,,,, -30350137,1261,,treats,,Nitroglycerin,,,,injury,,,,, -14891106,570,,affects,,Methylprednisolone,,,,kidney disorder,,,,, -8464737,570,,treats,,Methylprednisolone,,,,kidney disorder,,,,, -26974005,570,,related to,,Methylprednisolone,,,,hematopoietic and lymphoid system neoplasm,,,,, -15936572,570,,related to,,Methylprednisolone,,,,endocrine exophthalmos,,,,, -30360418,1652,,treats,,Furosemide,,,,nephrotic syndrome,,,,, -24586108,570,,related to,,Methylprednisolone,,,,alcoholic hepatitis,,,,, -26339812,570,,treats,,Methylprednisolone,,,,alcoholic hepatitis,,,,, -30342356,1523,,treats,,Letrozole,,,,polycystic ovary syndrome,,,,, -30362374,2193,,treats,,Calcitriol,,,,hypoparathyroidism,,,,, -8330909,570,,affects,,Methylprednisolone,,,,systemic lupus erythematosus,,,,, -8330903,570,,treats,,Methylprednisolone,,,,systemic lupus erythematosus,,,,, -11882768,570,,treats,,Methylprednisolone,,,,Cognitive impairment,,,,, -23934495,570,,prevents,,Methylprednisolone,,,,Cognitive impairment,,,,, -30355168,1300,,treats,,Sodium Chloride,,,,heart disorder,,,,, -7905007,570,,treats,,Methylprednisolone,,,,chronic progressive multiple sclerosis,,,,, -26050805,570,,related to,,Methylprednisolone,,,,ankylosing spondylitis,,,,, -25738014,570,,treats,,Methylprednisolone,,,,ankylosing spondylitis,,,,, -18938435,570,,related to,,Methylprednisolone,,,,graft versus host disease,,,,, -15186368,570,,affects,,Methylprednisolone,,,,graft versus host disease,,,,, -10289517,570,,treats,,Methylprednisolone,,,,graft versus host disease,,,,, -8291272,570,,prevents,,Methylprednisolone,,,,graft versus host disease,,,,, -30362734,1300,,treats,,Sodium Chloride,,,,Chronic pain,,,,, -14690661,570,,treats,,Methylprednisolone,,,,Meniere disease,,,,, -24475300,576,,affects,,Cefotaxime,,,,bacterial infectious disease,,,,, -8153267,576,,treats,,Cefotaxime,,,,bacterial infectious disease,,,,, -18672205,576,,affects,,Cefotaxime,,,,peritonitis,,,,, -15119078,576,,treats,,Cefotaxime,,,,peritonitis,,,,, -12905337,576,,related to,,Cefotaxime,,,,Sepsis,,,,, -23922029,576,,affects,,Cefotaxime,,,,Sepsis,,,,, -11176033,576,,treats,,Cefotaxime,,,,Sepsis,,,,, -15853591,576,,prevents,,Cefotaxime,,,,Sepsis,,,,, -16097513,576,,treats,,Cefotaxime,,,,osteomyelitis,,,,, -19081412,578,,prevents,,Ceftriaxone,,,,bacterial infectious disease,,,,, -26980543,578,,treats,,Ceftriaxone,,,,Lyme disease,,,,, -26401802,578,,treats,,Ceftriaxone,,,,Sepsis,,,,, -18413392,578,,treats,,Ceftriaxone,,,,bacterial pneumonia,,,,, -25827448,589,,related to,,Gefarnate,,,,gastric ulcer,,,,, -25810060,589,,treats,,Gefarnate,,,,gastric ulcer,,,,, -25993651,589,,disrupts,,Gefarnate,,,,gastric ulcer,,,,, -30342043,1829,,treats,,Nitric oxide,,,,malaria,,,,, -25784688,589,,treats,,Gefarnate,,,,duodenal ulcer,,,,, -19702373,589,,treats,,Gefarnate,,,,peptic ulcer disease,,,,, -22023951,590,,treats,,Regadenoson,,,,coronary artery disorder,,,,, -13297277,593,,treats,,Meldonium,,,,Ischemic stroke,,,,, -10690423,603,,related to,,Neobiotic,,,,burn,,,,, -24669492,603,,disrupts,,Neobiotic,,,,bacterial infectious disease,,,,, -26428369,603,,prevents,,Neobiotic,,,,bacterial infectious disease,,,,, -25624167,603,,treats,,Neobiotic,,,,pneumonia,,,,, -11022701,603,,treats,,Neobiotic,,,,bacterial infectious disease with sepsis,,,,, -20263460,603,,affects,,Neobiotic,,,,neoplasm,,,,, -17119153,603,,disrupts,,Neobiotic,,,,neoplasm,,,,, -17758516,603,,related to,,Neobiotic,,,,Inflammation,,,,, -19744068,603,,affects,,Neobiotic,,,,Inflammation,,,,, -21720587,612,,treats,,BLINATUMOMAB,,,,lymphoma,,,,, -22474123,612,,related to,,BLINATUMOMAB,,,,hematopoietic and lymphoid system neoplasm,,,,, -30344516,1541,,treats,,Rofecoxib,,,,Pain,,,,, -21947892,612,,related to,,BLINATUMOMAB,,,,acute lymphoblastic leukemia,,,,, -21932754,612,,treats,,BLINATUMOMAB,,,,acute lymphoblastic leukemia,,,,, -25579460,612,,related to,,BLINATUMOMAB,,,,Precursor B-Cell Lymphoblastic Leukemia-Lymphoma,,,,, -23073290,612,,treats,,BLINATUMOMAB,,,,Precursor B-Cell Lymphoblastic Leukemia-Lymphoma,,,,, -19572117,616,,related to,,Ciprofloxacin,,,,DNA Gyrase,,,,, -17007621,616,,coexists with,,Ciprofloxacin,,,,DNA Gyrase,,,,, -12385742,616,,coexists with,,Ciprofloxacin,,,,DNA Gyrase,,,,, -45032043,1362,,treats,,Cefazolin,,,,bacterial infectious disease with sepsis,,,,, -9387116,616,,physically interacts with,,Ciprofloxacin,,,,DNA Gyrase,,,,, -18400322,616,,affects,,Ciprofloxacin,,,,DNA Gyrase,,,,, -7781719,616,,affects,,Ciprofloxacin,,,,DNA Gyrase,,,,, -19572117,616,,related to,,Ciprofloxacin,,,,DNA Gyrase,,,,, -17007621,616,,coexists with,,Ciprofloxacin,,,,DNA Gyrase,,,,, -12385742,616,,coexists with,,Ciprofloxacin,,,,DNA Gyrase,,,,, -8212496,616,,physically interacts with,,Ciprofloxacin,,,,DNA Gyrase,,,,, -9387116,616,,physically interacts with,,Ciprofloxacin,,,,DNA Gyrase,,,,, -18400322,616,,affects,,Ciprofloxacin,,,,DNA Gyrase,,,,, -7781719,616,,affects,,Ciprofloxacin,,,,DNA Gyrase,,,,, -30361410,1980,,treats,,Acetaminophen,,,,Pruritus,,,,, -11628762,616,,treats,,Ciprofloxacin,,,,endophthalmitis,,,,, -12292532,616,,prevents,,Ciprofloxacin,,,,endophthalmitis,,,,, -8956825,616,,affects,,Ciprofloxacin,,,,cystic fibrosis,,,,, -7798648,616,,treats,,Ciprofloxacin,,,,cystic fibrosis,,,,, -11840711,616,,treats,,Ciprofloxacin,,,,cataract,,,,, -22484062,616,,treats,,Ciprofloxacin,,,,amyotrophic lateral sclerosis,,,,, -14284683,616,,treats,,Ciprofloxacin,,,,gastroenteritis,,,,, -8337570,616,,treats,,Ciprofloxacin,,,,bacterial infectious disease with sepsis,,,,, -10323767,616,,disrupts,,Ciprofloxacin,,,,bacterial infectious disease with sepsis,,,,, -30369697,1417,,treats,,Sevoflurane,,,,brain injury,,,,, -15459841,616,,predisposes,,Ciprofloxacin,,,,bacterial infectious disease with sepsis,,,,, -14398199,616,,treats,,Ciprofloxacin,,,,sinusitis,,,,, -11440816,616,,affects,,Ciprofloxacin,,,,typhoid fever,,,,, -7423320,616,,treats,,Ciprofloxacin,,,,typhoid fever,,,,, -45041161,569,,treats,,Hydrocortisone,,,,acute adrenal insufficiency,,,,, -24010235,616,,treats,,Ciprofloxacin,,,,chronic bronchitis,,,,, -8758764,616,,predisposes,,Ciprofloxacin,,,,gonorrhea,,,,, -10013051,616,,treats,,Ciprofloxacin,,,,plague,,,,, -14202377,616,,prevents,,Ciprofloxacin,,,,plague,,,,, -17154464,616,,causes,,Ciprofloxacin,,,,prostatitis,,,,, -9281470,616,,treats,,Ciprofloxacin,,,,prostatitis,,,,, -25648466,616,,causes,,Ciprofloxacin,,,,abscess,,,,, -30347599,886,,treats,,Capsaicin,,,,Pruritus,,,,, -14141218,616,,treats,,Ciprofloxacin,,,,castration-resistant prostate carcinoma,,,,, -14369807,616,,causes,,Ciprofloxacin,,,,neutropenia,,,,, -8194797,616,,treats,,Ciprofloxacin,,,,neutropenia,,,,, -9504629,616,,treats,,Ciprofloxacin,,,,Sepsis,,,,, -15438014,616,,prevents,,Ciprofloxacin,,,,Sepsis,,,,, -30353247,774,,treats,,Salsalate,,,,Insulin resistance,,,,, -16563368,616,,affects,,Ciprofloxacin,,,,Fever,,,,, -8669720,616,,affects,,Ciprofloxacin,,,,Fever,,,,, -8088120,616,,treats,,Ciprofloxacin,,,,Fever,,,,, -26984478,616,,disrupts,,Ciprofloxacin,,,,Fever,,,,, -11267024,616,,affects,,Ciprofloxacin,,,,eye infectious disorder,,,,, -11304087,616,,treats,,Ciprofloxacin,,,,eye infectious disorder,,,,, -30340302,1457,,treats,,Erythropoietin,,,,myocardial infarction,,,,, -27242944,616,,prevents,,Ciprofloxacin,,,,pyelonephritis,,,,, -10672042,616,,affects,,Ciprofloxacin,,,,Abdominal Infection,,,,, -8956827,616,,treats,,Ciprofloxacin,,,,Abdominal Infection,,,,, -9552171,616,,treats,,Ciprofloxacin,,,,otitis externa,,,,, -24716241,616,,causes,,Ciprofloxacin,,,,peritonitis,,,,, -8190776,616,,treats,,Ciprofloxacin,,,,peritonitis,,,,, -10087799,616,,treats,,Ciprofloxacin,,,,bacterial infectious disease,,,,, -9947057,616,,prevents,,Ciprofloxacin,,,,bacterial infectious disease,,,,, -11684450,616,,treats,,Ciprofloxacin,,,,cystitis,,,,, -8754779,616,,treats,,Ciprofloxacin,,,,rhinoscleroma,,,,, -45049616,568,,treats,,Prednisolone,,,,systemic lupus erythematosus,,,,, -13846017,616,,treats,,Ciprofloxacin,,,,lung disorder,,,,, -13950319,616,,causes,,Ciprofloxacin,,,,pneumonia,,,,, -30382356,1619,,treats,,Folic Acid,,,,Alzheimer disease,,,,, -30360972,1893,,treats,,Lansoprazole,,,,gastric ulcer,,,,, -26466958,616,,disrupts,,Ciprofloxacin,,,,pneumonia,,,,, -8364719,616,,prevents,,Ciprofloxacin,,,,pneumonia,,,,, -30344626,797,,treats,,Rifaximin,,,,diarrheal disease,,,,, -16125923,616,,affects,,Ciprofloxacin,,,,osteomyelitis,,,,, -7880629,616,,treats,,Ciprofloxacin,,,,osteomyelitis,,,,, -8956826,616,,affects,,Ciprofloxacin,,,,Pseudomonas infection,,,,, -11679354,616,,treats,,Ciprofloxacin,,,,Pseudomonas infection,,,,, -20040173,616,,treats,,Ciprofloxacin,,,,lymphoma,,,,, -14005051,616,,treats,,Ciprofloxacin,,,,acute myeloid leukemia,,,,, -19067853,616,,treats,,Ciprofloxacin,,,,B-cell chronic lymphocytic leukemia,,,,, -30648617,619,,treats,,DINUTUXIMAB,,,,neuroblastoma,,,,, -21996198,616,,affects,,Ciprofloxacin,,,,infectious disease,,,,, -9122989,616,,affects,,Ciprofloxacin,,,,infectious disease,,,,, -7228759,616,,treats,,Ciprofloxacin,,,,infectious disease,,,,, -18480207,616,,disrupts,,Ciprofloxacin,,,,infectious disease,,,,, -8054296,616,,prevents,,Ciprofloxacin,,,,infectious disease,,,,, -18366035,616,,predisposes,,Ciprofloxacin,,,,infectious disease,,,,, -13663890,616,,treats,,Ciprofloxacin,,,,otitis media,,,,, -16836665,616,,related to,,Ciprofloxacin,,,,Crohn disease,,,,, -12942741,616,,affects,,Ciprofloxacin,,,,Crohn disease,,,,, -7163480,616,,treats,,Ciprofloxacin,,,,Crohn disease,,,,, -30343558,1822,,treats,,Etoposide,,,,neoplasm,,,,, -11564697,616,,treats,,Ciprofloxacin,,,,chronic obstructive pulmonary disease,,,,, -30375773,2195,,treats,,Cholecalciferol,,,,depressive disorder,,,,, -9704134,616,,treats,,Ciprofloxacin,,,,bronchiectasis,,,,, -7544699,616,,treats,,Ciprofloxacin,,,,diarrheal disease,,,,, -16138544,616,,prevents,,Ciprofloxacin,,,,diarrheal disease,,,,, -21488232,616,,treats,,Ciprofloxacin,,,,Infection,,,,, -45049305,710,,treats,,Pirenzepine,,,,peptic ulcer disease,,,,, -10002223,616,,treats,,Ciprofloxacin,,,,anthrax infection,,,,, -7351604,617,,treats,,Chloramphenicol,,,,eye infectious disorder,,,,, -21241586,617,,prevents,,Chloramphenicol,,,,eye infectious disorder,,,,, -15493028,617,,disrupts,,Chloramphenicol,,,,acne,,,,, -10607698,617,,treats,,Chloramphenicol,,,,bacterial infectious disease,,,,, -9528501,617,,treats,,Chloramphenicol,,,,osteomyelitis,,,,, -16722213,618,,causes,,Rebamipide,,,,osteoarthritis,,,,, -19949890,618,,treats,,Rebamipide,,,,osteoarthritis,,,,, -10125846,618,,affects,,Rebamipide,,,,gastric ulcer,,,,, -10368387,618,,treats,,Rebamipide,,,,gastric ulcer,,,,, -10452606,618,,prevents,,Rebamipide,,,,gastric ulcer,,,,, -24500158,618,,treats,,Rebamipide,,,,gastroesophageal reflux disease,,,,, -8102739,618,,treats,,Rebamipide,,,,gastritis,,,,, -30343321,1523,,treats,,Letrozole,,,,neoplasm,,,,, -13727344,618,,prevents,,Rebamipide,,,,gastritis,,,,, -27679650,618,,affects,,Rebamipide,,,,peptic ulcer disease,,,,, -12062800,618,,treats,,Rebamipide,,,,peptic ulcer disease,,,,, -20953135,618,,prevents,,Rebamipide,,,,peptic ulcer disease,,,,, -13211904,618,,treats,,Rebamipide,,,,ulcerative colitis,,,,, -19364844,618,,treats,,Rebamipide,,,,dry eye syndrome,,,,, -27610972,619,,treats,,DINUTUXIMAB,,,,bone osteosarcoma,,,,, -23020953,619,,related to,,DINUTUXIMAB,,,,neoplasm,,,,, -21740095,619,,treats,,DINUTUXIMAB,,,,neoplasm,,,,, -12385638,619,,related to,,DINUTUXIMAB,,,,neuroblastoma,,,,, -30650155,1619,,treats,,Folic Acid,,,,colorectal carcinoma,,,,, -9445080,619,,treats,,DINUTUXIMAB,,,,neuroblastoma,,,,, -21569598,622,,treats,,BRENTUXIMAB VEDOTIN,,,,adult T-cell leukemia/lymphoma,,,,, -21657994,622,,related to,,BRENTUXIMAB VEDOTIN,,,,mature T-cell and NK-cell non-Hodgkin lymphoma,,,,, -22071488,622,,has part,,BRENTUXIMAB VEDOTIN,,,,mature T-cell and NK-cell non-Hodgkin lymphoma,,,,, -21657991,622,,treats,,BRENTUXIMAB VEDOTIN,,,,mature T-cell and NK-cell non-Hodgkin lymphoma,,,,, -23730531,622,,related to,,BRENTUXIMAB VEDOTIN,,,,mycosis fungoides,,,,, -21472937,622,,treats,,BRENTUXIMAB VEDOTIN,,,,mycosis fungoides,,,,, -23929422,622,,related to,,BRENTUXIMAB VEDOTIN,,,,anaplastic large cell lymphoma,,,,, -22808973,622,,treats,,BRENTUXIMAB VEDOTIN,,,,anaplastic large cell lymphoma,,,,, -22284390,622,,treats,,BRENTUXIMAB VEDOTIN,,,,neoplasm,,,,, -30355168,1300,,treats,,Sodium Chloride,,,,heart disorder,,,,, -23435913,622,,affects,,BRENTUXIMAB VEDOTIN,,,,lymphoma,,,,, -30342844,568,,treats,,Prednisolone,,,,contact dermatitis,,,,, -30340803,2167,,treats,,Bivalirudin,,,,myocardial infarction,,,,, -45032669,617,,treats,,Chloramphenicol,,,,typhoid fever,,,,, -30362717,1300,,treats,,Sodium Chloride,,,,multiple organ dysfunction syndrome,,,,, -21657993,622,,related to,,BRENTUXIMAB VEDOTIN,,,,primary cutaneous T-cell non-Hodgkin lymphoma,,,,, -21657990,622,,treats,,BRENTUXIMAB VEDOTIN,,,,primary cutaneous T-cell non-Hodgkin lymphoma,,,,, -23653011,622,,related to,,BRENTUXIMAB VEDOTIN,,,,diffuse large B-cell lymphoma,,,,, -45044752,570,,treats,,Methylprednisolone,,,,adrenocortical insufficiency,,,,, -10847016,628,,prevents,,Tetracycline,,,,inclusion conjunctivitis,,,,, -30357999,2086,,treats,,Labetalol,,,,hypertensive disorder,,,,, -19472933,628,,causes,,Tetracycline,,,,Helicobacter pylori infectious disease,,,,, -7227539,628,,treats,,Tetracycline,,,,Helicobacter pylori infectious disease,,,,, -10596737,628,,treats,,Tetracycline,,,,osteomyelitis,,,,, -30643640,1213,,treats,,Clemastine,,,,urticaria,,,,, -10513439,628,,treats,,Tetracycline,,,,bacterial infectious disease,,,,, -24565223,628,,prevents,,Tetracycline,,,,bacterial infectious disease,,,,, -20170701,628,,causes,,Tetracycline,,,,periodontitis,,,,, -18080767,628,,affects,,Tetracycline,,,,periodontitis,,,,, -30370500,1179,,treats,,Moxisylyte,,,,erectile dysfunction,,,,, -22346012,628,,treats,,Tetracycline,,,,Infection,,,,, -11754791,629,,related to,,(Alginate)n,,,,cystic fibrosis,,,,, -27435796,629,,affects,,(Alginate)n,,,,cystic fibrosis,,,,, -22788639,629,,treats,,(Alginate)n,,,,Pain,,,,, -10599430,629,,related to,,(Alginate)n,,,,obesity disorder,,,,, -23415127,629,,affects,,(Alginate)n,,,,obesity disorder,,,,, -23508922,629,,predisposes,,(Alginate)n,,,,obesity disorder,,,,, -12376615,629,,related to,,(Alginate)n,,,,gastroesophageal reflux disease,,,,, -27132270,629,,affects,,(Alginate)n,,,,gastroesophageal reflux disease,,,,, -19854419,629,,affects,,(Alginate)n,,,,gastroesophageal reflux disease,,,,, -11016107,629,,treats,,(Alginate)n,,,,gastroesophageal reflux disease,,,,, -8246131,629,,disrupts,,(Alginate)n,,,,gastroesophageal reflux disease,,,,, -11492096,629,,prevents,,(Alginate)n,,,,gastroesophageal reflux disease,,,,, -11597598,635,,related to,,Zolimidine,,,,peptic ulcer disease,,,,, -13503760,638,,affects,,Chlorhexidine,,,,periodontal disorder,,,,, -11792004,638,,treats,,Chlorhexidine,,,,periodontal disorder,,,,, -19905103,638,,prevents,,Chlorhexidine,,,,periodontal disorder,,,,, -19942414,638,,predisposes,,Chlorhexidine,,,,periodontal disorder,,,,, -16147932,638,,causes,,Chlorhexidine,,,,gingivitis,,,,, -8506996,638,,affects,,Chlorhexidine,,,,gingivitis,,,,, -7869752,638,,treats,,Chlorhexidine,,,,gingivitis,,,,, -11272633,638,,disrupts,,Chlorhexidine,,,,gingivitis,,,,, -7990742,638,,prevents,,Chlorhexidine,,,,gingivitis,,,,, -10593306,638,,treats,,Chlorhexidine,,,,eye infectious disorder,,,,, -7281939,638,,treats,,Chlorhexidine,,,,Acanthamoeba keratitis,,,,, -13955725,638,,treats,,Chlorhexidine,,,,bacterial infectious disease,,,,, -30376939,1721,,treats,,Losartan,,,,Left ventricular hypertrophy,,,,, diff --git a/docker-compose.yml b/docker-compose.yml new file mode 100644 index 0000000..1032d38 --- /dev/null +++ b/docker-compose.yml @@ -0,0 +1,17 @@ + +version: '3.11' + + +services: + db: + image: postgres:13.16 + container_name: biomedical + restart: always + environment: + POSTGRES_USER: ${DB_USERNAME} + POSTGRES_PASSWORD: ${DB_PASSWORD} + POSTGRES_DB: ${DB_NAME} + networks: + - default + ports: + - "5433:5432" diff --git a/env/LLMFactCheck.yml b/env/LLMFactCheck.yml index 28fd86b..fd0e1c7 100644 --- a/env/LLMFactCheck.yml +++ b/env/LLMFactCheck.yml @@ -16,3 +16,7 @@ dependencies: - llama-cpp-python - huggingface-hub - openai + + + # - psycopg2 + # - python-dotenv \ No newline at end of file diff --git a/json/local_items_single_3.json b/json/local_items_single_3.json new file mode 100644 index 0000000..27aa059 --- /dev/null +++ b/json/local_items_single_3.json @@ -0,0 +1,6022 @@ +[ + { + "input": { + "triple": "Excision TREATS Stage IA Ovarian Germ Cell Tumor", + "sentence": "CONCLUSION: Our experience emphasizes that patients with true stage Ia ovarian GCT are adequately managed by surgical resection followed by careful clinical, radiologic, and serologic surveillance." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Coronary Artery Bypass Surgery TREATS Ventricular Dysfunction, Left", + "sentence": "Percutaneous coronary intervention versus coronary artery bypass grafting in severe left ventricle dysfunction." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Pharmacotherapy TREATS Secondary malignant neoplasm of large intestine", + "sentence": "This observation is supported by clinical trials demonstrating that cetuximab improves tumor response when used in conjunction with modern chemotherapy in patients with metastatic colorectal cancer." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Vitamin B Complex TREATS Delirium", + "sentence": "In cases of concurrent alcohol withdrawal syndrome, delirium may be treated with haloperidol and a benzodiazepine and B-vitamins." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Selsun shampoo TREATS Seborrheic dermatitis", + "sentence": "Controlled comparison of Clinitar Shampoo and Selsun Shampoo in the treatment of seborrhoeic dermatitis of the scalp." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Drainage procedure TREATS Lesion", + "sentence": "The method may be used for temporary drainage before operation, in transient benign obstructions or as permanent drainage in unresectable lesions." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Catheter Ablation, Radiofrequency TREATS Tachycardia, Ventricular", + "sentence": "RFA is an effective and safe therapy in ventricular tachycardia in structurally normal heart." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Cyclooxygenase 2 Inhibitors TREATS Low Back Pain", + "sentence": "Selective COX-2 inhibitors are currently available and used for patients with low back pain." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "inhibitors TREATS Metastatic melanoma", + "sentence": "Four cases of erysipelas-like inflammation in patients with metastatic melanoma treated with checkpoint inhibitors." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "oxaliplatin TREATS Malignant neoplasm of stomach", + "sentence": "The purpose of this study was to determine the disease-free and overall survival (DFS and OS, respectively) in 991 postgastrectomy gastric cancer patients untreated (n = 372) or treated with either oxaliplatin-based (n = 376) or docetaxel-based (n = 243) chemotherapy and to identify prognostic factors that could help establish subgroups of patients who would benefit from such treatment." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Echinococcosis", + "sentence": "In these last few years we have seen an increase in the percentage of cardiac hydatid disease treated with surgery." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Therapeutic radiology procedure TREATS Malignant neoplasm of prostate", + "sentence": "METHODS AND MATERIALS: Between April 1989 and November 2004, 1,796 men with prostate cancer were treated with RT alone." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Anesthetics TREATS DYSTONIA 12", + "sentence": "Anesthetic Management of a Child With Rapid-Onset Dystonia-Parkinsonism (DYT12-ATP1A3): A Case Report." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Fixation of fracture using plate TREATS Fracture", + "sentence": "Submuscular double bridge plating for complex distal fractures of the humerus: an alternative, safe, and efficient treatment method." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Immunotherapy, Adoptive TREATS Malignant Neoplasms", + "sentence": "Accumulating clinical evidence suggests that adoptive T-cell immunotherapy could be a promising option for control of cancer; evident examples include the graft-vs-leukemia effect mediated by donor lymphocyte infusion (DLI) and therapeutic infusion of ex vivo-expanded tumor-infiltrating lymphocytes (TIL) for melanoma." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Malignant neoplasm of cervix uteri", + "sentence": "Anorectal dysfunction after surgical treatment for cervical cancer." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "inhibitors TREATS Colonic Neoplasms", + "sentence": "The effect of ChoKalpha inhibitors in combination with 5-FU as a new alternative for the treatment of colon tumors has been investigated both in vitro in CRC-tumour derived cell lines, and in vivo in mouse xenografts models." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Targeted Therapy Agent TREATS Indolent B-Cell Non-Hodgkin Lymphoma", + "sentence": "Targeted Agents in the Treatment of Indolent B-Cell Non-Hodgkin Lymphomas." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Immunotherapy TREATS Immune System Diseases", + "sentence": "Anti-tumor necrosis factor-alpha (TNF-alpha) immunotherapy is revolutionizing the treatment of immune disease, particularly Crohn's disease, rheumatoid arthritis, psoriatic arthritis and psoriasis." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Warfarin TREATS Atrial Fibrillation", + "sentence": "A 72-year-old man who had been treated for 20 years with warfarin for auricular fibrillation was scheduled for resection of a sessile mass (3.5 x 4 cm) on the posterior wall of the left atrium and a smaller mass (1.5 x 2 cm) in the right atrium." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Nephrolithotomy, Percutaneous TREATS Kidney Calculi", + "sentence": "METHODS: We prospectively evaluated patients with renal stones treated with percutaneous nephrolithotomy by a single institution's fellows employing the simplified bi-planar (0-90o) fluoroscopic puncture technique for renal access." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "intraperitoneal therapy TREATS Epithelial ovarian cancer", + "sentence": "PATIENTS AND METHODS: In this prospective observational study, from March 2013 to December 2015, the efficacy and tolerability of adjuvant IP/IV chemotherapy in optimally cytoreduced Stage III epithelial OC (EOC) patients were assessed." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Pharmacotherapy TREATS Locally Advanced Malignant Neoplasm", + "sentence": "OBJECTIVE: A computer-assisted technology has recently been proposed for the assessment of therapeutic responses to neoadjuvant chemotherapy in patients with locally advanced breast cancer (LABC)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Bilateral salpingectomy with oophorectomy TREATS Endometrial Carcinoma", + "sentence": "METHODS AND MATERIALS: Two hundred seventeen patients with Stage I-II endometrial carcinoma underwent total abdominal hysterectomy and bilateral salpingo-oophorectomy, followed by high-dose-rate (HDR) intracavitary irradiation, 5.5 Gy x 4 (22 Gy), to the upper 5 cm of the vagina." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "CyberKnife TREATS Intraocular melanoma", + "sentence": "Quality of life in the follow-up of uveal melanoma patients after enucleation in comparison to CyberKnife treatment." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Dopaminergic Agents TREATS Parkinson Disease", + "sentence": "PHNO differs from other dopaminergic drugs and may be useful in the treatment of Parkinson's disease." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antibiotic therapy TREATS Acute leukemia", + "sentence": "Sequential antibiotic therapy in acute leukemia." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Mexiletine TREATS Diabetic Neuralgia", + "sentence": "OBJECTIVE: To investigate the efficacy and safety of mexiletine in the treatment of painful diabetic neuropathy." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "macromolecule TREATS Vascular Diseases", + "sentence": "Evidence of the involvement of soluble, thermo-labile, and proteinase-inactivated macromolecules present in PO212 crude extracts in the control of Fusarium vascular disease in tomato plants was found." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antibiotics TREATS Influenza", + "sentence": "ANSWER: Use of antibiotics for treatment of viral infections such as influenza contributes to the emergence of resistant bacteria strains." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Cardiomyopathies", + "sentence": "Surgery for cardiomyopathy with mitral regurgitation and dyssynchrony." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Surgical Procedures, Laparoscopic TREATS Pregnancy, Tubal", + "sentence": "CONCLUSIONS: This meta-analysis shows that laparoscopic surgery is the most cost-effective treatment for tubal EP." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Peritoneal lavage TREATS Kidney Failure, Acute", + "sentence": "[The treatment of acute renal failure by peritoneal irrigation]." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Implantation procedure TREATS Hypertensive", + "sentence": "We compared the effects of telmisartan and valsartan on late lumen loss and inflammatory markers after sirolimus-eluting stent implantation in hypertensive patients." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Cognitive Therapy TREATS Hypochondriasis", + "sentence": "The aim of this study was to test CBT for hypochondriasis in a centre that was not involved in its development and compare both CBT and short-term psychodynamic psychotherapy (STPP) to a waiting-list control and to each other." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Artificial Ventricle TREATS Heart failure", + "sentence": "Expert opinion: Increasing use of VADs has facilitated a leading edge in management of advanced heart failure either as a bridge to transplantation or as a bridge to myocardial recovery." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Pharmacotherapy TREATS Leprosy", + "sentence": "Aims of the present study was to study the profile of RFT cases in leprosy treated with FD-MDT, who required extended MDT, duration between completion of FD -MDT and clinical presentation, Acid Fast Bacilli (AFB) status, histopathology and type of leprosy at the time of presentation." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Therapeutic radiology procedure TREATS Malignant neoplasm of prostate", + "sentence": "Role of principal component analysis in predicting toxicity in prostate cancer patients treated with hypofractionated intensity-modulated radiation therapy." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Surgical Procedures on the Penis TREATS Extravasation", + "sentence": "Forty-one patients underwent penile venous ligation surgery for pure cavernosal venous leakage diagnosed by infusion cavernosometry and cavernosography." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Percutaneous sperm aspiration TREATS Azoospermia", + "sentence": "Multiple needle-pass percutaneous testicular sperm aspiration as first-line treatment in azoospermic men." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Systemic Therapy TREATS Pancreatic Ductal Adenocarcinoma", + "sentence": "Although there have been advances in systemic, primarily cytotoxic, therapies, it has been a challenge to treat patients with PDA using targeted therapies." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antidotes TREATS Poisoning", + "sentence": "Review of oximes in the antidotal treatment of poisoning by organophosphorus nerve agents." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "artesunate TREATS Malaria", + "sentence": "Although artesunate is clearly superior, parenteral quinine is still used widely for the treatment of severe malaria." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "pirfenidone TREATS Hamman-Rich syndrome", + "sentence": "At present, no drugs are approved for the treatment of ILDs other than nintedanib and pirfenidone for the treatment of idiopathic pulmonary fibrosis." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Radiotherapy, Intensity-Modulated TREATS Nasopharyngeal carcinoma", + "sentence": "Methods: This was a retrospective study consisting of 156 NPC patients treated with IMRT." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "docetaxel TREATS Breast cancer metastatic", + "sentence": "The addition of capecitabine to docetaxel on a 3-week schedule resulted in superior response rate, increased time to progression (TTP), and improved overall survival in patients with anthracycline-pretreated metastatic breast cancer (MBC)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Idiopathic scoliosis", + "sentence": "SUMMARY OF BACKGROUND DATA: In common practice, patients who have undergone surgery for idiopathic scoliosis are followed up for a minimum of 2 years by clinical assessment and routine radiographic study at 3, 6, 12, and 24 months." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "intradermal injection TREATS Auriculotemporal Syndrome", + "sentence": "The remaining eight patients with recurrence of Frey's syndrome were successfully managed with a secondary intracutaneous injection of botulinum toxin type A." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Menotropins 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{ + "input": { + "triple": "Vitamin K antagonist TREATS Thromboembolism", + "sentence": "The vitamin K antagonists (VKAs) have been the standard treatment of thromboembolic diseases for more than 50 years." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Thyroxine TREATS Cretinism", + "sentence": "Neonates with CH have the worst rEI initially, but they reached the indices of the healthy infants thanks to L-thyroxin treatment." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Recombinant Growth Hormone TREATS Turner's Syndrome", + "sentence": "Patients with Turner syndrome were treated with recombinant human growth hormone (GH) for 3 years." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Insulin TREATS Diabetes Mellitus", + "sentence": "BACKGROUND: Insulin (INS) has been used in the treatment of diabetes mellitus." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Prophylactic treatment TREATS Migraine 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Localized Gastric Carcinoma", + "sentence": "Background: Surgical treatment is the key to cure localized gastric cancer." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Radiofrequency ablation TREATS Renal mass", + "sentence": "Pretreatment biopsy is performed more often for lesions treated by cryoablation than RFA with a significantly higher rate of indeterminate or unknown pathology for SRMs undergoing RFA versus cryoablation (P < 0.0001)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Thyrotoxicosis", + "sentence": "[Further remarks on non-toxic goiter following surgery for thyrotoxicosis]." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Experimental drug TREATS Diarrhea", + "sentence": "Shaman Pharmaceuticals is recruiting volunteers for a study of Provir (SP-303), an experimental drug being used to treat diarrhea." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antibiotics TREATS Septicemia", + "sentence": "Early recognition of sepsis, prompt treatment with antibiotics, and source control with surgical management allow for optimal chance of recovery." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Acarbose TREATS Hyperglycemia", + "sentence": "Acarbose improves postprandial hyperglycemia by delaying the release of glucose from complex carbohydrates in the absence of an increase in insulin secretion." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Ganciclovir TREATS Communicable Diseases", + "sentence": "Ganciclovir is effective in the treatment of human infections with viruses of the Herpesviridae family." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Molecular Target TREATS Malignant Neoplasms", + "sentence": "With the increasing knowledge of critical molecular targets in head and neck cancer (e.g. the epidermal growth factor receptor), many novel targeted 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"sentence": "Intraventricular administration of recombinant tissue-type plasminogen activator (rtPA) has proved successful in the treatment of spontaneous panventricular haemorrhage." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Phenylephrine TREATS Mean blood pressure", + "sentence": "CONCLUSION: Phen improves MAP and systemic and cerebral perfusion pressure in the prehospital phase but does not reduce secondary neuronal ischemia." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Nafcillin TREATS Staphylococcal Infections", + "sentence": "The nafcillin concentration of simultaneous cerebrospinal fluid (CSF) and serum specimens from nine patients being treated with parenteral nafcillin for staphylococcal infection were measured." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Dilator TREATS Renal Artery Stenosis", + "sentence": "A 6.5-Fr guiding catheter (Parent Plus 45, Medikit, Tokyo, Japan), composed of a hydrophilic 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"triple": "levofloxacin TREATS Febrile Neutropenia", + "sentence": "Oral Step-Down Therapy With Levofloxacin for Febrile Neutropenia in Children With Cancer.BACKGROUND: Although febrile neutropenia (FN) is a frequent complication in children with cancer receiving chemotherapy, there remains significant variability in selection of route (intravenous [IV] vs oral) and length of therapy." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Proctocolectomy, Restorative TREATS Ulcerative Colitis", + "sentence": "CONCLUSIONS: Restorative proctocolectomy for patients with MUC and coexisting colorectal cancer can be performed with a favorable prognosis and function." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antibiotics TREATS Superficial Infection", + "sentence": "BACKGROUND: Impetigo is a common superficial skin infection that affects people worldwide and is usually treated with antibiotics; therefore, its management has implications for global 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effects." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Terbutaline TREATS Diabetes Mellitus, Insulin-Dependent", + "sentence": "CONCLUSIONS: These data demonstrate substantial glycemic responses to Ala and terbutaline, through different mechanisms, in IDDM patients." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Microsurgery TREATS Cancer of Rectum", + "sentence": "Satisfactory results have been reported after CMT and TEM for the treatment of highly selected T2 N0 rectal cancers." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antirheumatic Agents TREATS Rheumatoid Arthritis", + "sentence": "INTRODUCTION: Disease-modifying anti-rheumatic drugs (DMARDs) currently form the mainstay of treatment of rheumatoid arthritis (RA)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "prednisolone TREATS Pain", + "sentence": "In a double-blind, placebo-controlled trial, treatment of patients with inflammatory OA of the hand (with pain, soft-tissue swelling and an ultrasound picture characteristic of inflammation) with 10 mg prednisolone per day for 6 weeks resulted in a larger decrease in pain than placebo did." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "inhibitors TREATS Virus Diseases", + "sentence": "While viral protease and polymerase inhibitors have shown great successes in treating chronic HCV infections, drugs that specifically target the helicase activity have not advanced." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Medical Nutrition Therapy TREATS Kidney Calculi", + "sentence": "Food and nutrition professionals provide medical nutrition therapy for patients with kidney stones." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Photochemotherapy TREATS Malignant Neoplasms", + "sentence": "Photodynamic therapy is an innovative approach to treat diverse cancers and diseases that involves the use of photosensitizing agents along with light of an appropriate wavelength to generate cytotoxic reactive oxygen species." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Molecular Target TREATS Leukemia, Lymphocytic, Acute", + "sentence": "The identification of the HSPA5 as a chemoresistance biomarker and molecular target for B-lineage ALL may lead to new anti-leukaemic treatment strategies that are much needed." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Monoclonal Antibody Therapy TREATS Solid tumor", + "sentence": "A further meta-analysis of 16 RCTs showed that anti-PD-1/PD-L1 mAb therapy had a benefit in patients with solid tumors (overall survival; hazard ratio = 0.73, 95% CI: 0.68-0.79; p < 0.001), supported by convincing evidence." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "HIV Vaccine TREATS Pediatric human immunodeficiency virus infection", + "sentence": "It is likely that additional intervention strategies, such as a maternal HIV vaccine, will be required to eliminate pediatric HIV infections." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Pilonidal Cyst", + "sentence": "OBJECTIVES: To determine the relative effects of open compared with closed surgical treatment for pilonidal sinus on the outcomes of time to healing, infection and recurrence rate." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antipsychotic Agents TREATS Aggressive behavior", + "sentence": "Studies reviewed in this article provide evidence for the use of psychostimulants, alpha-2 agonists, beta blockers, lithium, anticonvulsant mood-stabilizers, atypical antipsychotics, traditional antipsychotics, and selective serotonin reuptake inhibitors in treating pediatric aggression with the choice of medication dependent on symptomology." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Pharmacotherapy TREATS Dyslipidemias", + "sentence": "Pharmacotherapies targeting dyslipidemia, hypercholesterolemia, and neutralizing inflammatory cytokines (TNF-alpha, IL-1beta, IL-6, IL-17, and IL-12/23) have displayed proven promises although contradictory results." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Histone Deacetylase Inhibitor TREATS Inflammatory disorder", + "sentence": "Histone deacetylase inhibitors (HDACi) are currently in clinical trials for the treatment of inflammatory disorders." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Life support procedure TREATS Severe Acute Respiratory Syndrome", + "sentence": "Of these 405 patients, 255 were placed on ECLS for severe ARDS refractory to all other treatment." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Teriparatide therapy TREATS Bone necrosis", + "sentence": "Teriparatide therapy for alendronate-associated osteonecrosis of the jaw." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Calcitonin TREATS Pain", + "sentence": "CONCLUSIONS: We propose that clinicians consider use of intranasal calcitonin for the treatment of pain due to acute coccyx fractures." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Immunoglobulins, Intravenous TREATS Autoimmune Thrombocytopenia", + "sentence": "Fatal thrombotic events during treatment of autoimmune thrombocytopenia with intravenous immunoglobulin in elderly patients." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Therapeutic radiology procedure TREATS Malignant neoplasm of breast", + "sentence": "To the best of our knowledge, we report the first case of a pulmonary cutaneous fistula arising as a late effect of radiation therapy for breast cancer, which was successfully repaired using a free omental graft." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Proton therapy TREATS Locally Advanced Malignant Neoplasm", + "sentence": "PURPOSE: Dosimetric planning studies have described potential benefits for the use of proton radiation therapy (RT) for locally advanced breast cancer." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Traumatic injury", + "sentence": "Epilepsy surgery in bifrontal injury from prior craniopharyngioma resections." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Ribavirin TREATS Hepatitis C virus", + "sentence": "METHODS: A prospective study was performed to analyze HCV RNA load, liver function, and CD4+ count at weeks 0 (baseline), 12, 24, and 48 of treatment and at 24 weeks after drug discontinuation in 20 patients co-infected with HIV and HCV who failed standard interferon therapy and were then treated with PEG-INF-alphaand ribavirin." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Angioplasty, Balloon TREATS Obstruction", + "sentence": "OBJECTIVE: Minimally invasive interventions by recanalization, percutaneous transluminal angioplasty, and stenting in post-thrombotic syndrome (PTS) obstructions and iliac vein compression syndrome (IVCS) have shown good results." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Propranolol TREATS cardiac arrhythmia", + "sentence": "Propranolol, available commercially as a racemic mixture, is a non-selective beta-adrenergic blocking agent used in the treatment of hypertension, angina pectoris and cardiac arrhythmias." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Spinal Fusion TREATS Chronic low back pain", + "sentence": "BACKGROUND CONTEXT: Spinal fusion is a common but controversial treatment for chronic low back pain (LBP) with outcomes similar to those of programmed conservative care." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Systemic Therapy TREATS Cholangiocarcinoma", + "sentence": "The current review focuses on recent advances in the diagnosis and treatment of patients with cholangiocarcinoma and, in particular, on the role of endoscopy, surgery, transplantation, radiotherapy, systemic therapy, and liver-directed therapies in the curative or palliative treatment of these individuals." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Uterine Artery Embolization TREATS Abnormal uterine bleeding", + "sentence": "Efficacy of Uterine Artery Embolization for Treatment of Anticoagulant-Associated Abnormal Uterine Bleeding." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Levodopa TREATS Parkinson Disease", + "sentence": "Ropinirole as an adjunct to levodopa in the treatment of Parkinson's disease: a 16-week bromocriptine controlled study." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Cimetidine TREATS Ulcer", + "sentence": "The number of ulcers substantially decreased in the rat groups receiving either cimetidine or carbenoxolone pretreatment for two or more days before stress." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "nefazodone TREATS Stress Disorders, Post-Traumatic", + "sentence": "Through its mechanism inhibiting neuronal uptake of serotonin and norepinephrine and as a potent postsynaptic serotonergic antagonist, nefazodone has proven to be effective in treating post-traumatic stress disorder in several open-label trials." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Braces-Orthopedic appliances TREATS Patellar Dislocation", + "sentence": "The majority of patella dislocations can be reduced with simple manoeuvres or even spontaneously and can be managed conservatively by bracing and rehabilitation." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Allogeneic bone marrow transplantation TREATS Leukemia, Myelocytic, Acute", + "sentence": "A 64-year-old man underwent kidney transplantation for progressive chronic renal failure which had developed 8 years after allogeneic bone marrow transplantation for acute myeloid leukemia." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Aortic Aneurysm, Abdominal", + "sentence": "A 71-year-old male with abdominal aortic aneurysm, coronary artery disease and obstructive peripheral arteriosclerosis successfully underwent a combined operation of coronary artery bypass grafting (CABG), replacement of abdominal aortic aneurysm and femoro-popliteal bypass." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Radical prostatectomy TREATS Malignant neoplasm of prostate", + "sentence": "METHODS: PSA was assessed (PSA IMx, Abbott Diagnostic, Rungis, France) in serum and in the first voided urine before and after massage in 59 patients: 7 after cystoprostatectomy for bladder cancer, 22 with prostate in situ, and 30 after radical prostatectomy for prostate cancer." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "T cell therapy TREATS Communicable Diseases", + "sentence": "Since the first bone marrow transplantation, adoptive T cell therapy (ACT) has developed over the last 80 years to a highly efficient and specific therapy for infections and cancer." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Exercise, Aerobic TREATS Oxidative Stress", + "sentence": "Aerobic exercise mitigates oxidative stress and apoptosis caused by myocardial infarction (MI) even though the precise mechanisms remain completely elusive." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Epidural steroid injection TREATS Degenerative spondylolisthesis", + "sentence": "However, to our knowledge, there has been no study which has evaluated the outcomes of TFESI in patients with DLS." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Rectum excision TREATS Proctitis", + "sentence": "Many patients will require a proctectomy as the definitive treatment, especially for gangrenous proctitis." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "doramectin TREATS Lice Infestations", + "sentence": "CONCLUSION AND CLINICAL RELEVANCE: Injectable doramectin at a dosage of 200 micrograms/kg is safe and effective for treatment of gastrointestinal nematodiasis and louse infestations of cattle under field conditions." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Arthrodesis TREATS Giant Cell Tumors", + "sentence": "Resection arthrodesis for the management of aggressive giant cell tumor of the distal femur." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Local anesthesia TREATS Shoulder Impingement Syndrome", + "sentence": "OBJECTIVES: We evaluated the contribution of subacromial local anesthetic and corticosteroid injection to the conservative treatment of subacromial impingement syndrome." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Drug Combinations TREATS Malignant neoplasm of thorax", + "sentence": "This three-drug combination appears to be a reasonable treatment approach in patients with thoracic malignancies receiving an AUC >=5 mg/mL per minute of CBDCA-based regimen." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Gastrectomy TREATS Malignant neoplasm of stomach", + "sentence": "The Impact and Clinical Prediction of Hyperglycemia During Parenteral Nutrition for Nondiabetic Patients After Gastrectomy for Gastric Cancer." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Pancreaticojejunostomy TREATS Pancreatitis, Chronic", + "sentence": "AIM: To evaluate the possible advantages and disadvantages of S-PJ and L-PJ and to interpret the perspective of S-PJ in the treatment of CP." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Excision TREATS Lesion", + "sentence": "On an intent-to-treat basis, outcomes of surgery for transverse colon lesions (TC) were compared with outcomes of segmental colon resections for other lesions (OC)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Treatment Protocols TREATS Systemic arterial pressure", + "sentence": "Therefore the regimens of currently available drugs are being fine-tuned, resulting in the establishment of several novel fixed-dose combinations including triple combinations with the aim to facilitate proper blood pressure control." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Agent TREATS Coronavirus Infections", + "sentence": "These agents may be investigated further for the treatment of coronavirus infections." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Cefoxitin TREATS Acute appendicitis NOS", + "sentence": "CONCLUSIONS: We conclude that ceftizoxime is as effective as cefoxitin and can be surely employed in the treatment of acute appendicitis in children." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Behavior Therapy TREATS Tic disorder", + "sentence": "Pilot Open Case Series of Voice over Internet Protocol-delivered Assessment and Behavior Therapy for Chronic Tic Disorders." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Therapeutic radiology procedure TREATS Malignant Neoplasms", + "sentence": "Altered fractionated radiotherapy in head and neck cancer." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Intravenous therapy TREATS Vasculitis", + "sentence": "The vasculitis of SLE was probably responsible for this neuropathy and this case was successfully treated with intravenous cyclophosphamide pulse therapy." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Transplantation TREATS Liver carcinoma", + "sentence": "Liver transplantation for intermediate hepatocellular carcinoma: An adaptive approach." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "removal technique TREATS Chronic infectious disease", + "sentence": "Fistula decompression, bone resection, and urinary reconstruction effectively treats chronic infection, improves pain and ECOG scores." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Cervical arthrodesis TREATS Radiculopathy, Cervical", + "sentence": "Subjects and Methods: The charts of 89 consecutive patients with cervical radiculopathy treated surgically at one level with PCF and cages were reviewed." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Local anesthesia TREATS Pain", + "sentence": "CONCLUSION: The use of lidocaine spray for local anesthesia provided better satisfaction scores than the viscous solution, and both methods have the same effect with regards to the control of discomfort and pain." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antidotes TREATS overdose", + "sentence": "Furthermore, these results indicate that nicotinic acid is a potent antidote to treat GMX1777 overdose." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Aortic valvotomy TREATS Aortic Valve Stenosis", + "sentence": "Retrospective studies have been conducted in Lyon (33 patients) and Montreal (24 patients) in order to compare the results of transventricular valvotomy (TVV, 20 cases) and aortic valvotomy with cardiopulmonary bypass (CPB, 37 cases) in neonatal critical aortic stenosis." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Botulinum Toxins TREATS Pain, Intractable", + "sentence": "The use of Btx could be useful as an adjunctive treatment modality in the management of refractory myofascial pain." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Peripheral Stem Cell Transplantation TREATS Hematologic Neoplasms", + "sentence": "Allogeneic peripheral blood hematopoietic stem cell transplantation for patients with hematologic malignancies." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Durapatite TREATS Urinary Incontinence, Stress", + "sentence": "However, granuloma should be considered when a periurethral mass is encountered after injection of calcium hydroxylapatite for type III stress urinary incontinence." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antibiotics TREATS Bacteremia", + "sentence": "The first was an AIDS patient with relapsing H. cinaedi bacteraemia despite antibiotic treatment." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Angiotensin-Converting Enzyme Inhibitors TREATS Congestive heart failure", + "sentence": "Angiotensin-converting enzyme (ACE) inhibitors have been shown to prolong life expectancy in patients with congestive heart failure." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Angiotensin-Converting Enzyme Inhibitors TREATS COVID-19", + "sentence": "CONCLUSION: It is concluded that ACEIs and ARBs should be continued in COVID-19 patients, reinforcing the recommendations made by several medical societies." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "interferon-beta TREATS Cerebrovascular Disorders", + "sentence": "Autophagy/mitochondrial autophagy, nuclear factor E2-related factor-2 (Nrf2), interferon (IFN)-beta, sirtuin (SIRT), and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) reportedly alleviate cerebrovascular diseases by inhibiting NLRP3 inflammasome activation." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "wound care TREATS Foot Ulcer, Diabetic", + "sentence": "Therefore, the present review is focused on the efforts that have been made over the past years to find peptides possessing wound-healing properties, towards the development of new and effective wound care treatments for diabetic foot ulcers and other skin and soft tissue infections." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Electroconvulsive Therapy TREATS Bipolar Disorder", + "sentence": "Intractable manic-depressive psychosis with rapid cycling in an 18-year-old woman successfully treated with electroconvulsive therapy." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "gene therapy TREATS Atrial Fibrillation", + "sentence": "Recent advances in gene therapy for atrial fibrillation." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "formoterol TREATS Asthma", + "sentence": "CONCLUSION: This study shows that in adult patients whose mild-to-moderate asthma is not fully controlled on low doses of inhaled corticosteroids, single-inhaler therapy with budesonide and formoterol provides greater improvements in asthma control than increasing the maintenance dose of inhaled corticosteroid." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Hyperbaric Oxygenation TREATS Hemorrhagic cystitis", + "sentence": "We analyzed our data regarding HC in allogeneic HSCT patients in order to establish the efficacy of hyperbaric oxygen (HBO) therapy in severe HC and to document the main problems during its use." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Ciprofloxacin TREATS Lower respiratory tract infection", + "sentence": "BACKGROUND: Ciprofloxacin is usually used in the treatment of lower respiratory tract infections (LRTIs)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Surgical Procedures, Endoscopic TREATS Lesion", + "sentence": "Recent advances in endoscopic transnasal surgery have provided an additional approach for the treatment of these difficult lesions." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Lymph node excision TREATS Squamous cell carcinoma of esophagus", + "sentence": "Novel technique for lymphadenectomy along left recurrent laryngeal nerve during thoracoscopic esophagectomy.BACKGROUND: In esophageal squamous carcinoma, lymphadenectomy along the left recurrent laryngeal nerve (RLN) is recommended owing to its highly metastatic potential." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Interferon-alpha TREATS Myeloid Leukemia, Chronic", + "sentence": "SOCS3 mRNA expression in bone marrow cells from CML patients who responded well to IFN-alpha therapy was significantly lower than that in cells from healthy volunteers and patients who were resistant to IFN-alpha therapy." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Cefaclor TREATS Tonsillitis", + "sentence": "Comparative efficacy and safety of cefprozil versus penicillin, cefaclor and erythromycin in the treatment of streptococcal pharyngitis and tonsillitis." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Prophylactic treatment TREATS Pneumocystis jiroveci pneumonia", + "sentence": "SUMMARY: Prophylactic treatment for Pneumocystis carinii pneumonia should begin when the CD4 count falls below 200 cells per microL." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Metformin TREATS Diabetes Mellitus, Non-Insulin-Dependent", + "sentence": "Metformin is currently the most prescribed drug for treatment of type 2 diabetes mellitus in humans." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Standard plate TREATS Fracture with displacement", + "sentence": "Displaced distal tibia shaft fractures are effectively treated with standard plates and intramedullary nails." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Hip Replacement, Total TREATS Fracture", + "sentence": "The recommended treatment for fracture of ceramic bearing surfaces is complete synovectomy and revision total hip arthroplasty." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Nasal Continuous Positive Airway Pressure TREATS Sleep Apnea, Obstructive", + "sentence": "Diastolic BP of normotensive OSA patients did not change significantly by nCPAP treatment, but that of hypertensive OSA patients decreased significantly within 1 month-3 years of nCPAP treatment whether or not medication was used." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Radiosurgery TREATS Advanced Renal Cell Carcinoma", + "sentence": "Stereotactic radiosurgery and stereotactic body radiation therapy (SBRT) have led to a resurgence of the use of radiotherapy in the management of advanced renal cell carcinoma (RCC)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "rituximab TREATS Lymphoma", + "sentence": "Reactivation of hepatitis B virus (HBV) following rituximab (R)-containing chemotherapy for lymphoma is a major concern, and risk factors remain to be defined." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Staphylococcal Toxoid TREATS Fibromyalgia", + "sentence": "The results of this study support the authors>> hypothesis that treatment with staphylococcus toxoid may be a fruitful strategy in patients with fibromyalgia and chronic fatigue syndrome." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Obstruction", + "sentence": "A meta-analysis of endoscopic stenting as bridge to surgery versus emergency surgery for left-sided colorectal cancer obstruction." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "parthenolide TREATS Malignant neoplasm of breast", + "sentence": "Because parthenolide has shown safety in Phase I clinical trials, these findings have direct clinical relevance and provide support for the design of clinical studies combining antiestrogens and parthenolide in ER-positive breast cancer." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antibiotics TREATS Infection", + "sentence": "CONCLUSIONS: CSA-131 could be a potential antimicrobial agent for the treatment of S. maltophilia infections in CF, due to its low cytotoxicity on the CF cell line and good antimicrobial and antibiofilm effects." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Lobectomy TREATS Malignant neoplasm of lung", + "sentence": "Long-term survival in video-assisted thoracoscopic lobectomy vs open lobectomy in lung-cancer patients: a meta-analysis." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Diphosphonates TREATS Osteoarthritis, Knee", + "sentence": "BACKGROUND: The use of bisphosphonates has been reported to have potential beneficial effects on knee osteoarthritis, but existing studies have limitations." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Pharmacotherapy TREATS Lymphoma", + "sentence": "Mitoxantrone was selected for evaluation as single-agent chemotherapy for relapsing canine lymphoma based on its use in humans undergoing salvage chemotherapy for non-Hodgkin's lymphoma and its tumoricidal effect against canine lymphoma." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "iron TREATS Iron deficiency anemia", + "sentence": "CONCLUSION: Preoperative IDA management with intravenous iron is effective in improving hemoglobin level, thereby reducing intraoperative RBC transfusion rate particular if iron is administrated >7 days before surgery." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Pericardiectomy TREATS Cardiac Tamponade", + "sentence": "So emergent pericardiectomy and pericardial drainage were performed to relieve cardiac tamponade." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Percutaneous coronary intervention TREATS Angina Pectoris", + "sentence": "We investigated predictors of the filter no-reflow (FNR) phenomenon during PCI by using multimodality, such as hyperintense plaques (HIPs) in the coronary artery on T1-weighted imaging (T1WI) non-contrast magnetic resonance, plaque composition by using optical coherence tomography (OCT), and serum biomarkers, in patients with angina pectoris." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Methotrexate TREATS Rheumatoid Arthritis", + "sentence": "Nocardiosis associated with low dose methotrexate for rheumatoid arthritis." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Excision TREATS Neurilemmoma", + "sentence": "Intracapsular removal of schwannomas is relatively easy to perform, does not cause any additional damage to the nerve in most cases, and is therefore an excellent method for treatment of symptomatic schwannoma patients." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antioxidants TREATS Complications of Diabetes Mellitus", + "sentence": "AIMS/HYPOTHESIS: Increased oxidative stress has been causally linked to diabetic neurovascular complications, which are attenuated by antioxidants." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Loperamide TREATS Post-vagotomy syndrome", + "sentence": "We examined the effect of two drugs, codeine phosphate and loperamide, on upper intestinal transit and carbohydrate absorption, measured non-invasively by serial exhaled breath hydrogen monitoring, in patients with postvagotomy diarrhoea who had previously failed to gain relief from drug therapy." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Anti-Anxiety Agents TREATS Herpesviridae", + "sentence": "As an anti-viral agent for the herpes virus family, the author found that EPA (Omega 3 fish oil, Eicosa Pentaenoic Acid, C20:5 omega 3), at doses between 180 mg. and 350 mg (depending upon body weight) 4 times a day for 2 to 6 weeks, without prescribing the common anti-viral agent Acyclovir, often eliminated the symptoms due to viral infection including all well-known types of the herpes virus, such as herpes simplex virus, Epstein-Barr virus, and cytomegalovirus." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Excision TREATS Early gastric cancer", + "sentence": "A Single-Center Experience of Endoscopic Resection for Early Gastric Cancer with Lymphoid Stroma." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antiepileptic Agents TREATS CNS disorder", + "sentence": "Due to this situation, the future design of new AEDs must also include a potential in nonepileptic CNS disorders, such as bipolar disorder and neuropathic pain." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Diphosphonates TREATS Osteogenesis Imperfecta", + "sentence": "Antiresorptive bisphosphonates are commonly used to treat adult OI, but have shown mixed efficacy." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Combined Modality Therapy TREATS Carcinoma", + "sentence": "The trend toward multimodality treatment and the use of effective sphincter preserving procedures represent significant changes noted in this survey in the therapy of carcinoma of the rectum." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Excision TREATS Secondary malignant neoplasm of pancreas", + "sentence": "Surgical resection is more effective in treatment for 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most effective drugs used in the treatment of leishmaniasis and systemic fungal infections." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Behavior Therapy TREATS Impulse Control Disorders", + "sentence": "Post-treatment evaluation studies of behaviour therapy (BT) for trichotillomania (TTM) have shown that BT is successful in reducing symptoms in this impulse-control disorder." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Osteogenesis, Distraction TREATS Mandibular retrognathism", + "sentence": "This article evaluates the use of distraction osteogenesis in the treatment of mandibular retrognathia and laterognathia and the long term treatment results of the patients treated with this technique." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Nasogastric tube TREATS Persistent vomiting NOS", + "sentence": "Nine patients required NG tubes for persistent vomiting or abdominal distension." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antipsychotic Agents TREATS Hallucinations", + "sentence": "Atypical neuroleptic drugs are the preferred treatment for symptoms such as delusions, hallucinations, agitation and aggressive behaviour." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Bone Screws TREATS Fracture with displacement", + "sentence": "The Herbert screw is useful in the treatment of displaced fractures of the capitate since the screw maintains reduction, compresses the fracture site, and allows early wrist motion." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Masks TREATS Class III malocclusion", + "sentence": "MATERIALS AND METHODS: The material consisted of pretreatment and posttreatment lateral cephalometric radiographs of 28 subjects with Class III malocclusions treated with a face mask." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "reboxetine TREATS Bedwetting", + "sentence": "Reboxetine may be an 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"validation_result": "Yes" + }, + { + "input": { + "triple": "Emotion-Focused Therapy TREATS Generalized Anxiety Disorder", + "sentence": "A comparison of emotion-focused therapy and cognitive-behavioral therapy in the treatment of generalized anxiety disorder: Results of a feasibility randomized controlled trial." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Therapeutic radiology procedure TREATS Malignant Neoplasms", + "sentence": "During the last decade, some data indicate that regional deep hyperthermia therapy (RHT) combined with either chemo- and / or radiotherapy in malignancies is associated with AVN in young patients." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Melatonin TREATS Traumatic injury", + "sentence": "The aim of our study is to explore whether melatonin alleviates cardiac IR injury by modulating OPA1-related mitochondrial fusion." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical 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"triple": "Ciprofloxacin TREATS Chronic suppurative otitis media NOS", + "sentence": "The most effective antibiotic for treatment of bacterial chronic suppurative otitis media was ciprofloxacin." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Proteasome inhibitor TREATS Hematologic Neoplasms", + "sentence": "Proteasome inhibitors have shown remarkable success in the treatment of hematologic neoplasm." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Hemorrhage", + "sentence": "This treatment policy has as its major feature an early elective operation in patients with arterial bleeding and a visible vessel, providing that endoscopic control of the bleeding could be achieved." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Octreotide TREATS Vipoma", + "sentence": "In October 1988, octreotide received FDA-approved labeling for use in the management of carcinoid syndrome and vipomas." + }, 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+ { + "input": { + "triple": "Diuretics TREATS Hypertensive disease", + "sentence": "Although pharmacological therapy of asymptomatic hyperuricaemia is not recommended, primary prevention of gout can be achieved through lifestyle changes including weight loss, restricting protein and calorie intake, limiting alcohol consumption, avoiding the use of diuretics in the treatment of hypertension, and avoiding occupational exposure to lead." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antibiotics TREATS Pneumonia", + "sentence": "He was treated with antibiotics with improvement of his pneumonia, but his cerebellar symptoms persisted." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Lorazepam TREATS Generalized Anxiety Disorder", + "sentence": "Randomized, controlled trials confirm that pregabalin is superior to placebo and comparable with lorazepam, alprazolam and venlafaxine for the treatment of patients with moderate-to-severe GAD." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Carcinoma", + "sentence": "A 44-year old male with carcinoma of the upper third of the oesophagus and invasion of the trachea recently underwent surgical treatment at our institution." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Erbium Lasers TREATS Infertility, Male", + "sentence": "Seventeen live births after the use of an erbium-yytrium aluminum garnet laser in the treatment of male factor infertility." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Ablation TREATS Atrioventricular tachycardia", + "sentence": "However, 4 of 204 consecutive patients who underwent successful accessory pathway ablation (as shown by adenosine-induced transient AV block) had recurrent AV reciprocating tachycardia involving a second, previously nonmanifest accessory pathway." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Drug Combinations TREATS Malignant Neoplasms", + "sentence": "These metabolic antiglycolytic agents could be more effective if used in drug combinations to combat cancer." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "YM 31636 TREATS Chronic constipation", + "sentence": "Consequently, 5-HT3 receptor agonists like YM-31636 would be promising in the treatment of chronic constipation." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Lung Transplantation TREATS Primary pulmonary hypertension", + "sentence": "Indication, technique, postoperative care and results of lung transplantation for PPH are discussed." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Epicatechin TREATS Communicable Diseases", + "sentence": "Theaflavin:epicatechin combinations show real potential for future use as a treatment for infections caused by C. albicans." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Immunotherapy TREATS Neoplasm 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FOXQ1 and provided evidence that the miR-506/FOXQ1 axis plays an important role in the pathogenesis of cervical cancer, representing potential molecular targets for the development of anticancer agents for cervical cancer treatment." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "dimethyl fumarate TREATS Restenosis", + "sentence": "Dimethylfumarate attenuates restenosis after acute vascular injury by cell-specific and Nrf2-dependent mechanisms." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Excision TREATS Lymphadenitis", + "sentence": "METHODS: One hundred children with microbiologically proven nontuberculous mycobacterial cervicofacial lymphadenitis were randomly assigned to undergo surgical excision of the involved lymph nodes or to receive antibiotic therapy with clarithromycin and rifabutin for at least 12 weeks." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Finasteride TREATS Benign Prostatic Hyperplasia", + "sentence": "Blockade of intestinal cholesterol transport with ezetimibe induced prostate regression to a similar extent as the 5alpha-reductase inhibitor finasteride, a compound used to treat benign prostatic hyperplasia in humans." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Cetirizine TREATS Neuromyelitis Optica", + "sentence": "Objective: This pilot study preliminarily examined the efficacy and tolerability of cetirizine as an add-on to standard therapy for neuromyelitis optica (NMO)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Sodium-Glucose Transporter 2 Inhibitors TREATS Heart failure", + "sentence": "Together with ongoing large-scale clinical trials to evaluate the efficacy of SGLT2 inhibitors in patients with heart failure, intensive investigations regarding the mechanism through which SGLT2 inhibitors promote the restoration in cases of heart failure would lead to the establishment of these drugs as potent anti-heart failure 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"Hydroxyurea (HU) has traditionally been the first-line treatment for patients with polycythemia vera (PV) or essential thrombocythemia (ET) at high risk for vascular complications." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Microbicides TREATS Hand Injuries", + "sentence": "The use of parenteral prophylactic antimicrobial agents in the treatment of mutilating hand injuries was not significant in preventing infection, and their use does not seem to be indicated in farm implement-related injuries." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Excision TREATS Neurofibromatosis 2", + "sentence": "CONCLUSIONS: The function and appearance can be markedly improved after one-stage partial tumor resection, orbital reconstruction and blepharoplasty in patients with type II orbital neurofibromatosis." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Plasmapheresis TREATS Pemphigus", + "sentence": "Evaluating efficacy of 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"sentence": "Strictly superficial laser coagulation with tissue ablation therefore is a desirable option for the management of dysplasia in Barrett's esophagus because the tissue to be ablated is only about 2 mm thick." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Lobectomy TREATS Malignant neoplasm of lung", + "sentence": "PATIENTS AND TECHNIQUE: Between August 2006 and July 2007, 12 patients with clinical stage IA-lung cancer underwent the video-assisted thoracoscopic left upper lobectomy with bronchial dissection prior to anterior and apico-posterior pulmonary artery dissections following dissection of lingular segmental artery." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Sleeves TREATS Traumatic arthritis NOS", + "sentence": "CONCLUSIONS: Metaphyseal sleeves in combination with varus-valgus constrained (VVC) components and a rotating platform, have shown good clinical and radiological results in patients with post-traumatic knee arthritis and constitute a reliable alternative for treatment of this disease when the epiphyseal zone is deteriorated and has bone defects." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Radiofrequency ablation TREATS Secondary malignant neoplasm of liver", + "sentence": "CONCLUSION: RFA is an alternative approach to the treatment of unresectable CLM." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Percutaneous Coronary Intervention TREATS Acute myocardial infarction", + "sentence": "CONCLUSIONS: In patients undergoing PCI for acute MI complicated by CS, TRA may be associated with improved early outcomes, although the reason for this finding needs further research." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Amoxicillin-Potassium Clavulanate Combination TREATS Communicable Diseases", + "sentence": "Use of amoxicillin/clavulanate for treatment of infections due to Yersinia enterocolitica." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Esophagectomy TREATS Esophageal carcinoma", + "sentence": "Transhiatal oesophagectomy for carcinoma oesophagus." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Diphenoxylate TREATS Chronic diarrhea", + "sentence": "Loperamide is probably superior to diphenoxylate in providing symptomatic control of chronic diarrhoea such as that associated with chronic inflammatory bowel disease or following gastrointestinal surgery." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "candesartan TREATS Hypertensive", + "sentence": "The finding supports that the use of candesartan may offer a good alternative in the treatment of diabetic hypertensive subjects because it has an action that might be mediated through an antioxidant effect and beneficial effects on vascular endothelial permeability as well." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Cell Therapy TREATS Hereditary Diseases", + "sentence": "A combination of biological technologies, including induced pluripotent stem cells (iPSCs) and several gene-editing tools, allows us to develop gene and cell therapies for such inherited diseases." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Contraceptives, Oral TREATS Hirsutism", + "sentence": "Methods: We searched MEDLINE, EMBASE, and CENTRAL through January 2017 for randomized controlled trials (RCTs) with follow-up of at least 6 months that evaluated antiandrogens, insulin sensitizers, and oral contraceptives in women with hirsutism." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Heparin TREATS Pancreatitis", + "sentence": "[Fat emulsions and heparin in the treatment of acute pancreatitis]." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "zafirlukast TREATS Asthma", + "sentence": "OBJECTIVE: To investigate the efficacy of a single 20-mg dose of the oral LTRA zafirlukast in reducing the airway response to inhaled LTD4 in mild-to-moderate asthmatic patients receiving inhaled beta2-agonists and inhaled corticosteroids (ICS)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Partial excision of liver NOS TREATS Intrahepatic Cholangiocarcinoma", + "sentence": "Three hundred and twenty-two consecutive ICC patients undergoing partial hepatectomy at Liver Surgery Department of Zhongshan Hospital (Fudan University, Shanghai, China) between January 2005 and December 2011 were included in this retrospectively study." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Excision TREATS Secondary malignant neoplasm of liver", + "sentence": "C-reactive protein as a predictor of prognosis following curative resection for colorectal liver metastases." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antibiotics TREATS diabetic foot infection", + "sentence": "Is Routine Measurement of the Serum C-Reactive Protein Level Helpful During Antibiotic Therapy for Diabetic Foot Infection?" + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "magnesium sulfate TREATS Pre-Eclampsia", + "sentence": "STUDY DESIGN: Retrospective non-inferiority cohort study of women with preeclampsia with severe features treated with magnesium sulfate undergoing cesarean delivery with singleton pregnancies at tertiary care hospital from 2013 to 2018." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "inhibitors TREATS Metabolic Diseases", + "sentence": "Our findings demonstrate the possibility that NNMT inhibitors, which are expected to be used for the treatment of metabolic disorders, would be effective for the treatment of aggressive EC." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "adjuvant therapy TREATS Localized Malignant Neoplasm", + "sentence": "PURPOSE: To develop a prognostic nomogram to predict freedom from recurrence for patients treated with adjuvant hormonal therapy (HT) for localised breast cancer (BC)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Plug TREATS Pulmonary arteriovenous malformation", + "sentence": "RESULTS: Thirty-seven AVPs were used to close 36 feeding arteries in 35 PAVMs in seven male and 17 female patients aged 11-86 years (mean age, 50 y)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Excision TREATS Secondary malignant neoplasm of liver", + "sentence": "Both hepatic resection (HR) and RFA have been used increasingly in the treatment of colorectal liver metastases." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Guanfacine TREATS Hypertensive disease", + "sentence": "[Blood pressure and renin under treatment of hypertension with guanfacine (author's transl)]." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Hysterectomy TREATS Cervical Intraepithelial Neoplasia", + "sentence": "Because frozen section conization/immediate hysterectomy offers additional advantages of a single hospital admission, single anesthetic induction, and single postoperative recovery/convalescent period, this approach continues to deserve serious consideration in the management of patients with CIN when conization is necessary and subsequent hysterectomy is desired." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "isoniazid TREATS Tuberculosis, active", + "sentence": "Sixteen female hospital workers who were receiving INH for asymptomatic recent conversion of their Tb skin test, and 1 male physician under treatment with INH and rifampin for active tuberculosis as a result of a patient exposure, were studied over a 1-yr period." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Diet, Sodium-Restricted TREATS Uncomplicated hypertension", + "sentence": "A study of 56 males, aged 22 to 56 years, with uncomplicated essential hypertension, stages IB-IIA, where pretreatment examination was followed by repeat investigation after 4 or 5 weeks of treatment with diuretics or low-sodium diets with strict (less than 2 g), moderate (up to 3 g), or mild (4-4.5 g) restriction of sodium uptake, demonstrated a tendency to sodium retention with fluid redistribution from the interstitium to intravascular space in the presence of diuretic treatment." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Insulin TREATS Diabetes Mellitus, Insulin-Dependent", + "sentence": "The majority of patients with type 1 diabetes were treated with insulin, while most patients with type 2 diabetes were treated with metformin." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Cefaclor TREATS Bronchitis", + "sentence": "Oral cefaclor for treatment of bronchitis--a comparative double-blind study versus amoxycillin." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Mucosal resection TREATS Carcinoma", + "sentence": "Endoscopic mucosal resection is the therapy of first choice for such carcinomas." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Embolization, Therapeutic TREATS Aneurysm, Ruptured", + "sentence": "We report a case of ruptured renal artery aneurysm successfully treated by emergent transcatheter embolization with microcoils." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Physical therapy TREATS Multiple Sclerosis", + "sentence": "There is a need to develop PT interventions to reduce fall outcomes in non-ambulatory PwMS due to a scarcity of evidence in this population." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Total excision of bladder NOS TREATS Carcinoma, Transitional Cell", + "sentence": "PATIENTS AND METHODS: A retrospective review was performed of the 412 consecutive patients who underwent radical cystectomy and urinary diversion for transitional cell carcinoma of the bladder between 1986 and 2004." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Treatment Protocols TREATS Carcinoma, Non-Small-Cell Lung", + "sentence": "BACKGROUND: Bevacizumab combined with platinum-based chemotherapy has been recommended as the first-line agent in advanced nonsquamous non-small cell lung cancer (NSCLC) without driven gene, but this regimen is not common in the second-line or later-line treatment of non-squamous NSCLC." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Hysterectomy TREATS Pain", + "sentence": "This is based on claims that hysterectomy alleviates pain (dyspareunia and abnormal bleeding) and improves sexual response." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Lesion of liver", + "sentence": "In this study we have formally compared axial T2WSE images (TR 2000, TE 45/90) with TurboFLASH images (TR 135, TE 4, FA 80 degrees) acquired immediately after bolus injection of Gd-DTPA (0.1 mmol kg-1) in 41 patients referred for hepatic magnetic resonance imaging (MRI) prior to surgery for liver lesions." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antifungal Agents TREATS Pulmonary blastomycosis", + "sentence": "Current practice guidelines recommend that pulmonary blastomycosis be treated with antifungal agents such as amphotericin B and itraconazole." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Advanced cancer", + "sentence": "Enhanced Recovery After Surgery for Advanced Ovarian Cancer: A Systematic Review of Interventions Trialed." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Excision TREATS Barrett Esophagus", + "sentence": "The aim was to evaluate the safety of MBM and its efficacy for complete endoscopic removal of delineated target areas in Barrett's esophagus." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Ethanol TREATS Pruritus", + "sentence": "Complaints of itching decreased significantly following treatment with alcohol and boric acid solution in patients with normal flora (p<0.05)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Endoscopic Submucosal Dissection TREATS Malignant neoplasm of stomach", + "sentence": "To quantify the risk of cutting into cancer from the cutting-plane side during ESD, the proportion of lesions with VM1 /VMX among the pT1a gastric cancers treated by ESD was calculated." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Stapes Surgery TREATS Otosclerosis", + "sentence": "A wide variety of pistons are available for stapes surgery in otosclerosis." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Rifampin TREATS Bacteria", + "sentence": "The release profile showed an initial burst of rifampicin in the first six hours, enabling complete elimination of bacteria." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "cilostazol TREATS Claudication", + "sentence": "CONCLUSION: Naftidrofuryl oxalate and cilostazol are both effective treatments for claudication; naftidrofuryl oxalate is likely to be the most effective, with minimal serious adverse events." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Phosphodiesterase 5 inhibitor TREATS Spermatic Cord Torsion", + "sentence": "Recent researches have demonstrated that PDE5 inhibitors can also be employed in the treatment of lower urinary tract symptoms, renal ischemia/reperfusion injury and testicular torsion." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "inhibitors TREATS Toxic effect", + "sentence": "The attenuation of toxicity is the result of Abeta-inositol interaction, as inositol uptake inhibitors had no effect on neuronal survival." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "carprofen TREATS Degenerative polyarthritis", + "sentence": "Clinical efficacy and pharmacokinetics of carprofen in the treatment of dogs with osteoarthritis." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Lobectomy TREATS Malignant neoplasm of lung", + "sentence": "Non-temporary-type POAF occurred significantly later than transient type and caused poorer prognosis after lobectomy for lung cancer." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antibiotics TREATS Infected bursa", + "sentence": "Conventional treatment of septic bursitis consists of aspiration, antibiotics, and rest." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Care given by nurses TREATS Shivering", + "sentence": "Nursing care for postanesthesia shivering." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Angiogenesis Inhibitors TREATS Ovarian Carcinoma", + "sentence": "Significant improvements in the treatment of OC are expected from the development of novel compounds having combined cytotoxic and antiangiogenic properties that make them effective on refractory tumors." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Warfarin TREATS Atrial Fibrillation", + "sentence": "Some reports on anticoagulant evaluation (INR) and bleeding as complication of warfarin prescribed for AF treatment are not significantly different in elderly and younger patients." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Saline Solution, Hypertonic TREATS Intracranial Hypertension", + "sentence": "Within the limitations of the present study, these data suggest that giving 2 mL/kg hypertonic saline solution (approximately 480 mOsm/70 kg body weight) is an effective and safe initial treatment for intracranial hypertension episodes in head-trauma patients when osmotherapy is indicated." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "quetiapine TREATS Gilles de la Tourette syndrome", + "sentence": "Quetiapine in patients with Tourette's disorder: an open-label, flexible-dose study." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Oxytetracycline TREATS Pneumonia", + "sentence": "The production losses due to pneumonia in pigs treated with this combination were lower than among control pigs treated with Oxytetracycline, also a significantly lower ratio of death was observed among experimental weaners in comparison to the controls." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Precision Medicine TREATS Pancreatic carcinoma", + "sentence": "Further development of precise medicine for pancreatic cancer based on platforms using PDX and organoid model would promisingly help in effective improvement of clinical treatment." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Compression procedure TREATS Cardiac Output", + "sentence": "Under the most severe condition of heart failure, DCC improved cardiac output (CO) by 104% (0.80+/-0.33 to 1.63+/-0.40 L/min) and mean arterial pressure by 95% (45.6+/-11 to 89.0+/-18.2 mm Hg)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Nicotinic Agonists TREATS Learning performance", + "sentence": "Other nicotinic agonists also have been shown to improve learning performance." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Gentamicins TREATS Puerperal endometritis", + "sentence": "Ticarcillin disodium/clavulanate potassium versus clindamycin/gentamicin in the treatment of postpartum endometritis." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Debridement TREATS Communicable Diseases", + "sentence": "Multiple surgical debridements of the necrotic supraspinatus muscle were required to eradicate the infection." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Adenosine TREATS cardiac arrhythmia", + "sentence": "INTRODUCTION: Adenosine is an endogenous nucleoside that has an important role in the diagnosis and treatment of several cardiac arrhythmias." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Gastric Bypass TREATS Hypertension, Pulmonary", + "sentence": "CONCLUSIONS: Laparoscopic gastric bypass and sleeve gastrectomy in obese patients improves pulmonary hypertension in the short term." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Bronchodilator Agents TREATS Lung Diseases, Obstructive", + "sentence": "OBJECTIVE: To identify the role of bronchodilators in the maximal breath-hold time in patients with obstructive lung disease (OLD)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Cefoperazone TREATS Enterobacteriaceae", + "sentence": "These values were higher than MIC90 values of CPZ for Pseudomonas aeruginosa, Streptococcus pneumoniae, Haemophilus influenzae and Enterobacteriaceae." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Thermal techniques TREATS Asthma", + "sentence": "Elevation of antioxidant enzymes in the clinical effects of radon and thermal therapy for bronchial asthma." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "kinase inhibitor TREATS Arthritis, Psoriatic", + "sentence": "Tofacitinib is an oral Janus kinase inhibitor approved for the treatment of psoriatic arthritis (PsA)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Hysterectomy TREATS Menorrhagia", + "sentence": "Fibroids have been found in 10% of women with menorrhagia overall, and in 40% of women with severe menorrhagia; but half of women having a hysterectomy for menorrhagia are found to have a normal uterus." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Laparoscopic adrenalectomy TREATS Benign neoplasm of adrenal gland", + "sentence": "INTRODUCTION: Laparoscopic adrenalectomy (LA) is the procedure of choice for small benign adrenal tumors." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Bronchial Thermoplasty TREATS Severe asthma", + "sentence": "Effectiveness and Safety of Bronchial Thermoplasty in the Treatment of Severe Asthma with Smoking History: A Single-Center Experience." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Dietary Modification TREATS Inflammation", + "sentence": "Given the limitations of current pharmaceuticals, there is an intense research interest in identifying novel dietary interventions that can regulate and alleviate inflammation." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Insulin, Glargine, Human TREATS Diabetes Mellitus, Non-Insulin-Dependent", + "sentence": "OBJECTIVE: To assess and compare the total costs relevant to diabetes care in patients with type 2 diabetes mellitus (T2D) treated at specialised diabetes practices with either insulin glargine- or conventional basal insulin (neutral protamine Hagedorn [NPH])-based therapies from the German statutory health insurance (SHI) perspective." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Curettage procedure TREATS Bone Cysts, Aneurysmal", + "sentence": "We hereby report interesting and a rare case of aneurysmal bone cyst of medial end of clavicle in a eight year old lady which was treated with extended curettage and calcium sulfate bone grafting." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Thrombolytic Therapy TREATS Unstable angina", + "sentence": "Thrombolytic therapy and percutaneous coronary intervention in unstable angina." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "rituximab TREATS Lymphoma, Non-Hodgkin's", + "sentence": "A patient with stage IV non-Hodgkin's lymphoma and chronic hepatitis who was treated with chemotherapy and rituximab developed fatal reactivation of hepatitis B." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Levamisole TREATS Communicable Diseases", + "sentence": "Treatment of infections in animals and man either prophylactically or therapeutically, with thymic hormones, interferons, and thymomimetic drugs such as levamisole and isoprinosine, demonstrate the efficacy of this approach." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Laparoscopic appendectomy TREATS Appendicitis", + "sentence": "Randomised control trials of patients with signs and symptoms of appendicitis undergoing laparoscopic appendicectomy, with one arm being SILA were included." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "tocilizumab TREATS Rheumatoid Arthritis", + "sentence": "To investigate the clinical results of 1 year tocilizumab (TCZ) treatment of rheumatoid arthritis patients in clinical practice by using the clinical disease activity index (CDAI)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "hepatic arterial infusion TREATS Liver carcinoma", + "sentence": "[Efficacy of hepatic arterial infusion therapy for advanced hepatocellular carcinoma using 5-fluorouracil, epirubicin and mitomycin-C]." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Selective norepinephrine re-uptake inhibitor TREATS Major Depressive Disorder", + "sentence": "Duloxetine is a selective serotonin-noradrenaline reuptake inhibitor approved for treatment of major depressive disorder." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Medications, cardiovascular TREATS Coronary heart disease", + "sentence": "This review aimed to examine whether interventions improve adherence to multiple CV medications in a CHD population." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Congenital heart disease", + "sentence": "BACKGROUND: A comprehensive evaluation of postoperative arrhythmias following surgery for congenital heart disease by continuous Holter monitoring has not been carried out." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Agent TREATS Neoplasms", + "sentence": "With the ability to potentiate tumor-specific immune responses, these agents can result in durable tumor control." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Drug Repositioning TREATS Inflammatory Breast Carcinoma", + "sentence": "Literature-Wide Association Studies (LWAS) for a Rare Disease: Drug Repurposing for Inflammatory Breast Cancer." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Pharmacotherapy TREATS Gastrointestinal Neoplasms", + "sentence": "Oxaliplatin in combination with infusional 5-fluorouracil as first-line chemotherapy for elderly patients with metastatic colorectal cancer: a phase II study of the Spanish Cooperative Group for the Treatment of Digestive Tumors." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Cancer of Rectum", + "sentence": "The multimodal curative strategy for the treatment of unresectable obstructing rectal cancer with synchronous hepatic metastases, containing a two-stage surgical treatment with RFA of hepatic metastases and chemoradiation of the rectal tumor between the two stages of the procedure, is a promising method." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "stem cell therapy TREATS Adhesions of uterus", + "sentence": "In recent years, the mechanisms driving IUAs treatment has validated the application of hormones, and further stem cell therapy has also led to the development of novel therapeutic agents with promising efficacy in pre-clinical and initial clinical studies." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Streptomycin TREATS Diarrhea", + "sentence": "Inhibition of the beta-glucuronidase activity in the intestinal microflora by antibiotics (1 mg penicillin and 2 mg streptomycin per ml of drinking water) markedly ameliorated the diarrhea and reduced cecal damage." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Keratoplasty, Penetrating TREATS Endothelial dysfunction", + "sentence": "Penetrating keratoplasty is currently the only treatment for corneal endothelial dysfunction." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Injection procedure TREATS aldosterone hypertension", + "sentence": "PVN injections of either AdsiRNA-NOX2 or AdsiRNA-NOX4 significantly attenuated the development of Aldo/NaCl-induced hypertension." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Antidepressive Agents TREATS Depressive disorder", + "sentence": "Antidepressants are effective for the treatment of depression in MS patients although further clinical research into the neurobiological and psychological bases of depressive disorders in MS patients is clearly needed." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Sodium Bicarbonate TREATS Kidney Failure, Chronic", + "sentence": "MATERIALS AND METHODS: Six patients with chronic renal failure and acidosis underwent muscle biopsy before and after 1 month's treatment with sodium bicarbonate." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "seizure medication TREATS Epilepsy", + "sentence": "BACKGROUND: Epilepsy is a severe chronic neurologic disease with a prevalence of 0.7% worldwide; anti-seizure medications (ASMs) are the mainstay of epilepsy treatment." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Local excision TREATS Urethral Condyloma Acuminatum", + "sentence": "Urethral condyloma can be treated by local excision as an effective method for early improvement of voiding function." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Berberine TREATS Diabetes Mellitus, Non-Insulin-Dependent", + "sentence": "Berberine, one of the major constituents of Chinese herb Rhizoma coptidis, has been shown to improve several metabolic disorders, such as obesity and type II diabetes." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Recombinant Erythropoietin TREATS Amyotrophic Lateral Sclerosis", + "sentence": "CONCLUSIONS: Intravenous high-dose rhEPO is both safe and feasible for the treatment of ALS." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "hyperthermia treatment TREATS Breast Carcinoma", + "sentence": "Photodynamic therapy (PDT) utilizing hematoporphyrin derivative (Hpd) as photosensitizer and an argon-dye laser as the light source was used alone and in combination with a localized microwave hyperthermia treatment to treat the SMT-F mammary carcinoma in mice." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Dietary Modification TREATS Birth length", + "sentence": "Preconception nutrition intervention improved birth length and reduced stunting and wasting in newborns in South Asia: The Women First Randomized Controlled Trial.South Asia has >50% of the global burden of low birth weight (LBW)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Screw TREATS Unstable fracture", + "sentence": "CONCLUSION: CT fluoroscopy-guided placement of iliosacral screws is a safe and effective treatment in patients with unstable posterior pelvic fractures." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Pleurectomy TREATS Lupus Erythematosus, Systemic", + "sentence": "Refractory massive pleural effusion in systemic lupus erythematosus treated by pleurectomy." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Hydantoin TREATS Trigeminal Neuralgia", + "sentence": "[Diagnosis, differential diagnosis and possibilities for treatment of trigeminal neuralgia: with special reference to the conservative treatment with hydantoin drugs and vitamin B12]." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Cholecystectomy, Laparoscopic TREATS Cholelithiasis", + "sentence": "Laparoscopic cholecystectomy has become the treatment of choice for symptomatic cholelithiasis." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Therapeutic radiology procedure TREATS Cervix carcinoma", + "sentence": "UNLABELLED: The objective of this study was to evaluate the prognostic value of anemia in uterine cervical carcinoma patients treated with irradiation." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Transplantation TREATS Myocardial fibrosis", + "sentence": "CONCLUSION: We conclude that intravenous transplantation of MSCs and CM can attenuate myocardial fibrosis and increase Bcl-2 expression." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Bromocriptine TREATS adenoma", + "sentence": "Transsphenoidal surgery was found to be the most effective treatment for lasting control, and bromocriptine for temporary control, of prolactin adenomas." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Excision TREATS Communicable Diseases", + "sentence": "OBJECTIVE: Aortobifemoral graft (ABFG) infections presenting with apparent single-limb involvement can be 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"sentence": "The diagnosis of antibiotic-associated colitis was excluded in our patient by the negative stool examination for Clostridium difficile toxin, the failure to obtain supportive features on rectal biopsy, and the failure to demonstrate sigmoidoscopic improvement with vancomycin therapy." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Melphalan TREATS Pleural effusion disorder", + "sentence": "Transient improvement of the pleural effusion was observed after administration of combination chemotherapy of vincristine, melphalan, cyclophosphamide, prednisone (VMCP)/vincristine, cyclophosphamide, adriamycin, prednisone (VCAP)." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Agent TREATS Multiple Myeloma", + "sentence": "Evidence for the effectiveness of BMA for the treatment of lung cancer, breast cancer, prostate cancer, multiple myeloma, and other cancers is provided in each section of the guidelines." + }, + "validation_result": "Yes" 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"Pneumonectomy TREATS Lung mass", + "sentence": "A 70-year-old man presenting with a lung mass was investigated and treated with pneumonectomy for adenocarcinoma of the lung." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "telavancin TREATS Pneumonia, Bacterial", + "sentence": "Under the base case, hospital cost for patients with HABP treated with TLV was $42,564 and with VAN, it was $42,296." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Conservative therapy TREATS Immune thrombocytopenic purpura", + "sentence": "Trial of conservative management is safe in pregnant patient with ITP who develops subdural haematoma." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Coronary Arteriosclerosis", + "sentence": "A 71-year-old male with abdominal aortic aneurysm, coronary artery disease and obstructive peripheral arteriosclerosis successfully underwent a combined operation of coronary artery bypass grafting (CABG), replacement of abdominal aortic aneurysm and femoro-popliteal bypass." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Mechanical stimulation TREATS Parkinson Disease", + "sentence": "Mechanical Plantar Foot Stimulation in Parkinson's Disease: A Scoping Review.BACKGROUND: Parkinson's disease (PD) is the second most prevalent neurodegenerative disease in older individuals." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Clarithromycin TREATS Pneumonia", + "sentence": "OBJECTIVES: Amoxicillin and clarithromycin have been proven to be effective in the treatment of community-acquired pneumonia." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Immobilization TREATS Wounds and Injuries", + "sentence": "BACKGROUND: To protect the spine from secondary damage, spinal immobilization is a standard procedure in prehospital trauma management." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": 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"Electrophysiological studies before and after argon-laser photocoagulation in diabetic retinopathy." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Immunotherapy TREATS Neurodegenerative Disorders", + "sentence": "Immunotherapies for various neurodegenerative diseases have recently emerged as a promising approach for clearing pathological protein conformers in these disorders." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Haloperidol TREATS Delirium", + "sentence": "Haloperidol is the most commonly prescribed drug for delirium in the cancer setting because of its low cardiovascular and anticholinergic effects." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Topical form corticosteroids TREATS Pityriasis Lichenoides Chronica", + "sentence": "The foremost therapies for PLEVA and PLC are phototherapy, systemic antibacterials, and topical corticosteroids." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Microbicides TREATS Communicable Diseases", + "sentence": "The development of well-defined polymeric nanoparticles (NPs) as delivery carriers for antimicrobials targeting human infectious diseases requires rational design of the polymer template, an efficient synthetic approach, and fundamental understanding of the developed NPs, e.g., drug loading/release, particle stability, and other characteristics." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Transurethral Resection TREATS Fibroid Tumor", + "sentence": "[Leiomyoma of the urinary bladder treated by transurethral resection: a case report]." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Levofloxacin TREATS Stenotrophomonas maltophilia", + "sentence": "Risk factors for levofloxacin resistance in Stenotrophomonas maltophilia from respiratory tract in a regional hospital." + }, + "validation_result": "Yes" + }, + { + "input": { + "triple": "Referral to dermatology service TREATS 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"triple": "capecitabine TREATS Breast cancer metastatic", + "sentence": "Capecitabine is also effective in patients with taxoid-pretreated metastatic breast cancer, a population which previously had no established treatment options." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Tonsillectomy TREATS Down Syndrome", + "sentence": "Tonsillectomy and adenoidectomy in patients with Down syndrome usually relieves symptoms of upper airway obstruction due to adenotonsillar hypertrophy." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "water TREATS Diastasis", + "sentence": "In order to widen the potentiality of these carbonaceous materials and to overcome some of their limitations, particularly the inefficient separation of powdered formulations from treated water, the incorporation of magnetic nanoparticles has been explored." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "follow-up TREATS Ejection fraction", + "sentence": "Cox 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TREATS Malignant Neoplasms", + "sentence": "In this regard, cancer testis antigens have emerged as a potential targets for developing novel clinical biomarkers and immunotherapy for various malignancies." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Oseltamivir TREATS Communicable Diseases", + "sentence": "This helps to explain why K294 has predominantly been found in clinical cases of H7N9 infection under the selective pressure of oseltamivir treatment and not in the dominant human-infecting viruses." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Prenatal care TREATS Perinatal death", + "sentence": "To reduce the low birth weight infant rate by means of an effective family planning program and antenatal care may improve the perinatal mortality rate at Rajavithi Hospital." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Implants TREATS Neoplasm", + "sentence": "Induction heating of the implant, which is stereotactically 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"No" + }, + { + "input": { + "triple": "Percutaneous coronary intervention TREATS Myocardial Infarction", + "sentence": "CONCLUSION: Increased admission PCT level is associated independently with no-reflow after PPCI in STEMI patients." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Angioplasty, Transluminal, Percutaneous Coronary TREATS Lesion", + "sentence": "METHODS AND RESULTS: We studied 253 consecutive patients with 283 lesions who underwent attempted PTCA of CTO (mean time since occlusion 33 months, range 3-150 month)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Excision of left hemicolon NOS TREATS Malignant Neoplasms", + "sentence": "[Technic of anastomosis after left colectomy for cancer]." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "removal technique TREATS Advanced Malignant Neoplasm", + "sentence": "Pancreatectomy with AR for advanced pancreatic cancer showed acceptable procedure-related morbidity and 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"sentence": "Therefore, the benefit-risk profile of NOACs versus VKAs was investigated in AF patients treated with P-gp and/or CYP450-interacting drugs." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Percutaneous coronary intervention TREATS Acute coronary syndrome", + "sentence": "A total of 228 patients with acute coronary syndrome undergoing selective PCI were randomly divided into simvastatin 20-mg group (S20, n = 115) and simvastatin 80-mg group (S80, n = 113)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "infliximab TREATS Inflammation", + "sentence": "CONCLUSIONS: Crohn's disease patients have improvements in an index that measures both inflammation and nutrition (PINI) with infliximab therapy." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Proteasome inhibitor TREATS Thrombocytopenia", + "sentence": "BACKGROUND: Treatment with proteasome inhibitors like carfilzomib in patients with multiple myeloma (MM) can 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+ "validation_result": "No" + }, + { + "input": { + "triple": "Carbamazepine TREATS Tonic - clonic seizures", + "sentence": "Fifteen children (7 boys and 8 girls) with generalized tonic-clonic seizures (GTCS) and partial seizures with elementary or complex symptomatology, treated with carbamazepine (CBZ) alone (n = 7) or in combination with either phenobarbital (PB, n = 6) or clobazam (CLB, n = 2) given for at least 3 months at stable individualized doses and regimens, entered an open, within-patient, change-over study of consecutive periods, each lasting 2 weeks." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Cyclophotocoagulation TREATS Glaucoma", + "sentence": "BACKGROUND/AIMS: To compare the surgical outcome of glaucoma drainage device (GDD) implantation and diode laser cyclophotocoagulation (CPC) in the management of refractory glaucoma following vitrectomy with silicone oil (SO) injection." + }, + "validation_result": "No" + }, + { + "input": { + "triple": 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"input": { + "triple": "Evaluation TREATS Chronic Obstructive Airway Disease", + "sentence": "Postural Balance Evaluation in Patients with Chronic Obstructive Pulmonary Disease." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Drug Repositioning TREATS Inflammatory Bowel Diseases", + "sentence": "Drug repurposing strategies for IBD have had limited clinical success and have not typically offered individualized patient-level treatment recommendations." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Exploration procedure TREATS Diastasis", + "sentence": "This paper presents an exploration for separation of oil-in-water and coalescence of oil droplets in ultrasound field via lattice Boltzmann method." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Endoscopic dilatation TREATS Esophageal achalasia", + "sentence": "A review of factors predicting outcome of pneumatic dilation in patients with achalasia cardia." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Papain TREATS NEPHRITIS MEMBRANOUS", + "sentence": "Treatment of kidney membranes with papain resulted in release of the enzyme, as shown by Western blotting analysis of the solubilized fraction." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Detection TREATS Fatty Streak, Arterial", + "sentence": "Conclusion: We conclude that VSOP and, to a lesser extent, ferumoxytol increase light scattering and attenuation when taken up by macrophages and can serve as a multimodal imaging probe for MRI and OCT to improve macrophage detection in atherosclerotic plaques by OCT in the future." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Macrolides TREATS Streptococcus pneumoniae", + "sentence": "The resistant mechanisms of macrolides in S. pneumoniae is recognized as production of a 23s rRNA methylase encoded by ermB and efflux system mediated by mefA gene." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Binder TREATS Hyperphosphatemia", + "sentence": "Multicenter prospective randomized, double-blind comparative study between lanthanum carbonate and calcium carbonate as phosphate binders in Japanese hemodialysis patients with hyperphosphatemia." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Psilocybine TREATS Mental disorders", + "sentence": "The main psychedelic component of magic mushrooms is psilocybin, which shows promise as a treatment for depression and other mental disorders." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Aramine TREATS Normal blood pressure", + "sentence": "A comparison of the cerebral hemodynamic response to aramine and norepinephrine in the normotensive and hypotensive subject." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "adjuvant therapy TREATS Malignant neoplasm of breast", + "sentence": "The optimal duration and selection of adjuvant endocrine therapy for breast cancer: how long is enough?" + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Anti-Retroviral Agents TREATS Drug-Induced Liver Disease", + "sentence": "Patients were followed from admission until the earlier of death (10 with TB DILI, 2 with ART DILI and 9 with mixed DILI) or discharge (after a median (interquartile range) of 14.0 (9 - 23) days)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Vaccines TREATS Potomac horse fever", + "sentence": "This finding will improve the laboratory diagnosis of and vaccine for PHF, environmental risk assessment of PHF, and understanding of PHF pathogenesis and Neorickettsia biology in general." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Remoxipride TREATS Schizophrenia", + "sentence": "A double-blind comparative multicentre study of controlled-release remoxipride, immediate-release remoxipride and haloperidol in schizophrenia." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "immunoglobulins, intravenous TREATS Autoimmune Diseases", + "sentence": "Unfortunately, there is no established evidence of the efficacy of IVIg therapy for autoimmune diseases of the central nervous system." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Laparotomy TREATS patient state", + "sentence": "Despite conservative management, the patient's condition deteriorated and he underwent five laparotomies." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Lead Extraction TREATS Congenital heart block", + "sentence": "METHODS: Data on all attempted TLE procedures in patients with CCHB at two institutions between 2011 and 2021 were collected from a retrospective registry." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Ceftriaxone TREATS Neutropenia", + "sentence": "Efficacy of the cephalosporin, ceftriaxone, was compared with that of the combination of the aminoglycoside, netilmicin, and the penicillin, azlocillin, in the treatment of febrile episodes in immunocompromised neutropenic children undergoing chemotherapy for neoplastic disease." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "aclarubicin TREATS LEOPARD Syndrome", + "sentence": "The ACM phenotype may occur in other genetic cardiomyopathies, cardiocutaneous syndromes or neuromuscular disorders." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Human immunoglobulin TREATS Alzheimer's Disease", + "sentence": "CONCLUSIONS: Participants with mild to moderate AD showed good tolerability of treatment with low-dose human IVIg for 18 months but did not show beneficial effects on cognition or function relative to participants who received placebo." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Cyclophosphamide TREATS Leukopenia", + "sentence": "The no-reflow phenomenon seen after 30 minutes of severe bilateral hemispheric ischaemia during hypotensive reperfusion was compared in control animals and in a group made leukopenic by pretreatment with cyclophosphamide." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Brain natriuretic peptide TREATS Lung diseases", + "sentence": "Plasma amino-terminal pro B-type natriuretic peptide as a predictor of late cardiovascular mortality in patients with acute lung disorders: a prospective, observational cohort study." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Drugs, Non-Prescription TREATS Secondary malignant neoplasm of bone", + "sentence": "Approved pharmaceutical drugs for the treatment of bone metastasis, including bisphosphonate and denosumab, were designed to target bone stromal cell components." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Ethanol TREATS Depressed mood", + "sentence": "Since, a maximal depression in CO activity was seen with ethanol treatments of 75 mg/100 g, this dosing paradigm was adopted for subsequent experiments." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Heparin TREATS Asthma", + "sentence": "[The effect of inhaled heparin on airway responsiveness to metacholine in asthmatic children]." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Dietary Modification TREATS Autism spectrum disorder", + "sentence": "CONCLUSION: Based on available data, no evidence based recommendations regarding nutritional interventions for children and adolescents with autism spectrum disorders can be made." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "doxorubicin/fluorouracil/mitomycin/vincristine protocol TREATS Psoriasis", + "sentence": "Non-invasive clinical and microscopic evaluation of the response to treatment with clobetasol cream versus calcipotriol/betamethasone dipropionate foam in mild to moderate plaque psoriasis: an investigator-initiated, phase IV, unicentric, open, randomized clinical trial.BACKGROUND: Treatment response for psoriasis is typically evaluated using clinical scores." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Atypical antipsychotic TREATS Schizophrenia", + "sentence": "The cognitive efficacy of atypical antipsychotics in schizophrenia." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Triage TREATS COVID-19", + "sentence": "D-dimer Triage for COVID-19." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Functional behavioral assessment TREATS Leber's amaurosis", + "sentence": "Functional analyses of mutant recessive GUCY2D alleles identified in Leber congenital amaurosis patients: protein domain comparisons and dominant negative effects." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "ERBB2 gene TREATS Disease recurrence", + "sentence": "IMPORTANCE: ERBB2 (formerly HER2) is an important drug target in breast cancer, where anti-ERBB2 therapy has been shown to lead to improvements in disease recurrence and overall survival." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Hospitalization TREATS Heart failure", + "sentence": "Clinical and CMR features were analyzed with regard to major adverse cardiovascular events (MACE) (i.e., hospitalization for heart failure, sustained ventricular tachycardia, and all-cause mortality)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Brain hemorrhage", + "sentence": "The study included 224 patients after transcranial surgery for hemorrhagic stroke." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Dutasteride TREATS Prostate cancer recurrent", + "sentence": "MATERIALS AND METHODS: A total of 28 men with asymptomatic castration recurrent prostate cancer were treated with 3.5 mg dutasteride daily (luteinizing hormone-releasing hormone treatment continued), and evaluated monthly for response and toxicity." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Reconstructive Surgical Procedures TREATS Dislocation, incomplete", + "sentence": "Based on these findings, it appears that reconstruction of the MPFL is a useful addition to the treatment of recurrent patellar dislocation and subluxation." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Dehydroepiandrosterone Sulfate TREATS Coronary Arteriosclerosis", + "sentence": "OBJECTIVES: We studied the prevalence and prognostic consequences of deficiencies in circulating total and free testosterone (TT, FT) and dehydroepiandrosterone sulphate (DHEAS) in type II DM men with coronary artery disease (CAD)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Prescribed TREATS Alopecia", + "sentence": "BACKGROUND: Although intralesional triamcinolone acetonide(TA) is the most commonly prescribed treatment for localized alopecia areata(AA), the literature regarding the optimal concentration for attaining better efficacy with the most acceptable side effects is scarce." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Biological Response Modifiers TREATS Deleterious Mutation", + "sentence": "Specific unmet needs continue to exist for patients who develop disease progression after concurrent chemoradiation and immunotherapy, as well as defining the best treatment for patients with driver mutations." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Isolation procedure TREATS Atrial Fibrillation", + "sentence": "The Role of Superior Vena Cava Isolation in the Management of Atrial Fibrillation." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Immunoglobulins, Intravenous TREATS Immune thrombocytopenic purpura", + "sentence": "Intravenous immunoglobulin treatment of Epstein-Barr virus-related idiopathic thrombocytopenic purpura." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Isoflurane TREATS Hypothyroidism", + "sentence": "The dose of ISO in dogs with hypothyroidism 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{ + "triple": "Oral form ibuprofen TREATS Chronic pain", + "sentence": "Topical or oral ibuprofen for chronic knee pain in older people." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Lifesaving TREATS Heart failure", + "sentence": "METHODS: The Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF) registry is a comprehensive hospital-based registry and performance-improvement program for patients hospitalized with HF." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Acupuncture procedure TREATS Sleeplessness", + "sentence": "OBJECTIVE: To evaluate the efficacy and safety of acupuncture for residual insomnia and other residual symptoms associated with major depressive disorder (MDD)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Botulinum Toxins TREATS Spasm", + "sentence": "Efficacy of botulinum toxin A for treatment of unilateral spasms of the eyelid and its prognosis." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "atorvastatin TREATS Hyperemia", + "sentence": "Doppler coronary flow velocity and Doppler reserve measurement of distal left anterior descending were recorded at rest and adenosine infusion (140 microgxkg(-1)xmin(-1)) induced hyperemia state, CFR was calculated by the ratio of maximal hyperemia and baseline peak diastolic coronary flow velocity (hCFV and bCFV) before and after atorvastatin treatment." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "prucalopride TREATS Chronic constipation", + "sentence": "AIM: To evaluate the efficacy of the enterokinetic prucalopride (resolor) in patients with chronic constipation." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "omalizumab TREATS Asthma", + "sentence": "An Institutional Review Board-approved prospective pilot study was performed to assess the efficacy of omalizumab in 22 patients with persistent asthma and concomitant IgE-mediated food allergy." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "resiniferatoxin TREATS Pemphigus Vulgaris", + "sentence": "Methods and Materials: We evaluated the immunologic profile of 10 OPV patients treated with RTX as adjuvant by using the ELISA testing for anti-Dsg-1 and -3 titers and the immunophenotyping for B and T-cell lymphocyte subpopulations and compared them with the PDAI score for clinical remission." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Physostigmine TREATS Normal blood pressure", + "sentence": "The pressor response to physostigmine, but not to arecoline, was enhanced in adult, spontaneously-hypertensive rats, with respect to their normotensive controls." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Traction TREATS Wounds and Injuries", + "sentence": "Review of Lower Extremity Traction in Current Orthopaedic Trauma." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Aerosols TREATS Asthma", + "sentence": "[On the aerosol therapy of asthma in practice]." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Splenectomy TREATS Trauma", + "sentence": "A novel preoperative scoring system to predict technical difficulty in laparoscopic splenectomy for non-traumatic diseases." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Brachytherapy TREATS Pulse Rate", + "sentence": "CONCLUSIONS: According to the experience in our institute with 1,300 PDR treatments, we found that PDR is a safe brachytherapy treatment modality, both during and outside of office hours." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Alternative Therapies TREATS Seizures", + "sentence": "Taken as a whole, our data support that rapamycin has immediate antiseizure effects and could be a potential alternative therapy for seizure control in epilepsy." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "exenatide TREATS Risk factor, cardiovascular", + "sentence": "CONCLUSION: This case report suggests that the incretin mimetic exenatide decreases hepatic fat accumulation and may play a role in the future treatment of NAFLD, and the associated insulin resistance and cardiovascular risk factors in an ever-growing high-risk population." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Neuromuscular blocking therapy TREATS Lack of sensation", + "sentence": "[Effects of curarization of respiratory mechanics in anesthesia in patients with or without bronchopneumopathic obstruction]." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Protease Inhibitor TREATS Thickened", + "sentence": "Among individuals with HIV infection, variables associated with increased mean carotid artery wall thickness included lipoaccumulation [+0.09 mm; 95% confidence interval (CI) 0.03-0.14 mm; P = 0.003], Framingham risk score >= 5% (+0.07 mm; 95% CI 0.01-0.12; P = 0.02 mm), and increased duration of protease inhibitor therapy (+0.03 mm per 5 years; 95% CI 0.01-0.06 mm; P = 0.02)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Drug Delivery Systems TREATS Squamous cell carcinoma", + "sentence": "Therefore, it is of great importance to decipher mechanisms and identify new drug targets involved in squamous cell carcinoma development." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Wound dressing TREATS Encounter due to smallpox vaccination", + "sentence": "[The use of a plastic wound dressing in smallpox vaccination]." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Antioxidants TREATS Inflammatory disorder", + "sentence": "Furthermore, the good binding affinity of HGN for the active site of COX-2 may open novel vistas in therapeutic option with natural antioxidants like Cyathocline purpurea to treat various inflammatory disorders." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Antiepileptic Agents TREATS Pneumonia", + "sentence": "Hip-fracture patients, compared with matched controls of acute MI and pneumonia, had the largest pronounced differences in prescribed medications in the antiepileptics, antidepressants, antipsychotics and antiparkinson's drug classes." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "astragaloside IV TREATS Low Level", + "sentence": "In conclusion, astragaloside IV can reverse the low level of eNOS caused by OxLDL by regulating HDAC activity to protect myocardial cells from oxide damage, which is manifested by the decrease of BNP concentration." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Coronary Artery Bypass Surgery TREATS Diffuse acute inflammation", + "sentence": "Certain patients who have undergone coronary artery bypass grafts suffer from episodes of acute cellulitis, often repeatedly, in the saphenous vein donor extremity." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Repeat Surgery TREATS Cyst", + "sentence": "One intracranial and 2 spinal lesions caused by fertile cysts recurred to undergo repeated surgery." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Medicine, Folk TREATS Diabetes", + "sentence": "Salicornia herbacea has been used as a folk medicine for disorders such as constipation, obesity, diabetes, and cancer." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Ketoprofen TREATS Pain", + "sentence": "Excretion of ketoprofen and nalbuphine in human milk during treatment of maternal pain after delivery." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Osteotomy TREATS Rheumatoid Arthritis", + "sentence": "[High tibial osteotomy and double osteotomy of the knee in the treatment of rheumatoid arthritis]." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Partial excision of liver NOS TREATS Liver carcinoma", + "sentence": "Follow-up studies are available from 1 year to 27 years, after 41 patients with FL-HCC were treated with partial hepatectomy (PHx) (28 patients) or liver transplantation (13 patients)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Bypass TREATS Pancreatic carcinoma", + "sentence": "Bilio-digestive double bypass for nonresectable pancreatic cancer." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Microsurgery TREATS Nerve Degeneration", + "sentence": "When used in various combinations, these devices will facilitate a variety of high-throughput assays using whole animals, including mutagenesis and RNAi and drug screens at subcellular resolution, as well as high-throughput high-precision manipulations such as femtosecond laser microsurgery for large-scale in vivo neural degeneration and regeneration studies." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Basis TREATS CNS disorder", + "sentence": "We hope to provide a theoretical basis and novel 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"sentence": "[Clinical evaluation of the effectiveness of amoxicillin in bacterial bronchopneumopathies]." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Aspirin TREATS Glaucoma", + "sentence": "Treatment options include laser therapy for lightening of the birthmark, eye drops and surgery for glaucoma management, and aggressive anticonvulsant treatment, low dose aspirin, and neurosurgery where necessary." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Small cell carcinoma of lung", + "sentence": "We performed a prospective study of nephron sparing surgery for small renal cell carcinoma in renal grafts." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Exploration procedure TREATS Periampullary carcinoma", + "sentence": "How to Approach Para-Aortic Lymph Node Metastases During Exploration for Suspected Periampullary Carcinoma: Resection or Bypass?BACKGROUND: Intraoperative para-aortic lymph node (PALN) sampling during surgical exploration in patients with suspected pancreatic head cancer remains controversial." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Transcranial Magnetic Stimulation, Repetitive TREATS Autism spectrum disorder", + "sentence": "Here we report the results of a systematic literature review and meta-analysis on the use of rTMS to treat ASD." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Pharmacotherapy TREATS Carcinoma, Non-Small-Cell Lung", + "sentence": "Molecular basis of cellular response to cisplatin chemotherapy in non-small cell lung cancer (Review)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Immunotherapy TREATS Mouse Model", + "sentence": "Micelle-like particles have been developed with the ability to incorporate a range of tumor-specific antigens for immunotherapies in mouse models of cancer." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Lidocaine TREATS Liver carcinoma", + "sentence": "However, the function and underlying mechanisms of lidocaine in hepatocellular carcinoma both in vitro and in vivo have been poorly studied." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Screening procedure TREATS Frailty", + "sentence": "This would facilitate large-scale screening for frailty in older persons." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Implantation procedure TREATS Aortic Valve Stenosis", + "sentence": "Meta-Analysis of Impact of Baseline N-TerminalPro-Brain Natriuretic Peptide Levels on SurvivalAfter Transcatheter Aortic Valve Implantation for Aortic Stenosis." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Interferons TREATS Colitis, Ischemic", + "sentence": "Ischaemic colitis during interferon treatment for chronic hepatitis C: report of two cases and literature review." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "baicalein TREATS Cardiac Hypertrophy", + "sentence": "Baicalein attenuates cardiac hypertrophy in mice via suppressing oxidative stress and activating autophagy in cardiomyocytes." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Continuous Positive Airway Pressure TREATS Respiratory effort", + "sentence": "Therefore, we compared indexes of respiratory effort during sleep in 25 patients with OSA before and after 1 year of CPAP treatment." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Excision of axillary lymph nodes TREATS Micrometastasis", + "sentence": "As ALND is unnecessary in micrometastases, considering micrometastases 'N negative' increases the practical impact of AUS." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Terramycin TREATS Brucellosis", + "sentence": "Treatment of brucellosis with aureomycin or terramycin combined with dihydrostreptomycin." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Induction TREATS Malignant Neoplasms", + "sentence": "CONCLUSION: Fever induction under medical guidance may be considered as part of a therapy regimen for cancers of mesodermal origin." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Antibiotics TREATS Tendinitis", + "sentence": "Complications included 1 repeat surgery for ulnocarpal scar formation, 2 cases of transient tendonitis, and 1 portal site erythema without drainage that was treated with antibiotics." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "ORALIT TREATS Chronic Kidney Diseases", + "sentence": "Compared with men with an HSI < 30, men with 30 <= HSI <= 36 (OR: 1.50, 95% CI: 1.40-1.61) and HSI > 36 (OR: 2.14, 95% CI: 1.99-2.31) had significantly higher ORs for CKD." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Nerve operations TREATS Circulatory system disease NOS", + "sentence": "[SYMPATHETIC NERVE SURGERY IN ARTERIAL CIRCULATORY DISORDERS OF THE LEGS]." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "early detection of cervical cancer TREATS Scaling", + "sentence": "It is envisioned that this separation scheme will have clinical applications in settings where rapid cell enrichment and removal of contaminating blood will improve efficiency of screening and diagnosis such as cervical cancer screening based on mixed populations in exfoliated samples." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Interferons TREATS Infiltration", + "sentence": "Tumoral infiltrate after local treatment with interferon in squamous cell carcinoma." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Cisplatin TREATS Neurotoxicity Syndromes", + "sentence": "Neurotoxic effects of cisplatin therapy." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Iron TREATS Iron deficiency", + "sentence": "Decreased iron and zinc absorption in Turkish children with iron deficiency and geophagia." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Embolization, Therapeutic TREATS Pseudoaneurysm", + "sentence": "Pseudoaneurysm of the superficial temporal artery treated by embolization: report of a case." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Glucose TREATS Diabetes Mellitus, Insulin-Dependent", + "sentence": "Severe hyperkalemia (serum potassium level >6 mmol per liter [mEq per liter]), often with electrocardiographic disturbances, was noted at presentation in 30% of 73 hyperglycemic episodes (serum glucose concentration >25 mmol per liter [455 mg per dl]) observed in 15 in-hospital patients with insulin-dependent diabetes mellitus who were receiving long-term hemodialysis or peritoneal dialysis." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Iron TREATS Anemia", + "sentence": "The role of intravenous iron in anemia management and transfusion avoidance." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Diphosphonates TREATS Breast cancer metastatic", + "sentence": "BACKGROUND: Intravenous bisphosphonates have been used in metastatic breast cancer patients to reduce pathologic bone fracture and bone pain." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Iloprost TREATS Nerve conduction velocity", + "sentence": "Iloprost was found to improve the NCV in the diabetic rats." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Bifurcation TREATS Coronary Occlusion", + "sentence": "This study compared the procedural and mid-term outcomes of patients with bifurcation lesions in CTO treated with provisional stenting vs 2-stent techniques in a multicenter registry." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Metformin TREATS Insulin Resistance", + "sentence": "Metformin improves hepatic IRS2/PI3K/Akt signaling in insulin-resistant rats of NASH and cirrhosis." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Hyperthermic Intraperitoneal Chemotherapy TREATS Carcinomatosis", + "sentence": "OBJECTIVE: To compare the overall survival and progression-free survival of front-line cytoreductive surgery (CRs) +/- hyperthermic intraperitoneal chemotherapy versus intensive systemic chemotherapy alone, in patients with isolated peritoneal carcinomatosis of colorectal origin." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "MST TREATS Glioblastoma", + "sentence": "Two-year survivals and MSTs for the implanted GBM patients compared to the RTOG database were as follows: 74% vs." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Therapeutic Mobilization TREATS Coxitis", + "sentence": "[Radical reconstructive and mobilizing surgery in experimental tuberculous coxitis]." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "First line treatment TREATS anaphylaxis", + "sentence": "BACKGROUND: Epinephrine is the first-line therapy for patients with anaphylaxis, and intramuscular (IM) delivery is shownto be superior to subcutaneous (SC) delivery." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Splenectomy TREATS Fibrosis", + "sentence": "METHODS: All consecutive patients with cirrhosis who underwent splenectomy in Kyushu University Hospital between 1998 and 2004 were included in this retrospective study." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "ailanthoidol TREATS Skin Neoplasms", + "sentence": "Finally, AT was evaluated for its ability to inhibit the TPA-induced promotion in skin tumors of female CD-1 mice." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Paclitaxel TREATS Breast cancer metastatic", + "sentence": "Role of nab-paclitaxel in metastatic breast cancer: a meta-analysis of randomized clinical trials." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Suture Techniques TREATS Tear of meniscus of knee", + "sentence": "Outcomes of 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microflora to antibiotics without causing an essential influence on the content of microbes in the wound, and also has a favorable effect on the functional activity of the cells of the inflammation." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Gingival Recession", + "sentence": "Conventional surgical procedures designed for autogenous tissue material may not be appropriate when using acellular dermal matrix (ADM) for the treatment of gingival recessions." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Transplantation TREATS Liver diseases", + "sentence": "One hundred seventy-five patients underwent OLT for HBV-related liver diseases and were the subjects of this retrospective study." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Medical therapy TREATS Gangrene", + "sentence": "All patients presented a critical ischemia, with trophic lesions or gangrene in 76% of the cases (35/46) and who were previously treated unsuccessfully with medical therapy." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Prostatectomy TREATS Hemorrhage", + "sentence": "Blood loss was lower in those patients undergoing prostatectomy for carcinomatous disease." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Bone Marrow Transplantation TREATS Metachromatic leukodystrophy, juvenile type", + "sentence": "Long-term stabilization after bone marrow transplantation in juvenile metachromatic leukodystrophy." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Tuberculosis", + "sentence": "Management is prolonged and often complex, and close co-operation is required between the neurosurgical team and a physician experienced in the management of tuberculosis." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Immunotherapy TREATS Squamous cell carcinoma", + "sentence": "Further clinical trials in Asian countries are needed to test whether nivolumab immunotherapy is a safe and effective treatment for Asian patients with lung SCC." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "infliximab TREATS Ulcerative Colitis", + "sentence": "Endoscopic and clinical variables that predict sustained remission in children with ulcerative colitis treated with infliximab." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "testosterone enanthate TREATS Pseudovaginal Perineoscrotal Hypospadias", + "sentence": "Testosterone enanthate does not give good results in patients with 5-alpha reductase deficiency; dihydrotestosterone (DHT) has proven effectiveness in these cases." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "3,4-Methylenedioxyamphetamine TREATS Pre-Eclampsia", + "sentence": "RESULTS: The MDA level was significantly higher in the pre-eclampsia (3.15+/-0.28 nmol/mL) and eclampsia (4.01+/-0.66 nmol/mL) groups than in controls (1.85+/-0.18 nmol/mL); the difference between MDA levels in the pre-eclampsia and eclampsia groups was not statistically significant." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Sensors TREATS Glaucoma", + "sentence": "[Self-tonometry with a Telemetric Intraocular Pressure Sensor in Patients With Glaucoma]." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Therapeutic radiology procedure TREATS Malignant neoplasm of prostate", + "sentence": "Systematic review of hypofractionated radiation therapy for prostate cancer." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "TETROFOSMIN TREATS Ventricular Dysfunction, Left", + "sentence": "The aim of this study was to assess the influence of incremental nitroglycerin infusion (NTG+Inf) on the myocardial uptake of 99mTc-tetrofosmin (TF) in order to determine whether nitrates enhance the detection of viable myocardium with TF in patients with coronary artery disease (CAD) and left ventricular dysfunction." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Arthroplasty TREATS Nance-Horan syndrome", + "sentence": "Stringent patient selection complimented by a well-defined day-case arthroplasty pathway is fundamental for successful commencement of day-case UKA in the NHS." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Peritoneal Dialysis, Continuous Ambulatory TREATS Peritonitis", + "sentence": "Peritonitis in patients undergoing continuous ambulatory peritoneal dialysis." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Urea TREATS Diastasis", + "sentence": "It was characterized both in its cell-associated insoluble form and after separation by urea treatment." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Forecast of outcome TREATS Critical Illness", + "sentence": "The Use of Central Venous to Arterial Carbon Dioxide Tension Gap for Outcome Prediction in Critically Ill Patients: A Systematic Review and Meta-Analysis.OBJECTIVES: In this systematic review and meta-analysis, we assessed whether a high CO2 gap predicts mortality in adult critically ill patients with circulatory shock." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Chemotherapy, Adjuvant TREATS Advanced cancer", + "sentence": "[The predictive factors for the response to platinum/paclitaxel based first-line adjuvant chemotherapy in advanced ovarian cancer]." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Ara-C TREATS Leukemia, Myelocytic, Acute", + "sentence": "CONCLUSION: GM-CSF administered during induction treatment of AML with a DNR/Ara-C combination did not provide any clinical benefit." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Mechanical ventilation TREATS Neoplasm Metastasis", + "sentence": "There was an increase in the total number of patients with metastatic cancer who underwent intubation/MV during the study period, from 36,881 in 2001-2002 to 51,003 in 2009-2010 (P<.001)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Interstitial Radiation Therapy TREATS Malignant neoplasm of anus", + "sentence": "BACKGROUND: New techniques using image guidance other than computed tomography (CT) and traditional two-dimensional (2D) endosonography might improve interstitial brachytherapy in patients with anal cancer." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Thioguanine TREATS Crohn's disease", + "sentence": "Further experience with the use of 6-thioguanine in patients with Crohn's disease." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Decompressive incision TREATS Stenosis", + "sentence": "METHODS: Twelve patients who underwent operative decompression for symptomatic stenosis of the lower thoracic spine were followed up for an average period of 62.4 months." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "removal technique TREATS Malignant Neoplasms", + "sentence": "Combined Liver and Inferior Vena Cava Resection for Malignancies Is Safe and Feasible in a Group of High-Risk Patients." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Imaging Techniques TREATS Pulmonary Embolism", + "sentence": "Imaging techniques in treatment algorithms of pulmonary embolism." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Transplantation TREATS Demyelination", + "sentence": "In the current study, we evaluated the roles of E2 administration before SCs transplantation in targeting SCI-induced axonal degeneration and demyelination." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "levocarnitine TREATS Amyotrophic Lateral Sclerosis", + "sentence": "METHOD: This cross-sectional study evaluated the serum levels of L-carnitine in 30 patients with ALS (total-case) divided into two groups included 15 patients in the Oral-Fed (OF) group and 15 patients in the Enteral-Fed (EF) group, compared with 15 healthy people matched in age and sex in the control group." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Intrauterine artificial insemination TREATS Pregnancy Outcome", + "sentence": "Background: We investigated the impact of the choice of catheter type and tenaculum use on pregnancy related outcomes in intrauterine insemination (IUI) treatments." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Tamoxifen TREATS Malignant neoplasm of breast", + "sentence": "In this context, we have developed an ultra performance liquid chromatography-tandem mass spectrometry method (UPLC-MS/MS) requiring 100 MUL of plasma for the quantification of tamoxifen and three of its major metabolites in breast cancer patients." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Hospitalization TREATS Heart failure", + "sentence": "In this perspective, we highlight the results of the recent landmark EMPA-REG OUTCOME trial which has shown that empagliflozin, a member of the sodium-glucose co-transporter 2 (SGLT-2) inhibitor class of glucose lowering medications, reduces death from CV causes, hospitalisation for heart failure and progression to end stage kidney disease in patients with T2DM and established CV disease." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Patient identification TREATS Chronic pain", + "sentence": "OBJECTIVE: To develop a claims-based algorithm for identifying patients who are adherent versus nonadherent to published guidelines for chronic pain management." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Antiretroviral Therapy, Highly Active TREATS HIV", + "sentence": "Highly active antiretroviral therapy (HAART) has a positive influence on longevity in patients with HIV, substantially reducing morbidity and mortality, including resource-poor settings such as South Africa." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Evaluation procedure TREATS Pain", + "sentence": "Neuropathic pain: clinical classification and assessment in patients with pain due to cancer." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Placebos TREATS Urinary symptoms", + "sentence": "In a double-blind, randomised trial, 62 postmenopausal women with genito-urinary symptoms were treated with oestriol or matching placebo for 4 weeks." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Evoked potentials monitoring TREATS Lesion", + "sentence": "The modality is chosen in accordance with the affected neuronal system: visual-evoked potential (VEP) monitoring in the management of processes affecting the visual pathway, brain stem auditory-(BAER) and somatosensory-evoked potential (SSEP) monitoring in lesions affecting these pathways, in particular space-occupying lesions of the posterior fossa." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "First line treatment TREATS Advanced Ovarian Carcinoma", + "sentence": "Correction to: Niraparib: A Review in First-Line Maintenance Therapy in Advanced Ovarian Cancer." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Treatment Protocols TREATS Choriocarcinoma", + "sentence": "STUDY DESIGN: Seventy-four patients with GTT, 47 with invasive mole and 27 with choriocarcinoma were treated with FUDR-containing regimens." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Detection TREATS Cervical Squamous Cell Carcinoma", + "sentence": "This review article provides a comprehensive overview of literature over the past 5 years on the detection of circulating tumour cells (CTCs) in HNSCC; CTC biology and future perspectives." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Amino Acids TREATS Need for isolation", + "sentence": "It only incorporated amino acids in isolation to a small extent or not at all." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Bone Marrow Transplantation TREATS Non-Hodgkin's lymphoma refractory", + "sentence": "METHODS: Five patients with refractory non-Hodgkin lymphoma underwent bone-marrow transplantation from haploidentical related donors sharing at least one HLA A, B, or DR allele on the mismatched haplotype." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Transplantation TREATS Acute leukemia", + "sentence": "METHODS: To determine the effect of transplantation period, the authors divided 308 adults with de novo, acute leukemia who underwent T-cell-depleted haplo from 2005 to 2015 into 2 groups, according the year in which they underwent transplantation (2005-2011 [n = 191] and 2012-2015 [n = 117])." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "sham feeding TREATS Duodenal Ulcer", + "sentence": "Effects of proximal gastric vagotomy on gastric secretory and plasma hormonal responses to sham feeding in patients with duodenal ulcers." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Hemodilution TREATS Peripheral arterial occlusive disease", + "sentence": "[Isovolemic hemodilution in peripheral arterial occlusive diseases]." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Interleukin inhibitors TREATS Psoriasis", + "sentence": "After manually reviewing each article for discussion of IL-17 inhibitors for psoriasis, with data originating from clinical trials, and assessment for incidence of TB reactivation, 23 articles met the full inclusion criteria for our review." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Prophylactic treatment TREATS Aspergillosis", + "sentence": "Micafungin and caspofungin have been successfully used in targeted treatment of aspergillosis, prophylaxis, and empirical therapy, both as monotherapy and in combination with other antifungals." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Fludrocortisone TREATS Wasting", + "sentence": "Fludrocortisone treatment in a child with severe cerebral salt wasting." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Exploration procedure TREATS standing balance", + "sentence": "Exploration of a novel physical therapy protocol that uses a sensory substitution device to improve the standing postural balance of children with balance disorders.OBJECTIVE: To explore if an intensive balance training protocol that incorporated the BrainPort sensory substitution device improves the standing postural balance of children with balance disorders." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Secondary prevention TREATS Acute coronary syndrome", + "sentence": "BACKGROUND Clopidogrel is an antiplatelet medication that plays an important role in primary management and secondary prevention of thrombotic vascular events in patients with acute coronary syndrome." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Operative 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undergoing further clinical investigation." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Radical nephrectomy TREATS Carcinoma", + "sentence": "The analysis included 40 patients undergoing partial or radical nephrectomy for cRCC and 40 age- and sex-matched healthy adult volunteers." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Adrenergic beta-Antagonists TREATS Coronary Arteriosclerosis", + "sentence": "We conclude that in patients with coronary artery disease in whom chronic beta-blocker therapy is continued until the time of surgery, esmolol does not further attenuate the heart rate response but does attenuate the increase in blood pressure." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Microbicides TREATS Cicatrix", + "sentence": "CONCLUSIONS: These results suggest that PTX is effective in preventing renal scar formation in pyelonephritis when the initiation of antimicrobial treatment is delayed in this rat model of pyelonephritis." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Unithiol TREATS Lead Poisoning", + "sentence": "[On the problem of the use unithiol in lead poisoning]." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Quinine TREATS Malaria", + "sentence": "We evaluated the impact of the homeopathic medicine China rubra 7CH on the side-effects of quinine used as treatment for acute malaria in pregnant women in Cotonou, Benin." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Immune Checkpoint Inhibitors TREATS Venous Thromboembolism", + "sentence": "Immune checkpoint inhibitors for cancer and venous thromboembolic events." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Abortion, Induced TREATS Abortion, Missed", + "sentence": "We recorded 3 term deliveries, 1 induced abortion for sirenomelia, and 1 missed abortion." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "2-oxothiazolidine-4-carboxylate TREATS Protein-Energy Malnutrition", + "sentence": "Selective elevation of glutathione levels in target tissues with L-2-oxothiazolidine-4-carboxylate (OTC) protects against hyperoxia-induced lung damage in protein-energy malnourished rats: implications for a new treatment strategy." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Basis TREATS Protection", + "sentence": "This study would help to understand the role of C. joyneri in the material cycling and energy flow in Haizhou Bay ecosystem, and provide scientific basis for the protection and rational utilization of this species." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Tranexamic Acid TREATS Cerebral hemisphere hemorrhage", + "sentence": "Larger studies are needed to assess safety and efficacy of TA in ICH." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Therapeutic regimen TREATS Foramen Ovale, Patent", + "sentence": "The aim of this study was to evaluate the risk of recurrent ischaemic cerebrovascular events (stroke or transient ischaemic attack (TIA)) in patients with patent foramen ovale (PFO) or atrial septal aneurysm (ASA) treated with different therapeutic regimens." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Bariatric Surgery TREATS Hypertensive disease", + "sentence": "Impact of rapid weight loss on risk reduction of developing arterial hypertension in severely obese patients undergoing bariatric surgery." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Obesity", + "sentence": "CONCLUSIONS: The study found no differences between post-operative morbidity or mortality and the pre-operative nutrition status of obese patients who underwent surgery due to esophageal cancer." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Fasciotomy TREATS Burns, Electric", + "sentence": "Utility of Shoelace Technique in 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anesthesia in overweight and obese women." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Excision TREATS Gastrointestinal Stromal Tumors", + "sentence": "Endoscopic full-thickness resection for a gastrointestinal stromal tumor in a liver transplant recipient: A case report." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "gene therapy TREATS Optic Atrophy, Hereditary, Leber", + "sentence": "Gene Therapy for Leber Hereditary Optic Neuropathy: Initial Results." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Health education TREATS Crisis", + "sentence": "Health education for heart patients in crisis." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Anesthetics TREATS Muscle hypotonia", + "sentence": "The best treatment for an established case of tetanus is total muscle relaxation with anesthetic agents and intermittent positive pressure ventilation." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Leptin TREATS Acquired Immunodeficiency Syndrome", + "sentence": "Relationship between leptin levels and suppressed CD4 counts in HIV patients." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Detection TREATS Speech impairment", + "sentence": "Detection of a novel familial deletion of four genes between BP1 and BP2 of the Prader-Willi/Angelman syndrome critical region by oligo-array CGH in a child with neurological disorder and speech impairment." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Thymosin TREATS Immunologic Deficiency Syndromes", + "sentence": "Thymosin for immunodeficiency diseases and cancer." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Antibiotics TREATS Meconium Aspiration Syndrome", + "sentence": "It is concluded that empirical use of antibiotics in the routine management of meconium aspiration syndrome is of no benefit." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "cyclophosphamide/fluorouracil/methotrexate protocol TREATS Memory impairment", + "sentence": "The results point out that CMF changes the interhemispheric relations and result in memory malfunction." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Bronchopulmonary Sequestration", + "sentence": "Prenatal interventional and postnatal surgical therapy of extralobar pulmonary sequestration." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Sacrococcygeal teratoma", + "sentence": "The authors evaluate the time required for AFP levels to reach normal levels in 6 infants with prenatal diagnosis of SCT who underwent surgery for resection." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Operative Surgical Procedures TREATS Radiculopathy, Cervical", + "sentence": "OBJECTIVES: To evaluate the long-term outcome after 2 different surgical procedures in the treatment of cervical radiculopathy, compare them with each other and with previous data from other surgical techniques, and outline the indications, advantages, and disadvantages of each procedure." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "coronin, Annona muricata TREATS Chondromyces", + "sentence": "Southern blot analysis suggested that the coronin gene present in the P. polycephalum genome might be a single copy." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Sympathectomy TREATS Bromhidrosis", + "sentence": "We collected 108 patients with AO or AB treated by upper thoracic sympathectomy from July 1995 to July 2002." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Decompressive incision TREATS Spinal Stenosis", + "sentence": "Percutaneous endoscopic transforaminal lumbar spinal canal decompression for lumbar spinal stenosis." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Hydralazine TREATS Congestive 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"The use of night braces, besides a less severe influence on the patient's quality of life, is effective in stopping the progression of the curve in idiopathic scoliosis." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "denosumab TREATS Malignant neoplasm of prostate", + "sentence": "Bone metastasis from other tumors such as lung, breast, and prostate cancer, are more effectively treated with bisphosphonates and denosumab, thereby decreasing the need for palliative surgical intervention." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Dialysis Solutions TREATS Kidney Failure, Acute", + "sentence": "Using indirect calorimetry and analyzing the dialysate effluent for its dextrose concentration, we studied the effects of high dextrose-containing dialysate in five patients with ARF." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Fluid resuscitation TREATS Septicemia", + "sentence": "Fluid resuscitation in human sepsis: Time to 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"sentence": "CONCLUSIONS: Despite the rarity of the condition and despite the rarity of vertebral body lesion resolution, total vertebral body reconstruction was observed over a 7-year period." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Ablation TREATS Paroxysmal atrial fibrillation", + "sentence": "METHODS AND RESULTS: Cardiac magnetic resonance was performed pre-ablation, acutely (<3 h), and 3 months post-ablation in 41 patients with paroxysmal atrial fibrillation (AF) undergoing pulmonary vein (PV) isolation with PFA (n = 18) or thermal ablation (n = 23, 16 radiofrequency ablations, 7 cryoablations)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Induction TREATS Atherosclerosis", + "sentence": "Induction of mitochondrial manganese superoxide dismutase in macrophages by oxidized LDL: its relevance in atherosclerosis of humans and heritable hyperlipidemic rabbits." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Neoadjuvant Chemoradiotherapy TREATS Adenocarcinoma of rectum", + "sentence": "The impact of neoadjuvant concurrent chemoradiation (NCCR) on exosomal markers (CD63 and CD9) expression and their prognostic significance in patients with rectal adenocarcinoma are yet to be explored." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Stents TREATS Lesion", + "sentence": "AIMS: Our aim was to demonstrate the safety and efficacy of the Svelte sirolimus-eluting coronary stent-on-a-wire Integrated Delivery System (IDS) with bioresorbable drug coating compared to the Resolute Integrity zotarolimus-eluting stent with durable polymer in patients with de novo coronary artery lesions." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Surgical sutures TREATS Paralysed", + "sentence": "Complete removal of the suture and external neurolysis significantly improved the palsy." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Hemodialysis TREATS 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"triple": "Angioplasty, Transluminal, Percutaneous Coronary TREATS Shock, Cardiogenic", + "sentence": "There was only one death (no-reflow phenomenon in a rescue primary PTCA in a patient in cardiogenic shock) without other major periprocedural complications." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Sodium Chloride TREATS Reperfusion Injury", + "sentence": "CONCLUSIONS: Our findings suggest that HRS mitigates I/R injury by decreasing inflammation and, therefore, has the potential for application as a therapy for improving skin flap survival." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Nephrectomy TREATS Abnormal renal function", + "sentence": "The present case was a 59-year-old woman who underwent a right nephrectomy at 30 years of age, and in whom renal dysfunction occurred at 51 years of age." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "epigallocatechin gallate TREATS Neoplasm", + "sentence": "Comparable 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"Sublingual Immunotherapy TREATS Asthma", + "sentence": "Safety, Efficacy, and Preventive Role of Subcutaneous and Sublingual Allergen Immunotherapy for the Treatment of Pediatric Asthma." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "nimotuzumab TREATS Carcinoma, Non-Small-Cell Lung", + "sentence": "Nimotuzumab, a novel monoclonal antibody to the epidermal growth factor receptor, in the treatment of non-small cell lung cancer." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Calcitonin Gene-Related Peptide TREATS Endocrine Gland Neoplasms", + "sentence": "Calcitonin gene-related peptide in patients with endocrine tumors." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "inotersen TREATS Hereditary cardiac amyloidosis", + "sentence": "Inotersen preserves or improves quality of life in hereditary transthyretin amyloidosis." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "infliximab TREATS Rheumatoid 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"triple": "Choledochojejunostomy TREATS Liver calculus", + "sentence": "The goal of the present study was to evaluate the therapeutic safety and perioperative and long-term outcomes of choledochojejunostomy versus T-tube drainage for hepatolithiasis patients with sphincter of Oddi laxity (SOL)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Brain natriuretic peptide TREATS Congestive heart failure", + "sentence": "PURPOSE: B-type natriuretic peptide (BNP) has been in clinical use for the treatment of decompensated congestive heart failure." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Biomedical Monitors TREATS Eosinophilic esophagitis", + "sentence": "Endoscopies have to be repeated in order to diagnose, monitor, and treat EoE." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Extraction TREATS Myopia", + "sentence": "CONCLUSIONS: Small incision lenticule extraction for low myopia was found to be safe and effective with 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bleeding changes, headache, weight changes, mastalgia, and acne), continuation rates and reasons for termination, and removal." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Angioplasty, Balloon TREATS Lesion", + "sentence": "Although balloon angioplasty for femoropopliteal artery lesions has been associated with restenosis rates of up to 60% at 12 months, the mechanism of restenosis has not been fully evaluated." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Probes TREATS Hypersensitivity", + "sentence": "Highly stable quantum dots with silica-poly(EGDMA-co-MAA) synergistic protection and the preliminary application in immunoassay.For the application of biological quantitative probes, how to ameliorate chemical sensitivity and instability of quantum dots (QDs) under different environments is a longstanding issue." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "rituximab TREATS Lymphoma, Follicular", + "sentence": "Progressive multifocal leukoencephalopathy during rituximab maintenance after rituximab and bendamustine treatment for relapsed follicular lymphoma." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Blood Transfusion TREATS Cooley's anemia", + "sentence": "The aim of this study was to analyze the renal function and urine metabolomic profile of beta-TM patients undergoing transfusions and deferasirox (DFX) therapy, in order to better characterize and shed light on the pathogenesis of renal disease in this setting." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Treatment Protocols TREATS Hypertensive", + "sentence": "Both trials recently confirmed the safety and tolerability of both the regimen and goals of antihypertensive treatment in acutely hypertensive patients with ICH, as proposed in the present trial." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Coagulation procedure TREATS Hemorrhage", + "sentence": "RESULTS: Malignant disease was the primary cause of medical tamponade (74 patients; 65%), followed by viral history (11; 10%) and intra-pericardial bleeding due to anti-coagulation treatment (4; 3%)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Intra-Arterial Infusions TREATS Did not receive therapy or drug for", + "sentence": "The effects of combination therapy, the intra-arterial administration of 10 degrees C HemoAct (10H) initiated at the onset of reperfusion, were compared with those of monotherapies, the intra-arterial administration of 10 degrees C saline (10S) and 37 degrees C HemoAct (37H), and an untreated control under the condition of 2-hour ischemia/24-hour reperfusion." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Harvest of stem cells TREATS Advanced cancer", + "sentence": "Intensive-dose ifosfamide and etoposide with filgrastim for cytoreduction before peripheral blood stem cell collection in patients with advanced ovarian cancer." 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"validation_result": "No" + }, + { + "input": { + "triple": "Atropine TREATS Myopia", + "sentence": "We investigated whether lower doses of atropine would control myopia progression." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Introduction procedure TREATS Amyotrophic Lateral Sclerosis", + "sentence": "Introduction to the minireviews series on mitochondrial matters in amyotrophic lateral sclerosis, Lou Gehrig's disease." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Surgical Management TREATS Appendicitis", + "sentence": "This study compared management of appendicitis before and during the pandemic by assessing disease presentation severity, modes of investigation, surgical management and patient outcomes." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Punctal plug TREATS Dryness of eye", + "sentence": "Punctal plugs were placed in 18 dry eye patients of the aqueous-deficiency type who were on maximally tolerable 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}, + "validation_result": "No" + }, + { + "input": { + "triple": "Griseofulvin TREATS Raynaud Disease", + "sentence": "Griseofulvin in Raynaud's disease." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "moxifloxacin TREATS Neuroretinitis", + "sentence": "Our data support the use of 0.5 mg/L moxifloxacin in LJ for detection of FQ resistance, but not the recent increase in the ofloxacin critical concentration from 2 to 4 mg/L given in the WHO recommendations." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Reflexotherapy TREATS Myocardial Ischemia", + "sentence": "[Reflexotherapy in ischemic heart disease]." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Mechanical ventilation TREATS Tension", + "sentence": "Blood gas tensions were controlled by mechanical ventilation." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Keratomileusis, Laser In Situ TREATS Myopia", + "sentence": "METHODS: The study included 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"validation_result": "No" + }, + { + "input": { + "triple": "Dietary Modification TREATS Obesity", + "sentence": "This study concluded that physical activity and dietary interventions play an effective role in the management of obesity." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "simeprevir TREATS Hepatotoxicity", + "sentence": "In general, the obtained results demonstrate that simeprevir is susceptible to form reactive simeprevir-glutathione adducts and cyclopropansulfonamide, which may explain the implication of simeprevir in idiosyncratic adverse drug reactions (IADRs) or hepatotoxicity." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Radiotherapy, Adjuvant TREATS Malignant Neoplasms", + "sentence": "Costs of Definitive Chemoradiation, Surgery and Adjuvant Radiation, versus De-Escalated Adjuvant Radiation per *** in HPV+ Cancer of the Oropharynx." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Assessment procedure 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subjects." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Biological Response Modifiers TREATS Toxic effect", + "sentence": "Melatonin as a potent antioxidant has shown appropriate immune regulatory properties that may ameliorate toxicity induced by radiation in various organs." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Treatment Protocols TREATS Leukemia, Myelocytic, Acute", + "sentence": "Non-cardiotoxic anthracycline regimens in the treatment of acute myeloblastic leukaemia." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "GLUCOCORTICOID THERAPY TREATS Leukemia, Lymphocytic, Acute", + "sentence": "CONCLUSIONS: High-dose glucocorticoid therapy in ALL children may cause prolonged adrenal suppression and related clinical symptoms." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Open reduction of fracture TREATS LONG BONE FRACTURE", + "sentence": "Class I fractures (acute injuries) are managed by existing principles of long bone fracture management with a tendency to open reduction and internal fixation to dispense with the necessity of plaster casts on insensate skin." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Psychotherapy, Multiple TREATS Hyperparathyroidism, Secondary", + "sentence": "In conclusion, secondary hyperparathyroidism can be effectively controlled with combined oral therapy without significant hypercalcemia in selected patients with end-stage renal failure." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Tramadol TREATS Labor Pain", + "sentence": "Although tramadol has been used in myocardial emergencies, in trauma and obstetric pain, or to supplement balanced anaesthesia, most studies have investigated postoperative patients." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Virulence Factors TREATS Bacillus anthracis", + "sentence": "Anthrax toxin is a key virulence factor for Bacillus anthracis." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Placebos TREATS Skin Wrinkling", + "sentence": "In this pilot study, participants with moderate or severe crow's feet wrinkles were treated with Myobloc versus placebo." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "ergocalciferol TREATS Negative", + "sentence": "Vitamin D in Triple-Negative and BRCA1-Deficient Breast Cancer-Implications for Pathogenesis and Therapy." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "methotrexate TREATS Gestational Trophoblastic Neoplasms", + "sentence": "CONCLUSIONS: The Doppler-based predictive model, adding a non-invasive marker of tumor vascularity, could complement the FIGO Scoring system for the prediction of MTX-resistance in the low-risk GTN with myometrial invasion." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Mechanical thrombectomy TREATS Acute Ischemic Stroke", + "sentence": "This literature review assesses the clinical outcomes of AIS patients treated with both intravenous thrombolysis (IVT) prior to mechanical thrombectomy (MT) compared to those treated solely with mechanical thrombectomy." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Immunomodulators TREATS Extrinsic asthma NOS", + "sentence": "Taken together, our results indicated that administration of Ad-hIL-1ra may have therapeutic potential for the immunomodulatory treatment of allergic asthma." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Nasal Spray TREATS Nasal Polyps", + "sentence": "Therefore, the aim of this study was to compare the efficacy of beclomethasone aerosol and aqueous nasal sprays in the patients with nasal polyps." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Induction TREATS Primary open angle glaucoma", + "sentence": "There appear to be two different pathways of ECM remodelling and apoptosis induction in POAG." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Toll-like Receptor 7 Agonist TREATS melanoma", + "sentence": "Taken together, the combination therapy using the TGFbetaRI kinase inhibitor and TLR 7/8 agonist with EXOs may serve as a promising strategy to treat melanoma and prostate cancer." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Cisplatin TREATS Normal blood pressure", + "sentence": "Interaction of nimesulide, a cyclooxygenase-2 inhibitor, with cisplatin in normotensive and spontaneously hypertensive rats." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Triage TREATS Equivocal result", + "sentence": "Comparison of HPV genotyping and methylated ZNF582 as triage for women with equivocal liquid-based cytology results." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "bortezomib TREATS Multiple Myeloma", + "sentence": "METHODS: A total of 110 MM patients were treated with a bortezomib-based regimen at our hospital from January 2006 to February 2010." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Dissection TREATS hemangioblastoma", + "sentence": "PATIENTS AND METHODS: Since 2004, we have used a this device during tumor dissection for 36 patients with intramedullary spinal cord tumors (21 ependymomas, 7 astrocytomas, 6 hemangioblastomas, and 2 cavernomas) and 1 patient with an arteriovenous malformation." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Fatty Acids, Omega-3 TREATS Depressive disorder", + "sentence": "Omega-3 fatty acids for depression in adults." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Mohs Surgery TREATS Merkel cell carcinoma", + "sentence": "Response to \"Mohs surgery for early-stage Merkel cell carcinoma (MCC) achieves local control better than wide local excision +/- radiation therapy with no increase in MCC-specific death\"." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Forecast of outcome TREATS Pain", + "sentence": "Even in primary arthroplasty patients (n = 17), precision of outcome prediction for pain was no better that in the remaining collective (p = 0.634)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "tramadol hydrochloride TREATS Obsessive-Compulsive Disorder", + "sentence": "Open-label pilot study of tramadol hydrochloride in treatment-refractory obsessive-compulsive disorder." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Surgical Procedures, Laparoscopic TREATS Congenital malrotation", + "sentence": "We herein report two cases of colon cancer with intestinal malrotation treated with laparoscopic surgery and reviewed the literatures in Japan." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Iron TREATS Encounter due to counseling", + "sentence": "RELEVANCE TO CLINICAL PRACTICE: Knowledge about factors influencing children's iron intake and iron status may improve the nutritional advice and education from the Child Health Services to prevent or detect iron deficiency." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "daratumumab TREATS Refractory Plasma Cell Neoplasm", + "sentence": "The phase 2 MM-014 trial (NCT01946477) investigated pomalidomide, dexamethasone, and daratumumab after 1 to 2 prior treatment lines (62.5%, 1 prior line) in patients with RRMM and prior lenalidomide (75.0%, lenalidomide refractory)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "TAC TREATS Renal fibrosis", + "sentence": "CONCLUSIONS These results suggested that EVR addition and Tac reduction may attenuate kidney allograft fibrosis, and that the suppression of mTOR signaling process may be involved in the anti-fibrotic effect of this immunosuppressive regimen." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Induction TREATS Pseudomonas aeruginosa", + "sentence": "Specificity of beta-lactamase induction in Pseudomonas aeruginosa." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Nicotine TREATS Major Depressive Disorder", + "sentence": "The authors present findings from the first investigation of the use of alcohol, nicotine, and caffeine in nonsubstance-abusing outpatients with major depressive disorder." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Proton Pump Inhibitors TREATS Cholangitis", + "sentence": "Analysis of intrinsic anti-microbial resistance patterns was performed: Anti-microbial combination therapies were significantly more required to cover all isolated pathogens in cholangitis episodes with PPI than in cholangitis episodes without PPI (44/120 vs. 46/198, P = 0.01)." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "glutathione TREATS Traumatic Brain Injury", + "sentence": "Thus, hypobaria-induced enhancement of glutathione metabolism represents a potential therapeutic target for TBI management." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Division of adhesions TREATS Low Back Pain", + "sentence": "OBJECTIVES: The authors evaluated the effectiveness of percutaneous epidural adhesiolysis (PEA) in patients with low back pain due to contained disc herniation." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Anticoagulants TREATS STEMI", + "sentence": "Use of anticoagulants in ST-segment elevation myocardial infarction patients; a focus on low-molecular-weight heparin." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Embolization, Therapeutic TREATS Fibrosis", + "sentence": "BACKGROUND/AIMS: The aim of this prospective randomized controlled trial was to investigate the need for prophylactic antibiotherapy in patients with cirrhosis and hepatocellular carcinoma who underwent transarterial embolization and to establish the parameters that determine the development of fever > 38 degrees C after this procedure." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Idarubicin TREATS Lymphoma, Non-Hodgkin's", + "sentence": "Further studies employing idarubicin in non-Hodgkin's lymphoma should be considered." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Implantation procedure TREATS Sustained ventricular tachycardia", + "sentence": "A 46-year-old man with a history of sustained monomorphic ventricular tachycardia underwent an implantation of a third generation multiprogrammable implantable cardioverter defibrillator." + }, + "validation_result": "No" + }, + { + "input": { + "triple": "Anti-Arrhythmia Agents TREATS Ventricular arrhythmia", + "sentence": "CONCLUSION: RSDN appears to be a safe and effective treatment strategy in patients with prior failed antiarrhythmic drugs and catheter ablation for recurrent ventricular arrhythmia and electrical storm." + }, + "validation_result": "No" + } +] \ No newline at end of file diff --git a/main.py b/main.py deleted file mode 100644 index 3b94972..0000000 --- a/main.py +++ /dev/null @@ -1,43 +0,0 @@ -import os -import argparse -from config import OPENAI_API_KEY -from src.data_processing import read_data_from_files -from src.load_model import load_model -from src.processing import process_data - -os.environ["OPENAI_API_KEY"] = OPENAI_API_KEY - -result_folder = "result" -progress_folder = "progress" - - -def main() -> None: - """ - Main function to run the Fact-Checking App. - This function parses command-line arguments, - reads data from files, loads the language model, and initiates the data processing. - Returns: - None - """ - parser = argparse.ArgumentParser(description="Fact-Checking App") - parser.add_argument("--model", required=True, choices=['llama', 'gpt_4_0', 'gpt_3_5_turbo'], help="Model to use") - parser.add_argument("--icl", action='store_true', help="Use In-Context Learning") - parser.add_argument("--triple_file", required=True, help="Path to the SemMedDB triple file") - parser.add_argument("--sentence_file", required=True, help="Path to the SemMedDB sentence file") - args = parser.parse_args() - - triple_data, sentence_data = read_data_from_files(args.triple_file, args.sentence_file) - - model_info = load_model(args.model, args.icl) - - icl_suffix = '_icl' if args.icl else '' - result_file_name = f"{args.model}{icl_suffix}_semmed_result.csv" - progress_file_name = f"{args.model}{icl_suffix}_progress.csv" - - process_data(model_info, args.model, args.icl, triple_data, sentence_data, - os.path.join(result_folder, result_file_name), - os.path.join(result_folder, progress_folder, progress_file_name)) - - -if __name__ == "__main__": - main() diff --git a/process.py b/process.py deleted file mode 100644 index 1175a87..0000000 --- a/process.py +++ /dev/null @@ -1,161 +0,0 @@ -# -*- coding: utf-8 -*- -"""Process - -Automatically generated by Colab. - -Original file is located at - https://colab.research.google.com/drive/1Q1UxrmNHSKvNRqlksj7Lf0sObE5Zeq74 -""" - -import psycopg2 -import json -import os -from dotenv import load_dotenv -from llama_cpp import Llama -from huggingface_hub import hf_hub_download - -# Constants -MODEL_NAME = "TheBloke/Mixtral-8x7B-Instruct-v0.1-GGUF" -MODEL_PATH = hf_hub_download(repo_id=MODEL_NAME, filename="mixtral-8x7b-instruct-v0.1.Q5_K_M.gguf") -BATCH_SIZE = 10 # Number of records to process in each batch -TIMEOUT = 5000 # Statement timeout in milliseconds - -# Load Llama model -model = Llama( - model_path=MODEL_PATH, - n_threads=64, - n_batch=128, - n_ctx=4096, - n_gpu_layers=96, - mlock=True, - logits_all=True -) - -# Load environment variables -load_dotenv('.env') - -# Establish database connection -def create_db_connection(): - return psycopg2.connect( - dbname=os.getenv("DB_NAME"), - user=os.getenv("DB_USER"), - password=os.getenv("DB_PASSWORD"), - host=os.getenv("DB_HOST"), - port=os.getenv("DB_PORT"), - connect_timeout=10 # Set connection timeout to 10 seconds - ) - -# Set statement timeout for long-running queries -def set_statement_timeout(cursor, timeout=TIMEOUT): - cursor.execute(f"SET statement_timeout = {timeout};") - -# Read starting ID from environment -def read_starting_id(): - return int(os.getenv("STARTING_ID", 0)) - -# Save updated ID to the .env file -def save_updated_id(id_value): - with open('.env', 'r') as file: - lines = file.readlines() - - updated_lines = [ - f"STARTING_ID={id_value}\n" if line.startswith("STARTING_ID=") else line - for line in lines - ] - - if not any(line.startswith("STARTING_ID=") for line in lines): - updated_lines.append(f"STARTING_ID={id_value}\n") - - with open('.env', 'w') as file: - file.writelines(updated_lines) - -# Process a triple and sentence using Llama model -def process_triple(triple, sentence): - prompt=f""" - Context: - USER: (''Is the triple "Phase related to Follicle stimulating hormone measurement" directly or indirectly supported by the sentence: "In pre-menopause healthy females, blood was sampled weekly during one menstruation cycle and menstruation phases (follicular, ovulatory, luteal) were determined by FSH/LH levels."?',) - - ASSISTANT: Yes - - USER: (''Is the triple "Phase related to Sodium measurement" directly or indirectly supported by the sentence: "Based on a biophysical photoreceptor model, the Na(+)- and Ca(2+)-currents and concentration changes were determined from the first transient depolarization phase of the photoreceptor response."?',) - - ASSISTANT:Yes - - USER: (''Is the triple "Phase related to Bronchoalveolar Lavage" directly or indirectly supported by the sentence: "Challenge of the airways of sensitized guinea pigs with aerosolized ovalbumin resulted in an early phase of microvascular protein leakage and a delayed phase of eosinophil accumulation in the airway lumen, as measured using bronchoalveolar lavage (BAL)."?',) - - ASSISTANT: Yes - - USER: (''Does the phrase "Ciprofloxacin related to DNA Gyrase" receive at least indirect support from the statement: "Effect of ranolazine in preventing postoperative atrial fibrillation in patients undergoing coronary revascularization surgery."?',) - - ASSISTANT: No - - USER: (''Does the phrase "Ciprofloxacin related to Crohn disease" receive at least indirect support from the statement: "Recent evidence of beneficial effects of ranolazine (RAN) in type II diabetes motivates interest in the role of the late sodium current (INaL) in glucose-stimulated insulin secretion."?',) - - ASSISTANT: No - - USER: (''Does the phrase "Ciprofloxacin related to endophthalmitis" receive at least indirect support from the statement: "Furthermore, the activated Akt/mTOR signaling pathway induced by AF was further activated by ranolazine."?',) - - ASSISTANT: No - - - SYSTEM: You are a computational biologist tasked with evaluating scientific claims. Your role requires you to apply critical thinking and your expertise to interpret data and research findings accurately. Answer 'Yes' or 'No' to directly address the query posed. - - USER: ('\'Does the phrase "{triple}" receive at least indirect support from the statement: "{sentence}"?',). - - ASSISTANT: - - """ - - response = model(prompt=prompt, max_tokens=1, temperature=0, echo=False, logprobs=True) - return response["choices"][0]["text"], json.dumps(response["choices"][0]["logprobs"]) - -# Process batches of records from the database -def process_batches(cursor, starting_id): - while True: - cursor.execute(""" - SELECT "id", "triple", "sentence" - FROM public."tblBiomedicalFactcheck" - WHERE "id" >= %s - ORDER BY "id" - LIMIT %s - """, (starting_id, BATCH_SIZE)) - - records = cursor.fetchall() - if not records: - print("No more records to process.") - break - - for record in records: - record_id, triple, sentence = record - answer, logprops_json = process_triple(triple, sentence) - try: - cursor.execute(""" - UPDATE public."tblBiomedicalFactcheck" - SET "answer" = %s, "logprops" = %s - WHERE "id" = %s - """, (answer, logprops_json, record_id)) - except Exception as e: - print(f"Error updating record ID {record_id}: {e}") - conn.rollback() # Rollback in case of an error - - conn.commit() - starting_id += BATCH_SIZE - save_updated_id(starting_id) - print(f"Processed up to ID: {starting_id}") - -# Main processing function -def main(): - starting_id = read_starting_id() - conn = create_db_connection() - cursor = conn.cursor() - - try: - set_statement_timeout(cursor) - process_batches(cursor, starting_id) - finally: - cursor.close() - conn.close() - print("Data processing completed successfully.") - -if __name__ == "__main__": - main() diff --git a/src/data_processing.py b/src/data_processing.py deleted file mode 100644 index 9e71178..0000000 --- a/src/data_processing.py +++ /dev/null @@ -1,108 +0,0 @@ -import os -import csv -from typing import Tuple, TextIO -import pandas as pd - - -def read_data_from_files(triple_file: str, sentence_file: str) -> Tuple[pd.DataFrame, pd.DataFrame]: - """ - Read data from specified triple and sentence files into pandas DataFrames. - - This function reads two CSV files: one containing triples data and the other containing sentences. - It sets custom column names for the dataframes and performs basic preprocessing like stripping - quotes from the sentence strings. - - Parameters: - triple_file (str): File name of the triples CSV file located in the 'data' directory. - sentence_file (str): File name of the sentences CSV file located in the 'data' directory. - - Returns: - Tuple[pd.DataFrame, pd.DataFrame]: A tuple of two pandas DataFrames, one for triples and the other for sentences. - """ - triple_data = pd.read_csv(os.path.join('data', triple_file), delimiter=',', header=None, engine='python') - triple_data.columns = [ - "PREDICATION_ID", "SENTENCE_ID", "PMID", "PREDICATE", "SUBJECT_CUI", "SUBJECT_NAME", - "SUBJECT_SEMTYPE", "SUBJECT_NOVELTY", "OBJECT_CUI", "OBJECT_NAME", "OBJECT_SEMTYPE", - "OBJECT_NOVELTY", "Column", "Column", "Column" - ] - - sentence_data = pd.read_csv(os.path.join('data', sentence_file), delimiter=',', header=None, engine='python') - sentence_data.columns = [ - "SENTENCE_ID", "PMID", "TYPE", "NUMBER", "SENT_START_INDEX", "SENTENCE", - "SECTION_HEADER", "NORMALIZED_SECTION_HEADER", "Column", "Column" - ] - sentence_data["SENTENCE"] = sentence_data["SENTENCE"].str.strip('""') - return triple_data, sentence_data - - -def initialize_writers(result_file: str, progress_file_path: str) -> Tuple[csv.writer, csv.writer, TextIO, TextIO]: - """ - Initialize CSV writers for writing results and progress to files. - - This function opens the specified result and progress files in append mode and - initializes csv.writer objects for them. It handles exceptions during file opening - and raises them after logging. - - Parameters: - result_file (str): The file path for writing result data. - progress_file_path (str): The file path for writing progress data. - - Returns: - Tuple[csv.writer, csv.writer, TextIO, TextIO]: A tuple containing two csv.writer objects - and two file objects for results and progress. - """ - try: - console_results_file = open(result_file, mode="a", newline="") - progress_file = open(progress_file_path, mode="a", newline="") - console_results_writer = csv.writer(console_results_file) - progress_writer = csv.writer(progress_file) - return console_results_writer, progress_writer, console_results_file, progress_file - except Exception as e: - print(f"Error initializing writers: {e}") - raise - - -def save_state(progress_file_path: str, last_processed: dict) -> None: - """ - Save the last processed state to a progress file. - - This function writes the last processed sentence ID and predicate ID to the progress file. - It's used to keep track of progress in case of interruptions during processing. - - Parameters: - progress_file_path (str): The file path for the progress file. - last_processed (dict): A dictionary containing the 'sentence_id' and 'predicate_id' of the last processed item. - - Returns: - None - """ - with open(progress_file_path, 'a+', newline='') as progress_file: - csv_writer = csv.writer(progress_file) - csv_writer.writerow([last_processed['sentence_id'], last_processed['predicate_id']]) - - -def load_state(progress_file_path: str): - """ - Load the last processed state from a progress file. - - This function reads the progress file to find the last processed sentence ID and predicate ID. - It's used to resume processing from where it was last stopped. - - Parameters: - progress_file_path (str): The file path for the progress file. - - Returns: - dict or None: A dictionary containing the 'sentence_id' and 'predicate_id' of the last processed item, - or None if the file does not exist or is empty. - """ - try: - with open(progress_file_path, 'r') as progress_file: - reader = csv.reader(progress_file) - rows = list(reader) - if rows: - last_row = rows[-1] - return {'sentence_id': int(last_row[0]), 'predicate_id': int(last_row[1])} - else: - return None - except FileNotFoundError: - return None diff --git a/src/extract_filtered_data.py b/src/extract_filtered_data.py new file mode 100644 index 0000000..2defe3c --- /dev/null +++ b/src/extract_filtered_data.py @@ -0,0 +1,217 @@ +import json +import csv +import ast +import logging +import os +from typing import Dict, Any, Optional, List +import pandas as pd + +# This file defines a class KGDataExtractor that loads and filters knowledge graph data from JSONL files (nodes and edges), then writes the filtered results into CSV files. It extracts triples (subject-predicate-object) from edges, links them with sentences from publications_info, and produces several CSV outputs. + +class KGDataExtractor: + """ + A class to load and filter knowledge graph data from JSONL files (nodes and edges), + then write the filtered results into CSV files. It extracts triples (subject-predicate-object) + from edges, links them with sentences from publications_info, and produces several CSV outputs. + """ + + def __init__(self, + nodes_file_path: str, + edges_file_path: str, + output_csv_path: str, + base_name: str = "output"): + """ + Initialize the KGDataExtractor. + + Args: + nodes_file_path (str): Path to the nodes JSONL file. + edges_file_path (str): Path to the edges JSONL file. + output_csv_path (str): Path to the main filtered output CSV file. + base_name (str): Base name for additional CSV files for labeled_records, + sentence_data and triple_data. Default is "output". + """ + self.nodes_file_path = nodes_file_path + self.edges_file_path = edges_file_path + self.output_csv_path = output_csv_path + self.base_name = base_name + + self.nodes = {} + self.equivalent_curies_map = {} + + def run(self): + """Execute the extraction and filtering process.""" + self._load_nodes() + self._process_edges() + + def _load_nodes(self) -> None: + """ + Load all nodes into a dictionary for quick access by ID, + and build a map of equivalent CURIEs to names. + """ + with open(self.nodes_file_path, 'r', encoding='utf-8') as nodes_file: + for line in nodes_file: + node_data = json.loads(line) + name = self._get_node_name(node_data) + self.nodes[node_data['id']] = name + + # Map equivalent curies to the primary name + for curie in node_data.get('equivalent_curies', []): + self.equivalent_curies_map[curie] = name + + @staticmethod + def _get_node_name(node_data: Dict[str, Any]) -> str: + """ + Get the name of a node. If 'name' is not present, + try using the first element of 'all_names'. + If none found, return "Unknown". + """ + if node_data.get('name'): + return node_data['name'] + elif node_data.get('all_names'): + return node_data['all_names'][0] + return "Unknown" + + def _process_edges(self) -> None: + """ + Process edges that meet the criteria and write the filtered results. + This method: + - Filters edges by 'primary_knowledge_source' == 'infores:semmeddb' + - Extracts a sentence from publications_info + - Maps subject, predicate, object to their respective names + - Writes a main CSV file with filtered edges + - Creates and saves three additional CSV files: labeled_records, sentence_data, triple_data + """ + with open(self.edges_file_path, 'r', encoding='utf-8') as edges_file, \ + open(self.output_csv_path, 'w', newline='', encoding='utf-8') as output_file: + + csv_writer = csv.writer(output_file) + csv_writer.writerow(['ID', 'Fact', 'Source', 'Template', 'Reference', 'Name']) + + labeled_records = [] + sentence_records = [] + triple_records = [] + + sentence_columns = [ + "SENTENCE_ID", "PMID", "TYPE", "NUMBER", "SENT_START_INDEX", "SENTENCE", + "SECTION_HEADER", "NORMALIZED_SECTION_HEADER", "Column", "Column" + ] + + labeled_columns = [ + "Predicate ID", "Triple", "Sentence ID", "Sentence", "Question", "Label", + "Reference" + ] + + triple_columns = [ + "PREDICATION_ID", "SENTENCE_ID", "PMID", "PREDICATE", + "SUBJECT_CUI", "SUBJECT_NAME", "SUBJECT_SEMTYPE", "SUBJECT_NOVELTY", + "OBJECT_CUI", "OBJECT_NAME", "OBJECT_SEMTYPE", "OBJECT_NOVELTY", + "Column", "Column", "Column" + ] + + sentence_id = 0 + + for line in edges_file: + edge = json.loads(line) + + # Check the primary knowledge source + if edge.get('primary_knowledge_source') == 'infores:semmeddb': + # Extract the first available sentence from publications_info + sentence = self._extract_sentence(edge.get('publications_info', '{}')) + + subject_name, predicate_name, object_name = self._get_triple_names(edge) + fact = f"{subject_name} {predicate_name} {object_name}" + + # Write to the main output CSV + csv_writer.writerow([edge['id'], fact, sentence, '', '', '']) + + # Prepare labeled_record + labeled_records.append({ + "Predicate ID": edge['id'], + "Triple": fact, + "Sentence ID": sentence_id, + "Sentence": sentence, + "Question": f'Is the triple "{fact}" supported by the sentence: "{sentence}"?', + "Label": None, + "Reference": None + }) + + # Prepare sentence record + sentence_records.append({ + "SENTENCE_ID": sentence_id, + "PMID": None, + "TYPE": None, + "NUMBER": None, + "SENT_START_INDEX": None, + "SENTENCE": sentence, + "SECTION_HEADER": None, + "NORMALIZED_SECTION_HEADER": None, + "Column": None, + "Column": None + }) + + # Prepare triple record + triple_records.append({ + "PREDICATION_ID": edge['id'], + "SENTENCE_ID": sentence_id, + "PMID": None, + "PREDICATE": predicate_name, + "SUBJECT_CUI": None, + "SUBJECT_NAME": subject_name, + "SUBJECT_SEMTYPE": None, + "SUBJECT_NOVELTY": None, + "OBJECT_CUI": None, + "OBJECT_NAME": object_name, + "OBJECT_SEMTYPE": None, + "OBJECT_NOVELTY": None, + "Column": None, + "Column": None, + "Column": None + }) + sentence_id += 1 + + # Create DataFrames + labeled_records_df = pd.DataFrame(labeled_records, columns=labeled_columns) + sentence_df = pd.DataFrame(sentence_records, columns=sentence_columns) + triple_df = pd.DataFrame(triple_records, columns=triple_columns) + + # Save additional CSV files + labeled_records_df.to_csv(f"{self.base_name}_labeled_records.csv", index=False) + sentence_df.to_csv(f"{self.base_name}_sentence_data.csv", index=False) + triple_df.to_csv(f"{self.base_name}_triple_data.csv", index=False) + + logging.info("Filtered CSV file has been generated successfully.") + + def _extract_sentence(self, publications_info_raw: str) -> str: + """ + Extract the first available sentence from the publications_info field. + If parsing fails or no sentence found, returns an empty string. + """ + try: + publications_info = ast.literal_eval(publications_info_raw) + except ValueError as e: + logging.info(f"Error parsing publications_info: {publications_info_raw} with error: {e}") + return '' + + # Extract the first sentence found + return next((info.get('sentence', '') for info in publications_info.values()), '') + + def _get_triple_names(self, edge: Dict[str, Any]) -> tuple: + """ + Get human-readable names for subject, predicate, object from the edge, + using nodes or equivalent_curies_map. + """ + subject_name = self.nodes.get(edge['subject'], self.equivalent_curies_map.get(edge['subject'], edge['subject'])) + object_name = self.nodes.get(edge['object'], self.equivalent_curies_map.get(edge['object'], edge['object'])) + predicate_name = self.nodes.get(edge['predicate'], self.equivalent_curies_map.get(edge['predicate'], edge['predicate'])) + return subject_name, predicate_name, object_name + + +if __name__ == "__main__": + # Приклад використання + extractor = KGDataExtractor( + nodes_file_path='kg2c-2.8.4-nodes.jsonl', + edges_file_path='kg2c-2.8.4-edges.jsonl', + output_csv_path='output_filtered.csv', + base_name='output' + ) + extractor.run() diff --git a/src/fact_check_processor.py b/src/fact_check_processor.py new file mode 100644 index 0000000..3d54b22 --- /dev/null +++ b/src/fact_check_processor.py @@ -0,0 +1,169 @@ +import logging +import psycopg2 +import json +import os +from dotenv import load_dotenv +from llama_cpp import Llama +from huggingface_hub import hf_hub_download +from decouple import config + +# This file defines a class DBFactChecker that connects to a database, retrieves data, processes it using a language model, and updates the database with the results. + + +class DBFactChecker: + """ + A class that handles the logic of connecting to a database, retrieving data, + processing it using a language model, and updating the database with the results. + """ + def __init__(self, batch_size: int = 10, env_file: str = '.env'): + self.batch_size = batch_size + self.env_file = env_file + + # Load environment variables + load_dotenv(self.env_file) + + # Set up model + self.model_name = "TheBloke/Mixtral-8x7B-Instruct-v0.1-GGUF" + self.model_path = hf_hub_download(repo_id=self.model_name, filename="mixtral-8x7b-instruct-v0.1.Q5_K_M.gguf") + self.model = Llama(model_path=self.model_path, + n_threads=64, + n_batch=128, + n_ctx=4096, + n_gpu_layers=96, + mlock=True, + logits_all=True) + + # Connect to DB + + self.conn = psycopg2.connect( + dbname=config("DB_NAME"), + user=config("DB_USER"), + password=config("DB_PASSWORD"), + host=config("DB_HOST"), + port=config("DB_PORT"), + ) + self.cursor = self.conn.cursor() + self.cursor.execute("SET statement_timeout = 5000;") + + self.starting_id = self._read_starting_id() + + def _read_starting_id(self) -> int: + """Read the starting ID from the environment file.""" + return int(os.getenv("STARTING_ID", 0)) + + def _save_updated_id(self, id_value: int) -> None: + """Save the updated starting ID to the .env file.""" + updated_lines = [] + with open(self.env_file, 'r') as file: + lines = file.readlines() + + found = False + for line in lines: + if line.startswith("STARTING_ID="): + updated_lines.append(f"STARTING_ID={id_value}\n") + found = True + else: + updated_lines.append(line) + + if not found: + updated_lines.append(f"STARTING_ID={id_value}\n") + + with open(self.env_file, 'w') as file: + file.writelines(updated_lines) + + def _your_processing_function(self, triple: str, sentence: str): + """ + Process a triple and a sentence with the model and return the answer and logprobs. + This function uses a fixed prompt as defined in the original code. + """ + prompt = f""" + Context: + USER: (''Is the triple "Phase related to Follicle stimulating hormone measurement" directly or indirectly supported by the sentence: "In pre-menopause healthy females, blood was sampled weekly during one menstruation cycle and menstruation phases (follicular, ovulatory, luteal) were determined by FSH/LH levels."?',) + + ASSISTANT: Yes + + USER: (''Is the triple "Phase related to Sodium measurement" directly or indirectly supported by the sentence: "Based on a biophysical photoreceptor model, the Na(+)- and Ca(2+)-currents and concentration changes were determined from the first transient depolarization phase of the photoreceptor response."?',) + + ASSISTANT:Yes + + USER: (''Is the triple "Phase related to Bronchoalveolar Lavage" directly or indirectly supported by the sentence: "Challenge of the airways of sensitized guinea pigs with aerosolized ovalbumin resulted in an early phase of microvascular protein leakage and a delayed phase of eosinophil accumulation in the airway lumen, as measured using bronchoalveolar lavage (BAL)."?',) + + ASSISTANT: Yes + + USER: (''Does the phrase "Ciprofloxacin related to DNA Gyrase" receive at least indirect support from the statement: "Effect of ranolazine in preventing postoperative atrial fibrillation in patients undergoing coronary revascularization surgery."?',) + + ASSISTANT: No + + USER: (''Does the phrase "Ciprofloxacin related to Crohn disease" receive at least indirect support from the statement: "Recent evidence of beneficial effects of ranolazine (RAN) in type II diabetes motivates interest in the role of the late sodium current (INaL) in glucose-stimulated insulin secretion."?',) + + ASSISTANT: No + + USER: (''Does the phrase "Ciprofloxacin related to endophthalmitis" receive at least indirect support from the statement: "Furthermore, the activated Akt/mTOR signaling pathway induced by AF was further activated by ranolazine."?',) + + ASSISTANT: No + + + SYSTEM: You are a computational biologist tasked with evaluating scientific claims. Your role requires you to apply critical thinking and your expertise to interpret data and research findings accurately. Answer 'Yes' or 'No' to directly address the query posed. + + USER: ('\'Does the phrase "{triple}" receive at least indirect support from the statement: "{sentence}"?',). + + ASSISTANT: + + """ + + response = self.model(prompt=prompt, max_tokens=1, temperature=0, echo=False, logprobs=True) + logging.info(response) + return response["choices"][0]["text"], str(response["choices"][0]["logprobs"]) + + def process_data(self): + """Process data in batches, update the database, and track progress.""" + while True: + self.cursor.execute(""" + SELECT "id", "triple", "sentence" + FROM public."tblBiomedicalFactcheck" + WHERE "id" >= %s + ORDER BY "id" + LIMIT %s + """, (self.starting_id, self.batch_size)) + + records = self.cursor.fetchall() + logging.info(records) + if not records: + logging.info("No more records to process.") + break + + for record in records: + logging.info(record) + id, triple, sentence = record + logging.info(1) + answer, logprops = self._your_processing_function(triple, sentence) + logging.info(1) + logprops_json = json.dumps(logprops) + logging.info(id, answer, logprops_json) + + try: + self.cursor.execute(""" + UPDATE public."tblBiomedicalFactcheck" + SET "answer" = %s, "logprops" = %s + WHERE "id" = %s + """, (answer, logprops_json, id)) + except Exception as e: + logging.info(f"Error updating record ID {id}: {e}") + self.conn.rollback() + + self.conn.commit() + + logging.info(self.starting_id) + self.starting_id += self.batch_size + logging.info(self.starting_id) + self._save_updated_id(self.starting_id) + logging.info(f"Processed up to ID: {self.starting_id}") + + self.cursor.close() + self.conn.close() + logging.info("Data has been processed in batches and updated successfully.") + + +if __name__ == "__main__": + fact_checker = DBFactChecker(batch_size=10, env_file='.env') + fact_checker.process_data() diff --git a/src/get_result.py b/src/get_result.py deleted file mode 100644 index 5b852b2..0000000 --- a/src/get_result.py +++ /dev/null @@ -1,76 +0,0 @@ -def get_result(model_info, prompt, model_type): - """ - Get a result from a specified model. - - Args: - model_info (tuple or object): Information about the model, including the model itself and optional context. - prompt (str): The text prompt for the model. - model_type (str): The type of the model being used. - - Returns: - str: The generated result text. - - """ - if model_type.startswith('llama'): - # If using a Llama model - - if isinstance(model_info, tuple): - # If the Llama model has additional context - model, context = model_info - full_prompt = context + prompt - else: - # If using a standalone Llama model - model = model_info - full_prompt = prompt - - prompt_chunks = [full_prompt[i:i + 512] for i in range(0, len(full_prompt), 512)] - result_text = "" - for chunk in prompt_chunks: - # Interact with the Llama model - response = model(prompt=chunk, max_tokens=256, temperature=0.5, - top_p=0.95, repeat_penalty=1.2, top_k=150, echo=True) - result_text += response["choices"][0]["text"] - return result_text - - else: - # If using an OpenAI model - - return get_result_from_openai(model_info, prompt, model_type) - - -def get_result_from_openai(model_info, prompt, model_type): - """ - Get a result from an OpenAI model. - - Args: - model_info (tuple or object): Information about the OpenAI model, including the model itself and optional context. - prompt (str): The text prompt for the model. - model_type (str): The type of the OpenAI model being used. - - Returns: - str: The generated result text. - - """ - if 'icl' in model_type: - # If using an OpenAI model with Integrated Conversation Learning (ICL) - - client, (model, context) = model_info - full_prompt = context + '\n' + prompt - else: - # If using a standard OpenAI model - client, model = model_info - full_prompt = prompt - - try: - # Make a request to the OpenAI model - json_request = { - "model": model, - "messages": [{"role": "user", "content": full_prompt}] - } - - response = client.chat.completions.create(**json_request) - return response.choices[0].message.content - - except Exception as e: - print(f"Error: {e}") - return None diff --git a/src/kg_data_extractor.py b/src/kg_data_extractor.py new file mode 100644 index 0000000..b2fd8e2 --- /dev/null +++ b/src/kg_data_extractor.py @@ -0,0 +1,175 @@ +import json +import csv +import ast +import logging # Import the ast module for safely evaluating strings as Python expressions +import pandas as pd + +# This file defines a class KGDataExtractor that loads, filters, and exports knowledge graph data from JSONL files (nodes and edges) to CSV files. It extracts triples (subject-predicate-object) from edges, matches them with sentences, and stores results in multiple CSV outputs. + +class KGDataExtractor: + """ + A class to load, filter, and export knowledge graph edges and nodes data to CSV files. + It extracts triples from edges, matches them with sentences, and stores results in multiple CSV outputs. + """ + + def __init__(self, edges_file_path: str, nodes_file_path: str, output_csv_path: str, base_name: str = "output"): + """ + Initialize the data extractor with given file paths. + + Args: + edges_file_path (str): The path to the edges .jsonl file. + nodes_file_path (str): The path to the nodes .jsonl file. + output_csv_path (str): The path to the main filtered output CSV file. + base_name (str): Base name for the generated CSV files. Default is "output". + """ + self.edges_file_path = edges_file_path + self.nodes_file_path = nodes_file_path + self.output_csv_path = output_csv_path + self.base_name = base_name + + self.nodes = {} + self.equivalent_curies_map = {} + self.labeled_records = [] + self.sentence_records = [] + self.triple_records = [] + + def run(self): + """Run the data extraction and filtering process.""" + self._load_nodes() + self._process_edges() + self._save_dataframes() + logging.info("Filtered CSV file has been generated successfully.") + + def _load_nodes(self): + """Load nodes from the specified file, building a map of IDs to names and equivalent curies.""" + with open(self.nodes_file_path, 'r', encoding='utf-8') as nodes_file: + for line in nodes_file: + node_data = json.loads(line) + name = node_data.get('name') or ( + node_data.get('all_names')[0] if 'all_names' in node_data and node_data['all_names'] else "Unknown" + ) + self.nodes[node_data['id']] = name + for curie in node_data.get('equivalent_curies', []): + self.equivalent_curies_map[curie] = name + + def _process_edges(self): + """Process edges that meet the criteria, write to the main output CSV, and populate records.""" + with open(self.edges_file_path, 'r', encoding='utf-8') as edges_file, \ + open(self.output_csv_path, 'w', newline='', encoding='utf-8') as output_file: + + csv_writer = csv.writer(output_file) + csv_writer.writerow(['ID', 'Fact', 'Source', 'Template', 'Reference', 'Name']) + + sentence_id = 0 + for line in edges_file: + edge = json.loads(line) + + # Filter based on the knowledge source and retrieve the sentence + if edge.get('primary_knowledge_source') == 'infores:semmeddb': + sentence = self._extract_sentence(edge) + subject_name, predicate_name, object_name = self._get_names(edge) + + # Construct the Fact + fact = f"{subject_name} {predicate_name} {object_name}" + + # Write to the main CSV file + csv_writer.writerow([edge['id'], fact, sentence, '', '', '']) + + # Append to labeled_records + self.labeled_records.append({ + "Predicate ID": edge['id'], + "Triple": fact, + "Sentence ID": sentence_id, + "Sentence": sentence, + "Question": f'Is the triple "{fact}" supported by the sentence: "{sentence}"?', + "Label": None, + "Reference": None + }) + + # Append to sentence_records + self.sentence_records.append({ + "SENTENCE_ID": sentence_id, + "PMID": None, + "TYPE": None, + "NUMBER": None, + "SENT_START_INDEX": None, + "SENTENCE": sentence, + "SECTION_HEADER": None, + "NORMALIZED_SECTION_HEADER": None, + "Column": None, + "Column": None + }) + + # Append to triple_records + self.triple_records.append({ + "PREDICATION_ID": edge['id'], + "SENTENCE_ID": sentence_id, + "PMID": None, + "PREDICATE": predicate_name, + "SUBJECT_CUI": None, + "SUBJECT_NAME": subject_name, + "SUBJECT_SEMTYPE": None, + "SUBJECT_NOVELTY": None, + "OBJECT_CUI": None, + "OBJECT_NAME": object_name, + "OBJECT_SEMTYPE": None, + "OBJECT_NOVELTY": None, + "Column": None, + "Column": None, + "Column": None + }) + sentence_id += 1 + + def _extract_sentence(self, edge) -> str: + """Extract the first available sentence from the edge's publications_info.""" + publications_info_raw = edge.get('publications_info', '{}') + try: + publications_info = ast.literal_eval(publications_info_raw) + except ValueError as e: + logging.info(f"Error parsing publications_info: {publications_info_raw} with error: {e}") + publications_info = {} + + return next((info.get('sentence', '') for info in publications_info.values()), '') + + def _get_names(self, edge): + """Get subject, predicate, and object names using nodes or equivalent curies.""" + subject_name = self.nodes.get(edge['subject'], self.equivalent_curies_map.get(edge['subject'], edge['subject'])) + object_name = self.nodes.get(edge['object'], self.equivalent_curies_map.get(edge['object'], edge['object'])) + predicate_name = self.nodes.get(edge['predicate'], self.equivalent_curies_map.get(edge['predicate'], edge['predicate'])) + return subject_name, predicate_name, object_name + + def _save_dataframes(self): + """Save labeled_records, sentence_records, and triple_records to separate CSV files.""" + sentence_columns = [ + "SENTENCE_ID", "PMID", "TYPE", "NUMBER", "SENT_START_INDEX", "SENTENCE", + "SECTION_HEADER", "NORMALIZED_SECTION_HEADER", "Column", "Column" + ] + + labeled_columns = [ + "Predicate ID", "Triple", "Sentence ID", "Sentence", "Question", "Label", "Reference" + ] + + triple_columns = [ + "PREDICATION_ID", "SENTENCE_ID", "PMID", "PREDICATE", + "SUBJECT_CUI", "SUBJECT_NAME", "SUBJECT_SEMTYPE", "SUBJECT_NOVELTY", + "OBJECT_CUI", "OBJECT_NAME", "OBJECT_SEMTYPE", "OBJECT_NOVELTY", + "Column", "Column", "Column" + ] + + labeled_records_df = pd.DataFrame(self.labeled_records, columns=labeled_columns) + sentence_df = pd.DataFrame(self.sentence_records, columns=sentence_columns) + triple_df = pd.DataFrame(self.triple_records, columns=triple_columns) + + labeled_records_df.to_csv(f"{self.base_name}_labeled_records.csv", index=False) + sentence_df.to_csv(f"{self.base_name}_sentence_data.csv", index=False) + triple_df.to_csv(f"{self.base_name}_triple_data.csv", index=False) + + +if __name__ == "__main__": + extractor = KGDataExtractor( + edges_file_path='kg2c-2.8.4-edges.jsonl', + nodes_file_path='kg2c-2.8.4-nodes.jsonl', + output_csv_path='output_filtered.csv', + base_name='output' + ) + extractor.run() diff --git a/src/kg_data_processor.py b/src/kg_data_processor.py new file mode 100644 index 0000000..b10deb6 --- /dev/null +++ b/src/kg_data_processor.py @@ -0,0 +1,172 @@ +import json +import csv +import ast # Import the ast module for safely evaluating strings as Python expressions +import pandas as pd +import logging +# This file also defines a class KGDataExtractor with similar functionality but includes additional features: + +# Loading Nodes with Equivalent Curies: In addition to loading nodes, it builds a map of equivalent curies to node names. +# Processing Edges with Sentence Extraction: Similar to the previous file, but it includes a method to extract sentences from the edge's publications_info and uses equivalent curies to get node names if the primary ID is not found. +# Saving DataFrames: Similar to the previous file, it saves the records to separate CSV files. + + +class KGDataExtractor: + """ + A class for extracting and filtering knowledge graph data from JSONL files and exporting results to CSV. + """ + + def __init__(self, edges_file_path: str, nodes_file_path: str, output_csv_path: str, base_name: str = "output"): + """ + Initialize the data extractor. + + Args: + edges_file_path (str): Path to the edges JSONL file. + nodes_file_path (str): Path to the nodes JSONL file. + output_csv_path (str): Path to the main filtered output CSV file. + base_name (str): Base name for the auxiliary CSV files. + """ + self.edges_file_path = edges_file_path + self.nodes_file_path = nodes_file_path + self.output_csv_path = output_csv_path + self.base_name = base_name + + self.nodes = {} + self.labeled_records = [] + self.sentence_records = [] + self.triple_records = [] + + def run(self): + """Execute the data loading, filtering, and saving process.""" + self._load_nodes() + self._process_edges() + self._save_dataframes() + logging.info("Filtered CSV file has been generated successfully.") + + def _load_nodes(self): + """Load all nodes into a dictionary for quick access by ID.""" + with open(self.nodes_file_path, 'r', encoding='utf-8') as nodes_file: + for line in nodes_file: + node_data = json.loads(line) + # Get the name or the first alternative name if the primary name is absent + name = node_data.get('name') or ( + node_data.get('all_names')[0] if 'all_names' in node_data and node_data['all_names'] else "Unknown" + ) + self.nodes[node_data['id']] = name + + def _process_edges(self): + """Process edges that meet the criteria and write the main CSV file.""" + with open(self.edges_file_path, 'r', encoding='utf-8') as edges_file, \ + open(self.output_csv_path, 'w', newline='', encoding='utf-8') as output_file: + + csv_writer = csv.writer(output_file) + csv_writer.writerow(['ID', 'Fact', 'Source', 'Template', 'Reference', 'Name']) + + sentence_id = 0 + for line in edges_file: + edge = json.loads(line) + + # Filter based on the knowledge source and retrieve the sentence + if edge.get('primary_knowledge_source') == 'infores:semmeddb': + publications_info_raw = edge.get('publications_info', '{}') + try: + # Use ast.literal_eval to safely evaluate the string as a Python dictionary + publications_info = ast.literal_eval(publications_info_raw) + except ValueError as e: + logging.info(f"Error parsing publications_info: {publications_info_raw} with error: {e}") + publications_info = {} + + # Extracting the first available sentence from publications_info + sentence = next((info.get('sentence', '') for info in publications_info.values()), '') + + # Use names instead of IDs where possible + subject_name = self.nodes.get(edge['subject'], edge['subject']) + predicate_name = self.nodes.get(edge['predicate'], edge['predicate']) + object_name = self.nodes.get(edge['object'], edge['object']) + + # Construct the Fact + fact = f"{subject_name} {predicate_name} {object_name}" + + # Write to main CSV + csv_writer.writerow([edge['id'], fact, sentence, '', '', '']) + + self._append_records(edge, sentence_id, sentence, subject_name, predicate_name, object_name) + sentence_id += 1 + + def _append_records(self, edge, sentence_id, sentence, subject_name, predicate_name, object_name): + """Append records to labeled, sentence and triple lists.""" + self.labeled_records.append({ + "Predicate ID": edge['id'], + "Triple": f"{subject_name} {predicate_name} {object_name}", + "Sentence ID": sentence_id, + "Sentence": sentence, + "Question": f'Is the triple "{subject_name} {predicate_name} {object_name}" supported by the sentence: "{sentence}"?', + "Label": None, + "Reference": None + }) + + self.sentence_records.append({ + "SENTENCE_ID": sentence_id, + "PMID": None, + "TYPE": None, + "NUMBER": None, + "SENT_START_INDEX": None, + "SENTENCE": sentence, + "SECTION_HEADER": None, + "NORMALIZED_SECTION_HEADER": None, + "Column": None, + "Column": None + }) + + self.triple_records.append({ + "PREDICATION_ID": edge['id'], + "SENTENCE_ID": sentence_id, + "PMID": None, + "PREDICATE": predicate_name, + "SUBJECT_CUI": None, + "SUBJECT_NAME": subject_name, + "SUBJECT_SEMTYPE": None, + "SUBJECT_NOVELTY": None, + "OBJECT_CUI": None, + "OBJECT_NAME": object_name, + "OBJECT_SEMTYPE": None, + "OBJECT_NOVELTY": None, + "Column": None, + "Column": None, + "Column": None + }) + + def _save_dataframes(self): + """Save the DataFrames to CSV files.""" + sentence_columns = [ + "SENTENCE_ID", "PMID", "TYPE", "NUMBER", "SENT_START_INDEX", "SENTENCE", + "SECTION_HEADER", "NORMALIZED_SECTION_HEADER", "Column", "Column" + ] + + labeled_columns = [ + "Predicate ID", "Triple", "Sentence ID", "Sentence", "Question", "Label", "Reference" + ] + + triple_columns = [ + "PREDICATION_ID", "SENTENCE_ID", "PMID", "PREDICATE", + "SUBJECT_CUI", "SUBJECT_NAME", "SUBJECT_SEMTYPE", "SUBJECT_NOVELTY", + "OBJECT_CUI", "OBJECT_NAME", "OBJECT_SEMTYPE", "OBJECT_NOVELTY", + "Column", "Column", "Column" + ] + + labeled_records_df = pd.DataFrame(self.labeled_records, columns=labeled_columns) + sentence_df = pd.DataFrame(self.sentence_records, columns=sentence_columns) + triple_df = pd.DataFrame(self.triple_records, columns=triple_columns) + + labeled_records_df.to_csv(f"{self.base_name}_labeled_records.csv", index=False) + sentence_df.to_csv(f"{self.base_name}_sentence_data.csv", index=False) + triple_df.to_csv(f"{self.base_name}_triple_data.csv", index=False) + + +if __name__ == "__main__": + extractor = KGDataExtractor( + edges_file_path='kg2c-2.8.4-edges.jsonl', + nodes_file_path='kg2c-2.8.4-nodes.jsonl', + output_csv_path='output_filtered.csv', + base_name='output' + ) + extractor.run() diff --git a/src/langfuse_config.py b/src/langfuse_config.py new file mode 100644 index 0000000..e2cef86 --- /dev/null +++ b/src/langfuse_config.py @@ -0,0 +1,13 @@ +from decouple import config +from langfuse import Langfuse + +#Description: +#The code snippet initializes the Langfuse client. + +langfuse = Langfuse( + public_key=config("LANGFUSE_PUBLIC_KEY"), + secret_key=config("LANGFUSE_SECRET_KEY"), + host=config("LANGFUSE_HOST"), +) + +__all__ = ["langfuse"] diff --git a/src/langfuse_main.py b/src/langfuse_main.py new file mode 100644 index 0000000..77d669f --- /dev/null +++ b/src/langfuse_main.py @@ -0,0 +1,778 @@ +import json +import logging +import random +import re +from datetime import datetime + +from decouple import config +from dotenv import load_dotenv +from openai import OpenAI + +from langfuse_config import langfuse +from retrieval_rag import ChunkExpander +from logger_config import Logger + +#Description: +#The code snippet defines a class DatasetManager that handles dataset operations. + +class DatasetManager: + """Handles dataset operations.""" + + def __init__(self): + from langfuse_config import langfuse + self.langfuse = langfuse + + def load_local_dataset(self, file_path): + try: + with open(file_path, "r") as file: + data = json.load(file) + random.shuffle(data) + logging.info(f"Dataset loaded and shuffled from {file_path}.") + return data + except Exception as e: + logging.error(f"Error loading dataset from {file_path}: {e}") + raise e + + def get_dataset(self, dataset_name): + try: + return self.langfuse.get_dataset(dataset_name) + except Exception as e: + logging.error(f"Error retrieving dataset {dataset_name}: {e}") + return None + + def create_dataset(self, dataset_name): + try: + self.langfuse.create_dataset(name=dataset_name) + logging.info(f"Dataset {dataset_name} created successfully.") + except Exception as e: + logging.error(f"Error creating dataset {dataset_name}: {e}") + raise e + + def upload_items_to_langfuse(self, dataset_name, items): + for item in items: + try: + self.langfuse.create_dataset_item( + dataset_name=dataset_name, + input={ + "triple": item["input"]["triple"], + "sentence": item["input"]["sentence"], + }, + expected_output=item["validation_result"], + ) + langfuse.trace( + name="Dataset item uploaded", + input=item["input"], + expected_output=item["validation_result"], + ) + except Exception as e: + logging.error(f"Failed to upload item: {item} - {e}") + logging.info(f"All items uploaded to dataset {dataset_name}.") + + +class RAGProcessor: + """Handles processing of triples using Retrieval-Augmented Generation (RAG).""" + + def __init__(self, openai_client, model): + self.client = openai_client + self.model = model + + def extract_answer(self, llm_response): + """ + Extract the 'Answer' from LLM response. + Args: + llm_response (str): Full response from LLM. + Returns: + str: The extracted answer, or 'No Answer Found' if not present. + """ + if not isinstance(llm_response, str): + logging.error("Invalid input to extract_answer: not a string.") + return "No Answer Found" + + match = re.search(r"Answer:\s*(Yes|No)", llm_response, re.IGNORECASE) + return match.group(1) if match else "No Answer Found" + + def process_triple(self, triple, sentence): + question = f'Does the phrase "{triple}" receive at least indirect support from the statement: "{sentence}"?' + relevant_chunks = ChunkExpander.expand_chunks_with_tree(question) + + if not relevant_chunks: + logging.warning(f"No relevant documents found for triple: {triple}") + return "No Answer Found", "", "" + + prompt = self.create_prompt(triple, sentence, relevant_chunks) + try: + response = self.client.chat.completions.create( + model=self.model, messages=[{"role": "user", "content": prompt}] + ) + response_content = response.choices[0].message.content + final_answer = self.extract_answer(response_content) + except Exception as e: + logging.error(f"Error during OpenAI API call: {e}") + return "No Answer Found", prompt, "" + + return final_answer, prompt, response_content + + @staticmethod + def create_prompt(triple, sentence, relevant_chunks): + prompt = f""" + You are a computational biologist specializing in the evaluation of scientific claims. Your role is to apply critical thinking and domain-specific expertise to assess the validity of scientific statements based on provided evidence and data. + + Follow the instructions below to provide your answer. + ** instructions ** + Follow a structured, step-by-step approach: + 1. Analyze the provided triple and the associated statement step-by-step. + 2. Explain your reasoning process, detailing how (or if) the statement supports the triple. + 3. Determine if the triple receives at least indirect support from the statement. + - Answer "Yes" if the statement provides clear and sufficient support (direct or indirect). + - Answer "No" if the support is ambiguous, unclear, or absent. + 4. Provide your final conclusion in the exact format: + Answer: Yes + or + Answer: No + + Failure to provide this explicit answer will result in the response being marked as incomplete. + + --- + ** USER: ** + ``` + 'Does the phrase "{triple}" receive at least indirect support from the statement: "{sentence}"?' + ``` + ** ASSISTANT response: ** + ``` + + Answer: Yes or No + ``` + --- + + + Use the context below to evaluate the statement. The information is structured in hierarchical levels of relevance, from Level 1 (most relevant) to Level 3 (subordinate relationships). Your analysis should prioritize higher-level data when making decisions. + Based on your analysis and the context below, provide a conclusion: + ========= Relevant triples with subordinate clauses | BEGIN ========= + {relevant_chunks} + ========= Relevant triples with subordinate clauses | END ========= + + + --- + **Examples:** + --- + + + **USER:** + ``` + 'Is the triple "Phase related to Follicle stimulating hormone measurement" directly or indirectly supported by the sentence: "In pre-menopause healthy females, blood was sampled weekly during one menstruation cycle and menstruation phases (follicular, ovulatory, luteal) were determined by FSH/LH levels."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + + 1. The triple states: "Phase related to Follicle stimulating hormone measurement." + - This implies that a particular phase (in some physiological or biological context) is determined or associated with the measurement of Follicle Stimulating Hormone (FSH). + + 2. The sentence given is: "In pre-menopause healthy females, blood was sampled weekly during one menstruation cycle and menstruation phases (follicular, ovulatory, luteal) were determined by FSH/LH levels." + + 3. Breakdown of the sentence: + - The context is about menstrual cycles in pre-menopausal healthy females. + - Blood samples were taken weekly during a full menstruation cycle. + - The specific menstruation phases—follicular, ovulatory, and luteal—were identified (determined) by measuring the levels of hormones, specifically FSH and LH. + + 4. The phrase "were determined by FSH/LH levels" clearly indicates that the definition or identification of the menstrual phases relied, at least in part, on the measurement of Follicle Stimulating Hormone. In other words, the hormone levels are used as an indicator or criterion to decide which phase the menstrual cycle is currently in. + + 5. Therefore, the statement shows that the "Phase" (referring to the menstruation phase) is indeed related to the measurement of FSH, among other hormones (LH). The triple is effectively supported: the link between "Phase" and "Follicle stimulating hormone measurement" is explicitly mentioned. + + **Conclusion:** + The sentence provides direct support that menstrual cycle phases are related to FSH measurements. + + **Final Answer:** + Answer: Yes + + ``` + --- + **USER:** + ``` + 'Is the triple "Phase related to Sodium measurement" directly or indirectly supported by the sentence: "Based on a biophysical photoreceptor model, the Na(+)- and Ca(2+)-currents and concentration changes were determined from the first transient depolarization phase of the photoreceptor response."?' + ``` + + **ASSISTANT:** + ``` + + **Step-by-step reasoning:** + +1. Examine the triple: "Phase related to Sodium measurement." + - This triple suggests that there is a particular phase in a process that is relevant to or connected with measuring sodium (Na+) levels or currents. + +2. Examine the sentence: + "Based on a biophysical photoreceptor model, the Na(+)- and Ca(2+)-currents and concentration changes were determined from the first transient depolarization phase of the photoreceptor response." + +3. Breakdown of the sentence: + - The sentence describes a scenario where measurements of Na(+) and Ca(2+) currents (as well as their concentration changes) are being taken. + - These measurements are derived specifically from the "first transient depolarization phase" of the photoreceptor response. + +4. Linking the triple and the sentence: + - The triple indicates a relationship between some "phase" and the measurement of sodium (Na+). + - The sentence states that Na(+) currents and concentration changes were determined from a specific phase ("the first transient depolarization phase") in a photoreceptor model. + +5. Does the sentence support the triple? + - Yes. The sentence clearly shows that there is a phase during which Na(+) measurements (currents and concentration changes) are taken or determined. + - This directly connects the concept of a "phase" to the measurement of sodium, thus supporting the triple. + +**Conclusion:** +The sentence provides at least indirect (and arguably direct) support that sodium measurement is related to a specific phase. + +**Final Answer:** +Answer: Yes + ``` + --- + **USER:** + ``` + 'Is the triple "Phase related to Bronchoalveolar Lavage" directly or indirectly supported by the sentence: "Challenge of the airways of sensitized guinea pigs with aerosolized ovalbumin resulted in an early phase of microvascular protein leakage and a delayed phase of eosinophil accumulation in the airway lumen, as measured using bronchoalveolar lavage (BAL)."?' + ``` + + **ASSISTANT:** + ``` +**Step-by-step reasoning:** + +1. Triple under consideration: "Phase related to Bronchoalveolar Lavage" + - This means we are looking for whether a "phase" is associated or determined using bronchoalveolar lavage (BAL). + +2. Given sentence: + "Challenge of the airways of sensitized guinea pigs with aerosolized ovalbumin resulted in an early phase of microvascular protein leakage and a delayed phase of eosinophil accumulation in the airway lumen, as measured using bronchoalveolar lavage (BAL)." + +3. Breakdown of the sentence: + - The experiment involves sensitized guinea pigs challenged with aerosolized ovalbumin. + - Two phases are observed in the response: + - An early phase characterized by microvascular protein leakage. + - A delayed phase characterized by eosinophil accumulation. + - Crucially, these phases were measured using bronchoalveolar lavage (BAL). + +4. Link to the triple: + - The triple states that there is a "phase" related to BAL. + - The sentence explicitly says that the different phases (early and delayed) are measured by bronchoalveolar lavage. + - Thus, it shows a direct relationship between the phases of the response and the use of bronchoalveolar lavage as a measurement technique. + +5. Conclusion: + - The sentence confirms that BAL is used to identify or quantify the phases observed in the guinea pigs' airway response. + - Therefore, it supports the triple that indicates a relationship between a phase and bronchoalveolar lavage. + +**Final Answer:** +Answer: Yes + + ``` + --- + **USER:** + ``` + 'Does the phrase "Ciprofloxacin related to DNA Gyrase" receive at least indirect support from the statement: "Effect of ranolazine in preventing postoperative atrial fibrillation in patients undergoing coronary revascularization surgery."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple in question: "Ciprofloxacin related to DNA Gyrase" + + - This triple suggests a relationship between the antibiotic ciprofloxacin and DNA gyrase (which is a bacterial enzyme targeted by ciprofloxacin). + +2. The provided statement: + "Effect of ranolazine in preventing postoperative atrial fibrillation in patients undergoing coronary revascularization surgery." + +3. Breakdown of the statement: + - The statement focuses on the effect of the drug ranolazine in preventing a specific cardiac complication (postoperative atrial fibrillation) in patients who have undergone coronary revascularization surgery. + - It does not mention ciprofloxacin or any antibiotic. + - It does not mention DNA gyrase, which is typically associated with bacterial function and not directly related to the cardiac context described. + - No indirect references that might connect ranolazine or the procedure to ciprofloxacin or DNA gyrase are apparent. + +4. Does the statement support the triple? + - The triple is about ciprofloxacin and DNA gyrase, a known antibiotic-enzyme relationship. + - The statement is about ranolazine and atrial fibrillation in a cardiac surgery context, with no known link to ciprofloxacin, antibiotics, or DNA gyrase. + - Therefore, there is no support (direct or indirect) for the "Ciprofloxacin related to DNA Gyrase" triple from this statement. + +**Final Answer:** +Answer: No + ``` + --- + **USER:** + ``` + 'Does the phrase "Ciprofloxacin related to Crohn disease" receive at least indirect support from the statement: "Recent evidence of beneficial effects of ranolazine (RAN) in type II diabetes motivates interest in the role of the late sodium current (INaL) in glucose-stimulated insulin secretion."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple under evaluation: "Ciprofloxacin related to Crohn disease" + - This suggests a relationship between the antibiotic ciprofloxacin and the condition Crohn disease. + +2. The provided statement: + "Recent evidence of beneficial effects of ranolazine (RAN) in type II diabetes motivates interest in the role of the late sodium current (INaL) in glucose-stimulated insulin secretion." + +3. Breakdown of the given statement: + - The statement focuses on ranolazine and its beneficial effects in type II diabetes. + - It mentions interest in the late sodium current (INaL) and its role in insulin secretion. + - There is no mention of ciprofloxacin, no mention of any antibiotic, and no mention of Crohn disease or any inflammatory bowel condition. + +4. Does this statement support the triple? + - The triple requires some link between ciprofloxacin and Crohn disease. + - The statement is entirely about a cardiovascular/metabolic drug (ranolazine) in the context of type II diabetes, not about antibiotics, not about gastrointestinal diseases like Crohn. + - There is no direct or indirect support for linking ciprofloxacin to Crohn disease here. + +**Final Answer:** +Answer: No + ``` + --- + **USER:** + ``` + 'Does the phrase "Ciprofloxacin related to endophthalmitis" receive at least indirect support from the statement: "Furthermore, the activated Akt/mTOR signaling pathway induced by AF was further activated by ranolazine."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple under consideration: "Ciprofloxacin related to endophthalmitis." + - This implies a connection between the antibiotic ciprofloxacin and the eye infection endophthalmitis. + +2. The provided statement: + "Furthermore, the activated Akt/mTOR signaling pathway induced by AF was further activated by ranolazine." + +3. Breakdown of the statement: + - The sentence describes a molecular pathway (Akt/mTOR) being activated by AF, and this effect being further enhanced by the drug ranolazine. + - There is no mention of ciprofloxacin or any antibiotic. + - There is no mention of endophthalmitis, which is an ocular infection. + +4. Linking the triple and the statement: + - The triple is about ciprofloxacin and a specific eye condition (endophthalmitis). + - The statement deals with molecular signaling pathways and a different drug (ranolazine). There is no apparent link to antibiotics or eye infections. + +5. Conclusion: + - Since neither ciprofloxacin nor endophthalmitis is mentioned or even indirectly implied, the statement does not provide support for the triple. + +**Final Answer:** +Answer: No + ``` + --- + **USER:** + ``` + 'Is the triple "Gene X related to Protein Y expression" directly or indirectly supported by the sentence: "Overexpression of Gene X leads to an increase in Protein Y levels in neuronal cells."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple is: "Gene X related to Protein Y expression." + - This means we’re looking for a connection between Gene X and the expression (or levels) of Protein Y. + +2. The provided sentence is: "Overexpression of Gene X leads to an increase in Protein Y levels in neuronal cells." + - The sentence explicitly states that when Gene X is overexpressed, there is a corresponding increase in Protein Y levels. + - This implies a direct relationship between the presence or activity of Gene X and the expression of Protein Y. + +3. Since "overexpression" of Gene X results in increased Protein Y, the statement directly supports the notion that Gene X is related to (or influences) Protein Y expression. + +**Final Answer:** +Answer: Yes + ``` + --- + **USER:** + ``` + 'Does the phrase "Vitamin D related to Bone Density" receive at least indirect support from the statement: "Participants who received Vitamin D supplements showed improved calcium absorption rates."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple is: "Vitamin D related to Bone Density." + +2. The statement given is: "Participants who received Vitamin D supplements showed improved calcium absorption rates." + +3. Evaluating the connection: + - The statement directly links Vitamin D supplementation to improved calcium absorption. + - While the sentence does not explicitly mention bone density, it is well-established in medical and biological contexts that calcium absorption is a critical factor for maintaining and improving bone density. + - Increased calcium absorption, facilitated by Vitamin D, indirectly supports the idea that Vitamin D is related to bone density because better calcium uptake usually contributes to stronger, denser bones. + +4. Therefore, although the statement does not say "bone density" outright, it provides a key piece of evidence (improved calcium absorption) that is closely associated with bone density improvement. This can be seen as at least indirect support. + +**Final Answer:** +Answer: Yes + ``` + --- + **USER:** + ``` + 'Is the triple "Enzyme A related to Metabolic Pathway B" directly or indirectly supported by the sentence: "Inhibition of Enzyme A disrupts the metabolic pathway B, leading to reduced synthesis of essential metabolites."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple states: "Enzyme A related to Metabolic Pathway B." + - This means we are looking to see if there is a relationship between Enzyme A and Metabolic Pathway B. + +2. The sentence given is: "Inhibition of Enzyme A disrupts the metabolic pathway B, leading to reduced synthesis of essential metabolites." + - This sentence explicitly states that if Enzyme A is inhibited, Metabolic Pathway B is disrupted. + - Disruption of Metabolic Pathway B upon inhibition of Enzyme A suggests a direct link or dependency of the pathway on the enzyme. + +3. Since the sentence clearly connects Enzyme A activity to the proper function of Metabolic Pathway B, it provides direct support for the triple. + +**Final Answer:** +Answer: Yes + ``` + --- + **USER:** + ``` + 'Does the phrase "Antibiotic Z related to Heart Disease" receive at least indirect support from the statement: "Long-term use of Antibiotic Z has been associated with alterations in gut microbiota composition."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple is: "Antibiotic Z related to Heart Disease." + - This implies we are looking for some evidence that Antibiotic Z has a connection to heart disease. + +2. The provided statement: + "Long-term use of Antibiotic Z has been associated with alterations in gut microbiota composition." + +3. Evaluating the connection: + - The statement links long-term use of Antibiotic Z to changes in the gut microbiome. + - It does not mention heart disease or any cardiovascular condition. + - While the gut microbiota can have systemic effects, the statement does not indicate any direct or indirect link to heart disease. + - Without additional context or established scientific knowledge stated in the given sentence, it's not possible to infer a connection between Antibiotic Z and heart disease solely from altered gut microbiota composition. + +4. Conclusion: + - The provided sentence does not support, even indirectly, that Antibiotic Z is related to heart disease. + +**Final Answer:** +Answer: No + ``` + --- + **USER:** + ``` + 'Is the triple "Protein Z related to Cellular Apoptosis" directly or indirectly supported by the sentence: "Activation of Protein Z triggers the apoptotic pathways leading to programmed cell death."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple: "Protein Z related to Cellular Apoptosis" + - This states that Protein Z is related to or associated with the process of cellular apoptosis. + +2. The provided sentence: + "Activation of Protein Z triggers the apoptotic pathways leading to programmed cell death." + +3. Analysis: + - The sentence explicitly states that when Protein Z is activated, it initiates apoptotic pathways. + - "Apoptotic pathways" are the mechanisms by which cells undergo apoptosis (programmed cell death). + - Thus, the sentence clearly connects Protein Z activation to the induction of cellular apoptosis. + +4. Conclusion: + - The sentence directly supports the relationship between Protein Z and cellular apoptosis. + +**Final Answer:** +Answer: Yes + ``` + --- + **USER:** + ``` + 'Does the phrase "Hormone A related to Metabolic Syndrome" receive at least indirect support from the statement: "Studies have shown that Hormone A levels are elevated in individuals with insulin resistance."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple is: "Hormone A related to Metabolic Syndrome." + - This suggests that Hormone A should have some connection or association with metabolic syndrome. + +2. The provided statement: + "Studies have shown that Hormone A levels are elevated in individuals with insulin resistance." + +3. Consider the relationship between insulin resistance and metabolic syndrome: + - Insulin resistance is widely recognized as a key component and risk factor of metabolic syndrome. Metabolic syndrome is typically characterized by a cluster of conditions, including insulin resistance, high blood pressure, abnormal cholesterol levels, and excess body fat around the waist. + - Therefore, if Hormone A levels are elevated in individuals with insulin resistance, it indirectly links Hormone A to a core element of metabolic syndrome. + +4. Although the statement does not explicitly mention metabolic syndrome, the presence of elevated Hormone A in people with insulin resistance strongly hints at an involvement of Hormone A in metabolic syndrome. Thus, we can say the statement provides at least indirect support for the triple. + +**Final Answer:** +Answer: Yes + ``` + --- + **USER:** + ``` + 'Is the triple "Gene Y related to Immune Response" directly or indirectly supported by the sentence: "Knockout of Gene Y resulted in a diminished immune response to viral infections in mice."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple: "Gene Y related to Immune Response" implies there should be a connection between Gene Y and the immune response. + +2. The given sentence: "Knockout of Gene Y resulted in a diminished immune response to viral infections in mice." + +3. Analysis: + - The sentence clearly states that removing Gene Y (knockout) led to a reduced immune response. + - This indicates that Gene Y plays a role in normal immune functioning. + - By losing Gene Y, the mice show a diminished (weakened) immune response, directly linking Gene Y to immune response mechanisms. + +4. Conclusion: + - The statement directly supports the triple by showing Gene Y’s involvement in maintaining a proper immune response. + +**Final Answer:** +Answer: Yes + ``` + --- + **USER:** + ``` + 'Does the phrase "Medication B related to Kidney Function" receive at least indirect support from the statement: "Long-term use of Medication B has been linked to changes in renal biomarkers."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple: "Medication B related to Kidney Function." + - This indicates a potential relationship between Medication B and how the kidneys work or function. + +2. The given statement: + "Long-term use of Medication B has been linked to changes in renal biomarkers." + +3. Analysis: + - "Renal" refers to the kidneys. + - Biomarkers are measurable substances in the body whose changes can indicate alterations in organ function or health status. + - Changes in renal biomarkers generally reflect changes in kidney function or health. + - Thus, if Medication B is linked to changes in renal biomarkers, it implies that Medication B affects kidney-related parameters. + +4. Conclusion: + - Since renal biomarkers are directly associated with kidney function, the statement indirectly supports that Medication B is related to kidney function. + +**Final Answer:** +Answer: Yes + ``` + --- + **USER:** + ``` + 'Is the triple "Receptor C related to Neurotransmitter D release" directly or indirectly supported by the sentence: "Binding of ligand E to Receptor C modulates the release of Neurotransmitter D in synaptic clefts."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple is: "Receptor C related to Neurotransmitter D release." + - This suggests a connection between Receptor C and the release of Neurotransmitter D. + +2. The sentence: "Binding of ligand E to Receptor C modulates the release of Neurotransmitter D in synaptic clefts." + - This statement explicitly states that when ligand E binds to Receptor C, it influences how much Neurotransmitter D is released. + - This indicates that Receptor C is indeed involved in regulating or affecting the release of Neurotransmitter D. + +3. Since the sentence clearly shows a relationship between Receptor C and the release of Neurotransmitter D, it provides direct support for the triple. + +**Final Answer:** +Answer: Yes + ``` + --- + **USER:** + ``` + 'Does the phrase "Supplement F related to Muscle Growth" receive at least indirect support from the statement: "Participants taking Supplement F showed increased protein synthesis rates post-exercise."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple: "Supplement F related to Muscle Growth." + - This suggests a connection between taking Supplement F and muscle growth. + +2. The statement: "Participants taking Supplement F showed increased protein synthesis rates post-exercise." + - Protein synthesis is a key physiological process that underlies muscle repair and hypertrophy (growth) after exercise. + - While the statement does not explicitly mention "muscle growth," increased protein synthesis rates in a post-exercise context are commonly linked to muscle recovery and growth over time. + +3. Since protein synthesis is a critical step in the process of building muscle, an increase in protein synthesis rates can be considered an indirect indicator that Supplement F supports or is related to muscle growth. + +**Final Answer:** +Answer: Yes + ``` + --- + **USER:** + ``` + 'Is the triple "Factor G related to Cell Cycle Regulation" directly or indirectly supported by the sentence: "Overexpression of Factor G disrupts normal cell cycle progression, leading to uncontrolled cell proliferation."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple: "Factor G related to Cell Cycle Regulation." + - This means we need to see if Factor G influences or is involved in controlling the cell cycle. + +2. The provided sentence: + "Overexpression of Factor G disrupts normal cell cycle progression, leading to uncontrolled cell proliferation." + +3. Analysis: + - The sentence explicitly states that when Factor G is overexpressed, it disrupts normal cell cycle progression. + - Disrupting normal cell cycle progression is a direct indication that Factor G affects how the cell cycle is regulated. + - Since cell cycle progression is a key part of cell cycle regulation, this sentence clearly links Factor G to the regulation of the cell cycle. + +**Conclusion:** +The sentence provides direct support for the triple, confirming that Factor G is related to cell cycle regulation. + +**Final Answer:** +Answer: Yes + ``` + --- + **USER:** + ``` + 'Does the phrase "Compound H related to Liver Toxicity" receive at least indirect support from the statement: "Exposure to Compound H has been associated with elevated liver enzymes in clinical studies."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple: "Compound H related to Liver Toxicity." + - This implies Compound H is associated with harmful effects on the liver. + +2. The statement: + "Exposure to Compound H has been associated with elevated liver enzymes in clinical studies." + +3. Analysis: + - Elevated liver enzymes (such as ALT, AST) are commonly used as indicators of liver injury or stress. + - Although the statement does not explicitly say "toxicity," elevated liver enzymes strongly suggest liver damage or impairment. + - Therefore, the statement provides at least indirect evidence that Compound H is related to liver toxicity, as these elevated enzymes typically reflect liver dysfunction. + +**Conclusion:** +Since elevated liver enzymes are a known biomarker for liver damage, the sentence indirectly supports the connection between Compound H and liver toxicity. + +**Final Answer:** +Answer: Yes + ``` + --- + **USER:** + ``` + 'Is the triple "Molecule I related to Inflammatory Response" directly or indirectly supported by the sentence: "Molecule I acts as a key mediator in the inflammatory response during infection."?' + ``` + + **ASSISTANT:** + ``` + **Step-by-step reasoning:** + +1. The triple is: "Molecule I related to Inflammatory Response." + - This suggests that Molecule I should have some connection with the inflammatory response. + +2. The given sentence: + "Molecule I acts as a key mediator in the inflammatory response during infection." + +3. Analysis: + - The sentence explicitly states that Molecule I is a "key mediator" in the inflammatory response. + - Being a "key mediator" directly places Molecule I in a central role in the inflammatory response process. + +4. Conclusion: + - The sentence provides direct support for the triple, as it clearly states Molecule I is involved in the inflammatory response. + +**Final Answer:** +Answer: Yes + ``` + --- + + USER: ('\'Does the phrase "{triple}" receive at least indirect support from the statement: "{sentence}"?',). + + ASSISTANT: + + ''' + """ + + return prompt + + +class ExperimentRunner: + """Runs experiments using RAG.""" + + def __init__(self, dataset_name, rag_processor): + self.dataset_name = dataset_name + self.rag_processor = rag_processor + + def run(self, experiment_name): + try: + dataset = langfuse.get_dataset(self.dataset_name) + if not dataset: + logging.error(f"Dataset {self.dataset_name} could not be retrieved.") + return + + for idx, item in enumerate(dataset.items, 1): + try: + completion, prompt, response_content = ( + self.rag_processor.process_triple( + item.input["triple"], item.input["sentence"] + ) + ) + + generation = langfuse.generation( + name=experiment_name, + input=prompt, + output=response_content, + model=self.rag_processor.model, + start_time=datetime.now(), + end_time=datetime.now(), + ) + item.link(generation, experiment_name) + + generation.score( + name="exact_match", value=item.expected_output in completion + ) + except KeyError as e: + logging.exception(f"Missing key in item {idx}: {e}") + except Exception as e: + logging.exception(f"Error processing item {idx}: {e}") + + logging.info(f"Experiment '{experiment_name}' completed.") + except Exception as e: + logging.error(f"Error running experiment '{experiment_name}': {e}") + + +if __name__ == "__main__": + Logger.setup_logging() + + try: + load_dotenv() + openai_api_key = config("OPENAI_API_KEY") + client = OpenAI(api_key=openai_api_key) + + rag_processor = RAGProcessor( + openai_client=client, + model="gpt-4o-mini", + ) + + dataset_manager = DatasetManager() + local_items = dataset_manager.load_local_dataset( + "./json/local_items_single_3.json" + ) + + dataset_name = "RAG_biomedical_factchecks_human_yes_without_semmed__6" + dataset = dataset_manager.get_dataset(dataset_name) + + if not dataset: + logging.info( + f"Dataset {dataset_name} not found. Creating and uploading dataset..." + ) + with open("./json/local_items_single_3.json", "r") as file: + local_items = json.load(file) + dataset_manager.create_dataset(dataset_name) + dataset_manager.upload_items_to_langfuse(dataset_name, local_items) + else: + logging.info(f"Dataset {dataset_name} exists. Starting experiment...") + + + experiment_runner = ExperimentRunner( + dataset_name=dataset_name, + rag_processor=rag_processor, + ) + experiment_name = ( + f"exp_{datetime.now().strftime('%m_%d_%Y__%H_%M_%S')}__human_labeled" + ) + experiment_runner.run(experiment_name) + except Exception as e: + logging.error(f"Unexpected error: {e}") + + diff --git a/src/load_documents_chromadb.py b/src/load_documents_chromadb.py new file mode 100644 index 0000000..2382aca --- /dev/null +++ b/src/load_documents_chromadb.py @@ -0,0 +1,197 @@ +import ast +import json +import logging + +import openai +from decouple import config +from dotenv import load_dotenv + +from load_model import ChromaDBInitializer +from logger_config import Logger + +#Description: +#The code snippet defines a class FileReader that handles reading and processing of files. + +class FileReader: + """Handles reading and processing of files.""" + + @staticmethod + def count_lines(file_path): + with open(file_path, "r") as f: + return sum(1 for _ in f) + + @staticmethod + def read_lines(file_path): + with open(file_path, "r") as f: + for line in f: + yield line + + +class NodeProcessor: + """Processes node data from the nodes file.""" + + def __init__(self, nodes_file_path, sampling_rate): + self.nodes_file_path = nodes_file_path + self.sampling_rate = sampling_rate + self.nodes = {} + self.equivalent_curies_map = {} + + def load_nodes(self): + total_nodes = FileReader.count_lines(self.nodes_file_path) + max_nodes = int(total_nodes * self.sampling_rate) + logging.info( + f"Processing first {max_nodes} nodes ({self.sampling_rate * 100:.2f}% of total)." + ) + + try: + for line_number, line in enumerate( + FileReader.read_lines(self.nodes_file_path), 1 + ): + node_data = json.loads(line) + name = node_data.get("name") or ( + node_data.get("all_names")[0] + if "all_names" in node_data and node_data["all_names"] + else "Unknown" + ) + self.nodes[node_data["id"]] = name + for curie in node_data.get("equivalent_curies", []): + self.equivalent_curies_map[curie] = name + + if line_number % 500000 == 0: + logging.info(f"Processed {line_number} nodes.") + + logging.info(f"Loaded {len(self.nodes)} nodes into memory.") + except Exception as e: + logging.error(f"Error loading nodes: {e}") + exit(1) + + +class EdgeProcessor: + """Processes edge data and prepares documents for indexing.""" + + def __init__(self, edges_file_path, nodes, equivalent_curies_map, sampling_rate): + self.edges_file_path = edges_file_path + self.nodes = nodes + self.equivalent_curies_map = equivalent_curies_map + self.sampling_rate = sampling_rate + self.documents = [] + + def process_edges(self): + total_edges = FileReader.count_lines(self.edges_file_path) + max_edges = int(total_edges * self.sampling_rate) + logging.info( + f"Processing first {max_edges} edges ({self.sampling_rate * 100:.2f}% of total)." + ) + + try: + for line_number, line in enumerate( + FileReader.read_lines(self.edges_file_path), 1 + ): + edge = json.loads(line) + + if edge.get("primary_knowledge_source") != "infores:semmeddb": + publications_info_raw = edge.get("publications_info", "{}") + try: + publications_info = ast.literal_eval(publications_info_raw) + except ValueError as e: + logging.error( + f"Error parsing publications_info: {publications_info_raw} with error: {e}" + ) + publications_info = {} + + sentence = next( + ( + info.get("sentence", "") + for info in publications_info.values() + ), + "", + ) + subject_name = self.nodes.get( + edge["subject"], + self.equivalent_curies_map.get( + edge["subject"], edge["subject"] + ), + ) + object_name = self.nodes.get( + edge["object"], + self.equivalent_curies_map.get(edge["object"], edge["object"]), + ) + predicate_name = self.nodes.get( + edge["predicate"], + self.equivalent_curies_map.get( + edge["predicate"], edge["predicate"] + ), + ) + fact = f"{subject_name} {predicate_name} {object_name}" + doc_text = f"Sentence: {sentence}\nTriple: {fact}" + + self.documents.append({"id": edge["id"], "text": doc_text}) + + if len(self.documents) > 200000: + break + + if line_number % 500000 == 0: + logging.info(f"Processed {line_number} edges.") + + logging.info(f"Prepared {len(self.documents)} documents for indexing.") + except Exception as e: + logging.error(f"Error processing edges: {e}") + exit(1) + + +class ChromaDBIndexer: + """Indexes documents into ChromaDB.""" + + def __init__(self, collection): + self.collection = collection + + def index_documents(self, documents, batch_size=256): + logging.info("Indexing documents into ChromaDB.") + for idx in range(0, len(documents), batch_size): + batch = documents[idx : idx + batch_size] + ids = [doc["id"] for doc in batch] + texts = [doc["text"] for doc in batch] + self.collection.add(ids=ids, documents=texts) + if (idx + batch_size) % 1000 == 0 or (idx + batch_size) >= len(documents): + logging.info( + f"Indexed {min(idx + batch_size, len(documents))} documents." + ) + logging.info("Indexing completed.") + + +class DataPipeline: + """Manages the entire data processing and indexing pipeline.""" + + def __init__(self, nodes_file_path, edges_file_path, sampling_rate=0.002): + self.nodes_file_path = nodes_file_path + self.edges_file_path = edges_file_path + self.sampling_rate = sampling_rate + self.collection = ChromaDBInitializer.initialize_chromadb() + + def execute(self): + node_processor = NodeProcessor(self.nodes_file_path, self.sampling_rate) + node_processor.load_nodes() + + edge_processor = EdgeProcessor( + self.edges_file_path, + node_processor.nodes, + node_processor.equivalent_curies_map, + self.sampling_rate, + ) + edge_processor.process_edges() + + indexer = ChromaDBIndexer(self.collection) + indexer.index_documents(edge_processor.documents) + + +if __name__ == "__main__": + Logger.setup_logging() + load_dotenv() + openai.api_key = config("OPENAI_API_KEY") + + pipeline = DataPipeline( + nodes_file_path="./data/kg2c-2.8.4-nodes.jsonl", + edges_file_path="./data/kg2c-2.8.4-edges.jsonl", + ) + pipeline.execute() + diff --git a/src/load_model.py b/src/load_model.py index 604adcf..0d4c523 100644 --- a/src/load_model.py +++ b/src/load_model.py @@ -1,79 +1,25 @@ -import os -from openai import OpenAI -from config import OPENAI_API_KEY -from llama_cpp import Llama -from huggingface_hub import hf_hub_download -from sklearn.model_selection import train_test_split -import pandas as pd +from decouple import config -# Define the file path to the CSV data -file_path = os.path.join('data', 'true_false_chembl_labeled.csv') +#Description: +#The code snippet initializes the ChromaDB collection. +class ChromaDBInitializer: + """Initializes the ChromaDB collection.""" -def load_model(model_type, use_icl): - """ - Load a language model for inference. + @staticmethod + def initialize_chromadb(): + from chromadb import PersistentClient + from chromadb.utils import embedding_functions - Args: - model_type (str): The type of the model to load ('llama', 'gpt_3_5_turbo', or 'gpt_4_0'). - use_icl (bool): Whether to use Integrated Conversation Learning (ICL) for OpenAI models. + OPENAI_API_KEY = config("OPENAI_API_KEY") + openai_ef = embedding_functions.OpenAIEmbeddingFunction( + api_key=OPENAI_API_KEY, + model_name="text-embedding-ada-002", + ) - Returns: - tuple or object: A tuple containing the client and model for OpenAI models, or just the model for Llama models. + chroma_client = PersistentClient(path="chroma_persistent_storage") + collection = chroma_client.get_or_create_collection( + name="kg2c_collection", embedding_function=openai_ef + ) - Raises: - ValueError: If an unknown model type is provided. - - """ - if model_type == 'llama': - # Load a Llama model - model_name = "TheBloke/Llama-2-7B-GGUF" - model_path = hf_hub_download(repo_id=model_name, filename="llama-2-7b.Q4_K_M.gguf") - model = Llama(model_path=model_path, n_threads=1000, n_batch=5120, n_gpu_layers=640, n=128, mlock=True) - if use_icl: - return prepare_icl(model, model_type) - return model - else: - # Load an OpenAI model - client = OpenAI(api_key=OPENAI_API_KEY) - if model_type == 'gpt_3_5_turbo': - model = 'gpt-3.5-turbo' - elif model_type == 'gpt_4_0': - model = 'gpt-4' - else: - raise ValueError(f"Unknown model type: {model_type}") - if use_icl: - return client, prepare_icl(model, model_type) - return client, model - - -def prepare_icl(model, model_type): - """ - Prepare context for models using Integrated Conversation Learning (ICL). - - Args: - model (object): The language model (OpenAI model). - model_type (str): The type of the model being used. - - Returns: - tuple: A tuple containing the model and context for OpenAI models. - - """ - df = pd.read_csv(file_path) - - if not os.path.exists(os.path.join('data', f'test_df_{model_type}_icl.csv')) or \ - not os.path.exists(os.path.join('data', f'train_df_{model_type}_icl.csv')): - - train_df, test_df = train_test_split(df, test_size=0.8, random_state=42) - - test_df.to_csv(os.path.join('data', f'test_df_{model_type}_icl.csv'), index=False) - train_df.to_csv(os.path.join('data', f'train_df_{model_type}_icl.csv'), index=False) - else: - train_df = pd.read_csv(os.path.join('data', f'train_df_{model_type}_icl.csv')) - - context_entries = train_df.sample(n=10) - - context = context_entries.apply( - lambda row: f"{row['Question']} Answer: {'Yes' if row['Label'] else 'No'}\n", - axis=1).str.cat() - return model, context \ No newline at end of file + return collection diff --git a/src/logger_config.py b/src/logger_config.py new file mode 100644 index 0000000..a663ad2 --- /dev/null +++ b/src/logger_config.py @@ -0,0 +1,13 @@ + +import logging + +#Description: This class sets up the logging configuration for the application. + +class Logger: + + @staticmethod + def setup_logging(): + logging.basicConfig( + level=logging.INFO, format="%(asctime)s %(levelname)s:%(message)s" + ) + \ No newline at end of file diff --git a/src/process_result.py b/src/process_result.py deleted file mode 100644 index d696f80..0000000 --- a/src/process_result.py +++ /dev/null @@ -1,34 +0,0 @@ -import re -from typing import Tuple - - -def process_result(result: str) -> Tuple[str, str]: - """ - Process a result string to extract the answer and determine its correctness. - - The function searches for patterns in the result string to classify the answer - as 'Yes', 'No', or 'Undefined'. If the result contains 'Yes' or 'No', it is - considered the answer with the corresponding correctness. If it ends with a - question mark followed by text, the text is extracted as the answer with - 'Undefined' correctness. Otherwise, the entire result is taken as the answer - with 'Undefined' correctness. - - Parameters: - result (str): The result string to be processed. - - Returns: - Tuple[str, str]: A tuple containing the correctness of the answer ('Yes', 'No', - or 'Undefined') and the extracted answer. - """ - match = re.search(r"\b(Yes|No)\b", result) - if match: - answer = result[match.start():] - is_correct = match.group(0) == 'Yes' - else: - match = re.search(r"\?([^?]+)$", result) - if match: - answer = match.group(1).strip() - else: - answer = result.strip() - is_correct = "Undefined" - return is_correct, answer diff --git a/src/processdb.py b/src/processdb.py new file mode 100644 index 0000000..6b6c75b --- /dev/null +++ b/src/processdb.py @@ -0,0 +1,121 @@ +import json +import ast +import psycopg2 +from psycopg2.extras import execute_batch +from decouple import config +from logger_config import Logger +import logging + +class DatabaseConnection: + """Manages the database connection and cursor.""" + + def __init__(self): + self.conn = psycopg2.connect( + dbname=config("DB_NAME"), + user=config("DB_USER"), + password=config("DB_PASSWORD"), + host=config("DB_HOST"), + port=config("DB_PORT"), + ) + self.cursor = self.conn.cursor() + + def execute_batch_insert(self, data_batch, query): + """Executes batch insert into the database.""" + execute_batch(self.cursor, query, data_batch) + self.conn.commit() + + def close(self): + """Closes the database connection.""" + self.cursor.close() + self.conn.close() + +class NodeLoader: + """Loads nodes and equivalent CURIEs from the nodes file.""" + + def __init__(self, nodes_file_path): + self.nodes_file_path = nodes_file_path + self.nodes = {} + self.equivalent_curies_map = {} + + def load_nodes(self): + """Loads all nodes into memory.""" + with open(self.nodes_file_path, "r") as nodes_file: + for line in nodes_file: + node_data = json.loads(line) + name = node_data.get("name") or ( + node_data.get("all_names")[0] + if "all_names" in node_data and node_data["all_names"] + else "Unknown" + ) + self.nodes[node_data["id"]] = name + for curie in node_data.get("equivalent_curies", []): + self.equivalent_curies_map[curie] = name + +class EdgeProcessor: + """Processes edges and prepares data for database insertion.""" + + def __init__(self, edges_file_path, nodes, equivalent_curies_map, batch_size=10000): + self.edges_file_path = edges_file_path + self.nodes = nodes + self.equivalent_curies_map = equivalent_curies_map + self.batch_size = batch_size + self.insert_data = [] + + def process_edges(self): + """Processes edges and prepares them for database insertion.""" + with open(self.edges_file_path, "r") as edges_file: + for line in edges_file: + edge = json.loads(line) + + if edge.get("primary_knowledge_source") == "infores:semmeddb": + publications_info_raw = edge.get("publications_info", "{}") + publications_info = self._parse_publications_info(publications_info_raw) + + sentence = next( + (info.get("sentence", "") for info in publications_info.values()), "" + ) + subject_name = self._get_node_name(edge["subject"]) + object_name = self._get_node_name(edge["object"]) + predicate_name = self._get_node_name(edge["predicate"]) + fact = f"{subject_name} {predicate_name} {object_name}" + + self.insert_data.append((edge["id"], fact, sentence)) + + if len(self.insert_data) >= self.batch_size: + yield self.insert_data + self.insert_data.clear() + + # Yield any remaining data + if self.insert_data: + yield self.insert_data + +def main(): + # Initialize components + Logger.setup_logging() + db = DatabaseConnection() + node_loader = NodeLoader("kg2c-2.8.4-nodes.jsonl") + node_loader.load_nodes() + + edge_processor = EdgeProcessor( + edges_file_path="kg2c-2.8.4-edges.jsonl", + nodes=node_loader.nodes, + equivalent_curies_map=node_loader.equivalent_curies_map, + ) + + # Database insertion query + query = """ + INSERT INTO public."tblkg2c-2-8-4Dataset" ("nodeDataID", "triple", "sentence") + VALUES (%s, %s, %s) + """ + + # Process edges and insert data into the database + try: + for data_batch in edge_processor.process_edges(): + db.execute_batch_insert(data_batch, query) + logging.info("Data has been inserted into the database successfully.") + finally: + db.close() + + +if __name__ == "__main__": + main() diff --git a/src/processing.py b/src/processing.py deleted file mode 100644 index 8807fbe..0000000 --- a/src/processing.py +++ /dev/null @@ -1,77 +0,0 @@ -import pandas as pd - -from src.data_processing import initialize_writers -from src.get_result import get_result -from src.process_result import process_result -from src.progress import read_progress, write_progress -from src.result_writing import write_result_to_csv -from src.triple_processing import process_triple_row - - -def create_prompt(triple_text, sentence, context=""): - """ - Constructs a prompt for the model to process. - - Args: - triple_text (str): The triple text. - sentence (str): The sentence text. - context (str, optional): Additional context to include in the prompt. Defaults to "". - - Returns: - str: The constructed prompt. - """ - return f"{context}'Is the triple \"{triple_text}\" supported by the sentence: \"{sentence}\"?" - - -def process_data(model_info, model_type, use_icl, triple_data: pd.DataFrame, sentence_data: pd.DataFrame, - result_file: str, progress_file_path: str): - print("Initializing data processing...") - - sentence_dict = {} - model_key = model_type + ('_icl' if use_icl else '') - progress = set(read_progress(model_key)) - - last_processed = max(progress, key=lambda x: (x[0], x[1])) if progress else None - print(f"Last processed: {last_processed}") - - # Check filtering logic - if last_processed: - triple_data = triple_data[triple_data['SENTENCE_ID'].astype(int) >= int(last_processed[0])] - - (console_results_writer, progress_writer, console_results_file, - progress_file) = initialize_writers(result_file, progress_file_path) - - if not last_processed: - console_results_writer.writerow( - ["Predicate ID", "Triple", "Sentence ID", "Sentence", "Is Correct", "Question", "Answer"]) - - for index, row in triple_data.iterrows(): - sentence_id, predicate_id, triple = process_triple_row(row) - if sentence_id not in sentence_dict: - sentence_dict[sentence_id] = [] - sentence_dict[sentence_id].append((sentence_id, predicate_id, triple)) - - for sentence_id, triples in sentence_dict.items(): - sentence = sentence_data[sentence_data['SENTENCE_ID'].astype(int) == int(sentence_id)]['SENTENCE'].values[0] - for triple in triples: - process_triple(model_info, sentence_id, sentence, triple, - progress, console_results_writer, model_key, use_icl, progress_writer) - - console_results_file.close() - progress_file.close() - print("Data processing completed.") - - -def process_triple(model_info, sentence_id, sentence, triple, - progress, console_results_writer, model_key, use_icl, _): - - triple_sentence_id, predicate_id, triple_text = triple - if (triple_sentence_id, predicate_id) not in progress: - prompt = create_prompt(triple_text, sentence, model_info[1] if use_icl else "") - result = get_result(model_info, prompt, model_key) - - question = f"Is the triple '{triple_text}' supported by the sentence: '{sentence}'?" - is_correct, answer = process_result(result) - write_result_to_csv(console_results_writer, predicate_id, triple_text, sentence_id, - sentence, is_correct, question, answer.strip() if answer else None) - write_progress(model_key, sentence_id, predicate_id) diff --git a/src/progress.py b/src/progress.py deleted file mode 100644 index 53ac9fb..0000000 --- a/src/progress.py +++ /dev/null @@ -1,60 +0,0 @@ -import csv -import os -from typing import Any, List, Tuple, Union -from src.progress_path import PROGRESS_FILES - - -def read_progress(model_name: str) -> Union[List[Tuple[int, ...]], List[Any]]: - """ - Read the progress of a specified model from its corresponding CSV file. - - Parameters: - model_name (str): The name of the model for which progress needs to be read. - Valid values are keys of the PROGRESS_FILES dictionary. - - Returns: - Union[List[Tuple[int, ...]], List[Any]]: A list of tuples, where each tuple - represents a row in the CSV file. - Returns an empty list if file is not found. - - Raises: - ValueError: If the model_name is not a valid key in PROGRESS_FILES. - """ - progress_file = PROGRESS_FILES.get(model_name) - if not progress_file: - raise ValueError("Invalid model name") - - try: - with open(progress_file, "r") as file: - reader = csv.reader(file) - next(reader, None) # Skip the header - return [tuple(map(int, row)) for row in reader] - except FileNotFoundError: - return [] - - -def write_progress(model_key, sentence_id, predicate_id): - - """ - Write a progress record to the CSV file of a specified model. - - Parameters: - model_name (str): The name of the model for which progress needs to be written. - Valid values are keys of the PROGRESS_FILES dictionary. - sentence_id (int): The ID of the sentence for which progress is being tracked. - predicate_id (int): The ID of the predicate for which progress is being tracked. - - Raises: - ValueError: If the model_name is not a valid key in PROGRESS_FILES. - """ - progress_file = PROGRESS_FILES.get(model_key) - if not progress_file: - raise ValueError(f"Invalid model name: {model_key}") - - file_exists = os.path.isfile(progress_file) - is_empty = os.stat(progress_file).st_size == 0 if file_exists else False - with open(progress_file, "a", newline="") as file: - writer = csv.writer(file) - if is_empty or not file_exists: - writer.writerow(["Sentence ID", "Predicate ID"]) - writer.writerow([sentence_id, predicate_id]) diff --git a/src/progress_path.py b/src/progress_path.py deleted file mode 100644 index d4bd158..0000000 --- a/src/progress_path.py +++ /dev/null @@ -1,36 +0,0 @@ -import os - -# Dictionary mapping task names to their progress file paths -PROGRESS_FILES = { - 'llama': os.path.join('result', 'progress', 'llama_progress.csv'), - 'llama_icl': os.path.join('result', 'progress', 'llama_icl_progress.csv'), - 'gpt_3_5_turbo': os.path.join('result', 'progress', 'gpt_3_5_turbo_progress.csv'), - 'gpt_3_5_turbo_icl': os.path.join('result', 'progress', 'gpt_3_5_turbo_icl_progress.csv'), - 'gpt_4_0': os.path.join('result', 'progress', 'gpt_4_0_progress.csv'), - 'gpt_4_0_icl': os.path.join('result', 'progress', 'gpt_4_0_icl_progress.csv') -} - - -# This module defines a mapping of various processing tasks to their corresponding -# progress file paths. These file paths are used to store the progress of each task. -# -# The 'os.path.join' method is used to construct the file paths, ensuring correct -# path formatting across different operating systems. -# -# Structure: -# - Key: A string representing the name of the processing task. -# - Value: The file path where the progress of the corresponding task is stored. -# -# Tasks and their file paths: -# - 'llama': Path to the progress file for the 'llama' task. -# - 'llama_icl': Path to the progress file for the 'llama_icl' task. -# - 'gpt_3_5_turbo': Path to the progress file for the 'gpt_3_5_turbo' task. -# - 'gpt_3_5_turbo_icl': Path to the progress file for the 'gpt_3_5_turbo_icl' task. -# - 'gpt_4_0': Path to the progress file for the 'gpt_4_0' task. -# - 'gpt_4_0_icl': Path to the progress file for the 'gpt_4_0_icl' task. -# -# Example: -# To access the file path for the 'llama' task's progress: -# >>> filepath = PROGRESS_FILES['llama'] -# >>> print(filepath) -# 'result/progress/llama_progress.csv' diff --git a/src/result_writing.py b/src/result_writing.py deleted file mode 100644 index 68c769a..0000000 --- a/src/result_writing.py +++ /dev/null @@ -1,50 +0,0 @@ -import csv - - -def write_result_to_csv(console_results_writer, predicate_id, triple_text, - sentence_id, sentence, is_correct, question, answer): - """ - Write the results of processing to a CSV file using a CSV writer. - - This function takes various pieces of information related to the processing - of semantic triples, and writes them to a CSV file. It includes details - such as predicate ID, the text of the triple, sentence ID, the original - sentence, correctness of the triple, and any associated question and answer. - - Parameters: - console_results_writer (csv.writer): A CSV writer object used for writing to a file. - predicate_id (int): The ID of the predicate. - triple_text (str): The text of the semantic triple. - sentence_id (int): The ID of the sentence from which the triple is derived. - sentence (str): The original sentence. - is_correct (bool): Flag indicating whether the triple is correct. - question (str, optional): A related question, if any. - answer (str, optional): The answer to the related question, if any. - - Returns: - None - """ - console_results_writer.writerow([ - predicate_id, triple_text, sentence_id, sentence, is_correct, - question if question else '', - answer.strip() if answer else '' - ]) - - -def write_progress(writer: csv.writer, sentence_id: int, predicate_id: int) -> None: - """ - Write the progress of processing to a CSV file. - - This function records the current progress of processing by logging the - sentence ID and predicate ID to a CSV file. It's useful for tracking - which sentences and predicates have been processed. - - Parameters: - writer (csv.writer): A CSV writer object used for writing to a file. - sentence_id (int): The ID of the sentence being processed. - predicate_id (int): The ID of the predicate being processed. - - Returns: - None - """ - writer.writerow([sentence_id, predicate_id]) diff --git a/src/retrieval_rag.py b/src/retrieval_rag.py new file mode 100644 index 0000000..81ea0e0 --- /dev/null +++ b/src/retrieval_rag.py @@ -0,0 +1,140 @@ +import logging + +import networkx as nx + +from load_model import ChromaDBInitializer + +#Description +#The code snippet defines a class ChromaDBQuery that handles querying documents from ChromaDB. + +class ChromaDBQuery: + """Handles querying documents from ChromaDB.""" + + @staticmethod + def query_documents(question, n_results=10): + """ + Query the initial relevant documents from ChromaDB. + + Args: + question (str): User's query. + n_results (int): Number of results to retrieve. + + Returns: + list: List of top relevant documents (text). + """ + collection = ChromaDBInitializer.initialize_chromadb() + if collection is None: + raise ValueError("ChromaDB collection is not initialized properly.") + + results = collection.query(query_texts=[question], n_results=n_results) + + if "documents" not in results or not results["documents"][0]: + logging.warning("No documents found.") + return [] + + return results["documents"][0] + + +class RelevanceGraph: + """Manages the relevance graph and its operations.""" + + def __init__(self, initial_question, max_depth=2, n_results=10): + self.initial_question = initial_question + self.max_depth = max_depth + self.n_results = n_results + self.graph = nx.DiGraph() + self.graph.add_node(initial_question, depth=0, text=initial_question) + + def deep_search_relevant_chunks(self): + """ + Perform a deep search for relevant chunks and store results in a graph. + + Returns: + nx.DiGraph: Graph representing relevant chunks and their connections. + """ + initial_chunks = ChromaDBQuery.query_documents( + self.initial_question, n_results=self.n_results + ) + + def expand_chunks(current_question, parent_node, current_depth): + if current_depth > self.max_depth: + return + + child_chunks = ChromaDBQuery.query_documents( + current_question, n_results=self.n_results + ) + + for i, chunk in enumerate(child_chunks): + chunk_node = f"{parent_node}_child_{i}" + self.graph.add_node(chunk_node, depth=current_depth, text=chunk) + self.graph.add_edge(parent_node, chunk_node) + expand_chunks(chunk, chunk_node, current_depth + 1) + + for i, chunk in enumerate(initial_chunks): + chunk_node = f"root_child_{i}" + self.graph.add_node(chunk_node, depth=1, text=chunk) + self.graph.add_edge(self.initial_question, chunk_node) + expand_chunks(chunk, chunk_node, current_depth=2) + + return self.graph + + +class TreeFormatter: + """Formats the relevance graph as a tree structure.""" + + @staticmethod + def format_relevance_tree(relevance_graph): + """ + Format the relevance graph as a tree structure for the prompt. + + Args: + relevance_graph (nx.DiGraph): Graph representing relevant chunks and their connections. + + Returns: + str: Formatted string in a tree structure. + """ + tree_formatted = [] + + for node in relevance_graph.nodes: + depth = relevance_graph.nodes[node]["depth"] + text = relevance_graph.nodes[node]["text"] + + if depth == 0: # Root query + tree_formatted.append(f"Level 1: {text}\n") + child_nodes = list(relevance_graph.successors(node)) + for i, child_node in enumerate(child_nodes, 1): + child_text = relevance_graph.nodes[child_node]["text"].replace( + "\n", "\t\n" + ) + tree_formatted.append(f"\t└─ Level 2 ({i}):\n\t{child_text}\n") + + grandchild_nodes = list(relevance_graph.successors(child_node)) + for j, grandchild_node in enumerate(grandchild_nodes, 1): + grandchild_text = relevance_graph.nodes[grandchild_node][ + "text" + ].replace("\n", "\t\t\n") + tree_formatted.append( + f"\t\t└─ Level 3 ({j}):\n\t\t{grandchild_text}\n" + ) + + return "".join(tree_formatted) + + +class ChunkExpander: + """Expands relevant chunks and formats the output as a tree.""" + + @staticmethod + def expand_chunks_with_tree(question): + """ + Expand relevant chunks into a tree structure. + + Args: + question (str): The initial question to retrieve relevant chunks. + + Returns: + str: A formatted tree string for the prompt. + """ + graph_manager = RelevanceGraph(question) + relevance_graph = graph_manager.deep_search_relevant_chunks() + return TreeFormatter.format_relevance_tree(relevance_graph) + diff --git a/src/triple_processing.py b/src/triple_processing.py deleted file mode 100644 index a57d23f..0000000 --- a/src/triple_processing.py +++ /dev/null @@ -1,41 +0,0 @@ -import pandas as pd -from typing import Tuple - - -def process_triple_row(row: pd.Series) -> Tuple[int, int, str]: - """ - Process a row of a DataFrame to extract and format a semantic triple. - - This function takes a pandas Series object representing a row of data, - extracts the relevant information, and formats it into a semantic triple. - The function handles special cases in the data formatting, such as - replacing 'isa' with 'is a', removing specific characters, and converting - text to lowercase. - - Parameters: - A single row of a DataFrame, expected to contain the columns - 'SENTENCE_ID', 'PREDICATION_ID', 'PREDICATE', 'SUBJECT_NAME', - and 'OBJECT_NAME'. - - Returns: - Tuple[int, int, str]: A tuple containing the sentence ID, predicate ID, and - the formatted semantic triple as a string. - - Example: - "SENTENCE_ID": 1, - "PREDICATION_ID": 101, - "PREDICATE": '"_isa_"', - "SUBJECT_NAME": '"_Cat_"', - "OBJECT_NAME": '"_Animal_"' - - (1, 101, 'Farm animals is an Animals') - """ - sentence_id = row["SENTENCE_ID"] - predicate_id = row["PREDICATION_ID"] - predicate_raw = row["PREDICATE"].strip('""_').replace('_', ' ').lower() - predicate = "is a" if predicate_raw == "isa" else predicate_raw - subject_name = row["SUBJECT_NAME"].strip('""_') - object_name = row["OBJECT_NAME"].strip('""_') - - triple = f"{subject_name} {predicate} {object_name}" - return sentence_id, predicate_id, triple diff --git a/test/__init__.py b/test/__init__.py deleted file mode 100644 index e69de29..0000000 diff --git a/test/test_data_processing.py b/test/test_data_processing.py deleted file mode 100644 index 024e466..0000000 --- a/test/test_data_processing.py +++ /dev/null @@ -1,58 +0,0 @@ -import os -import pandas as pd -import pytest -from src import data_processing - -os.makedirs(os.path.join('test', 'test_result'), exist_ok=True) - -# Define a constant for the progress file name -PROGRESS_FILE = 'llama_progress.csv' - - -@pytest.fixture -def sample_data(): - return pd.Series({ - "SENTENCE_ID": 1, - "PREDICATION_ID": 1, - "PREDICATE": '"isa"', - "SUBJECT_NAME": '"subject"', - "OBJECT_NAME": '"object"' - }) - - -@pytest.mark.parametrize("file1,file2", [ - ("semmed_triple_data.csv", "semmed_sentence_data.csv") -]) -def test_read_data_from_files(file1, file2): - triple_data, sentence_data = data_processing.read_data_from_files(file1, file2) - assert isinstance(triple_data, pd.DataFrame) - assert isinstance(sentence_data, pd.DataFrame) - - -def test_initialize_writers(): - result_file_path = os.path.join('test', 'test_result', 'llama_semmed_result.csv') - progress_file_path = os.path.join('test', 'test_result', PROGRESS_FILE) - - (console_results_writer, progress_writer, console_results_file, - progress_file) = data_processing.initialize_writers(result_file_path, progress_file_path) - assert console_results_writer is not None - assert progress_writer is not None - assert console_results_file is not None - assert progress_file is not None - - -def test_save_state(): - state = {'sentence_id': 1, 'predicate_id': 1} - progress_file_path = os.path.join('test', 'test_result', PROGRESS_FILE) - data_processing.save_state(progress_file_path, state) - - with open(progress_file_path, 'r') as f: - last_line = f.readlines()[-1] - assert last_line == '1,1\n' - - -def test_load_state(): - expected_state = {'sentence_id': 1, 'predicate_id': 1} - progress_file_path = os.path.join('test', 'test_result', PROGRESS_FILE) - state = data_processing.load_state(progress_file_path) - assert state == expected_state diff --git a/test/test_process_result.py b/test/test_process_result.py deleted file mode 100644 index 843866a..0000000 --- a/test/test_process_result.py +++ /dev/null @@ -1,46 +0,0 @@ -import pytest -from src.process_result import process_result - - -@pytest.fixture -def result_yes(): - return "Yes, the statement is correct." - - -@pytest.fixture -def result_no(): - return "No, the statement is incorrect." - - -@pytest.fixture -def result_question(): - return "Is the statement correct? It is unclear." - - -@pytest.fixture -def result_ambiguous(): - return "The statement is ambiguous." - - -def test_process_result_yes(result_yes): - is_correct, answer = process_result(result_yes) - assert is_correct is True - assert answer == 'Yes, the statement is correct.' - - -def test_process_result_no(result_no): - is_correct, answer = process_result(result_no) - assert is_correct is False - assert answer == 'No, the statement is incorrect.' - - -def test_process_result_question(result_question): - is_correct, answer = process_result(result_question) - assert is_correct == 'Undefined' - assert answer == 'It is unclear.' - - -def test_process_result_ambiguous(result_ambiguous): - is_correct, answer = process_result(result_ambiguous) - assert is_correct == 'Undefined' - assert answer == 'The statement is ambiguous.' diff --git a/test/test_progress.py b/test/test_progress.py deleted file mode 100644 index ddebb55..0000000 --- a/test/test_progress.py +++ /dev/null @@ -1,45 +0,0 @@ -from unittest.mock import patch, mock_open, call -from src.progress import read_progress, write_progress - - -@patch('src.progress.PROGRESS_FILES', {'test_model': 'test_model.csv'}) -@patch('builtins.open', new_callable=mock_open, read_data="Sentence ID,Predicate ID\n1,2\n3,4\n") -def test_read_progress(_): - result = read_progress('test_model') - assert result == [(1, 2), (3, 4)] - - -@patch('src.progress.PROGRESS_FILES', {'test_model': 'test_model.csv'}) -@patch('builtins.open', new_callable=mock_open) -@patch('os.path.isfile', return_value=True) -@patch('os.stat') -def test_write_progress(mock_stat, _, mock_file): - mock_stat.return_value.st_size = 10 - write_progress('test_model', 5, 6) - calls = [call('5,6\r\n')] - mock_file.return_value.write.assert_has_calls(calls) - - -@patch('src.progress.PROGRESS_FILES', {'test_model': 'test_model.csv'}) -@patch('builtins.open', new_callable=mock_open) -@patch('os.path.isfile', return_value=False) -@patch('os.stat') -def test_write_progress_new_file(mock_stat, _, mock_file): - mock_stat.return_value.st_size = 0 - write_progress('test_model', 5, 6) - calls = [call('Sentence ID,Predicate ID\r\n'), call('5,6\r\n')] - mock_file.return_value.write.assert_has_calls(calls) - - -def test_read_progress_invalid_model(): - try: - read_progress('invalid_model') - except ValueError: - pass - - -def test_write_progress_invalid_model(): - try: - write_progress('invalid_model', 5, 6) - except ValueError: - pass diff --git a/test/test_result_writing.py b/test/test_result_writing.py deleted file mode 100644 index daae156..0000000 --- a/test/test_result_writing.py +++ /dev/null @@ -1,39 +0,0 @@ -import pytest -from unittest.mock import MagicMock -from src.result_writing import write_result_to_csv, write_progress - - -@pytest.fixture -def mock_writer(mocker): - return MagicMock() - - -def test_write_result_to_csv(mock_writer): - write_result_to_csv( - mock_writer, - predicate_id="predicate_id_test", - triple_text="triple_text_test", - sentence_id="sentence_id_test", - sentence="sentence_test", - is_correct="is_correct_test", - question="question_test", - answer="answer_test" - ) - mock_writer.writerow.assert_called_once_with([ - "predicate_id_test", - "triple_text_test", - "sentence_id_test", - "sentence_test", - "is_correct_test", - "question_test", - "answer_test" - ]) - - -def test_write_progress(mock_writer): - write_progress( - mock_writer, - sentence_id=1, - predicate_id=2 - ) - mock_writer.writerow.assert_called_once_with([1, 2]) diff --git a/test/test_triple_processing.py b/test/test_triple_processing.py deleted file mode 100644 index a0b3e98..0000000 --- a/test/test_triple_processing.py +++ /dev/null @@ -1,22 +0,0 @@ -import pandas as pd -import pytest -from src.triple_processing import process_triple_row - - -@pytest.fixture -def sample_row(): - data = { - "SENTENCE_ID": [1], - "PREDICATION_ID": [101], - "PREDICATE": ['"_isa_"'], - "SUBJECT_NAME": ['"_Cat_"'], - "OBJECT_NAME": ['"_Animal_"'] - } - return pd.DataFrame(data).iloc[0] - - -def test_process_triple_row(sample_row): - sentence_id, predicate_id, triple = process_triple_row(sample_row) - assert sentence_id == 1 - assert predicate_id == 101 - assert triple == 'Cat is a Animal' diff --git a/util/chembl/chembl_triple.py b/util/chembl/chembl_triple.py deleted file mode 100644 index 2c089a9..0000000 --- a/util/chembl/chembl_triple.py +++ /dev/null @@ -1,55 +0,0 @@ -import requests -import pandas as pd -import re - -api_endpoint = "https://arax.ncats.io/api/arax/v1.4/meta_knowledge_graph" - - -def get_query_results(): - response = requests.get(api_endpoint) - - if response.status_code == 200: - data = response.json() - - edges = data.get('edges', []) - - triple = [] - for edge in edges: - triple.append({ - 'subject': edge.get('subject'), - 'predicate': edge.get('predicate'), - 'object': edge.get('object') - }) - - # Convert the list of triple to a pandas DataFrame - triple_df = pd.DataFrame(triple) - - return triple_df - - else: - print("Request failed") - return None - - -def process_text(text): - text = text.replace("biolink:", "") - text = camel_case_to_words(text) - text = text.replace("_", " ") - return text - - -def camel_case_to_words(text): - return re.sub(r'([A-Z])', r' \1', text).lower() - - -triple_df = get_query_results() - -triple_list = [] -for index, row in triple_df.iterrows(): - subject = process_text(row['subject']) - predicate = process_text(row['predicate']) - object = process_text(row['object']) - triple = f"{subject} {predicate} {object}" - triple_list.append(triple) - -print("\n".join(triple_list)) diff --git a/util/chembl/convert.py b/util/chembl/convert.py deleted file mode 100644 index e05d24a..0000000 --- a/util/chembl/convert.py +++ /dev/null @@ -1,89 +0,0 @@ -import json -import pandas as pd - - -def create_csvs(json_path: str, name: str): - with open(json_path, 'r', encoding='utf-8-sig') as json_file: - data = json.load(json_file) - - sentence_columns = ["SENTENCE_ID", "PMID", "TYPE", "NUMBER", "SENT_START_INDEX", "SENTENCE", - "SECTION_HEADER", "NORMALIZED_SECTION_HEADER", "Column", "Column"] - sentence_records = [] - - labeled_columns = ["Predicate ID", "Triple", "Sentence ID", "Sentence", "Question", "Label", - "Reference"] - labeled_records = [] - #Predicate ID,Triple,Sentence ID,Sentence,Question,Label,Reference - - triple_columns = ["PREDICATION_ID", "SENTENCE_ID", "PMID", "PREDICATE", - "SUBJECT_CUI", "SUBJECT_NAME", "SUBJECT_SEMTYPE", "SUBJECT_NOVELTY", - "OBJECT_CUI", "OBJECT_NAME", "OBJECT_SEMTYPE", "OBJECT_NOVELTY", - "Column", "Column", "Column"] - triple_records = [] - sentence_id = 1000 - for item in data: - segments = item['p3']['segments'][0] - - subject_data = segments['end']['properties'] - object_data = segments['start']['properties'] - predicate_data = segments['relationship']['properties'] - - subject_name = subject_data['name'] - object_name = object_data['name'] - predicate = predicate_data['predicate'].split('biolink:', 1)[1].replace('_', ' ') - sentence = eval(predicate_data['publications_info']) - print(sentence) - sentence= sentence[list(sentence.keys())[0]]["sentence"] - print(sentence) - sentence_id = sentence_id+1 - predicate_id = predicate_data['id'] - - labeled_records.append({ - "Predicate ID": predicate_id, - "Triple": f"{subject_name} {predicate} {object_name}", - "Sentence ID": sentence_id, - "Sentence": sentence, - "Question": f"Is the triple \"{subject_name} {predicate} {object_name}\" supported by the sentence: \"{sentence}\"?", - "Label": True, - "Reference": None - }) - sentence_records.append({ - "SENTENCE_ID": sentence_id, - "PMID": None, - "TYPE": None, - "NUMBER": None, - "SENT_START_INDEX": None, - "SENTENCE": sentence, - "SECTION_HEADER": None, - "NORMALIZED_SECTION_HEADER": None, - "Column": None, - "Column": None - }) - - triple_records.append({ - "PREDICATION_ID": predicate_id, - "SENTENCE_ID": sentence_id, - "PMID": None, - "PREDICATE": predicate, - "SUBJECT_CUI": None, - "SUBJECT_NAME": subject_name, - "SUBJECT_SEMTYPE": None, - "SUBJECT_NOVELTY": None, - "OBJECT_CUI": None, - "OBJECT_NAME": object_name, - "OBJECT_SEMTYPE": None, - "OBJECT_NOVELTY": None, - "Column": None, - "Column": None, - "Column": None - }) - labeled_records_df=pd.DataFrame(labeled_records, columns=labeled_columns) - sentence_df = pd.DataFrame(sentence_records, columns=sentence_columns) - triple_df = pd.DataFrame(triple_records, columns=triple_columns) - - labeled_records_df.to_csv(f"{name}_labeled_records.csv", index=False) - sentence_df.to_csv(f"{name}_sentence_data.csv", index=False) - triple_df.to_csv(f"{name}_triple_data.csv", index=False) - - -create_csvs('/neo4j.json', 'true') diff --git a/util/chembl/create_dataset.py b/util/chembl/create_dataset.py deleted file mode 100644 index 9dbe64e..0000000 --- a/util/chembl/create_dataset.py +++ /dev/null @@ -1,89 +0,0 @@ -import json -import csv -import os - - -def create_dataset_from_json(json_file_name: str, dataset_name: str): - """ - Creates a CSV file with data retrieved from a json file - - This function reads data from a json file and creates a CSV file to which it writes the data from the json. - The created dataset is saved to the data folder, which is located in the project root. - - Parameters - ---------- - json_file_name : str - Name of the JSON file that was received from the neo4j service. The file must be in the root of the project - dataset_name : str - Name of the dataset to be created. - - Returns - ------- - None - - Raises - ------- - FileNotFoundError - If the json file is not found. - json.JSONDecodeError - If JSON decoding fails. - """ - try: - json_path = os.path.abspath(json_file_name + '.json') - print(json_path) - - if not os.path.exists(json_path): - raise FileNotFoundError('JSON file not found') - - path_to_save_df = os.path.join(os.getcwd(), 'data', f'{dataset_name}.csv') - - with open(path_to_save_df, 'w', newline='', encoding='utf-8-sig') as csv_file: - writer = csv.writer(csv_file) - writer.writerow(['Predicate ID', 'Triple', 'Sentence ID', 'Sentence', 'Question', 'Label', 'Reference']) - write_data(json_path, writer) - - except FileNotFoundError as e: - print(f"Error: {e}. File not found.") - except json.JSONDecodeError as e: - print(f"Error: {e}. JSON decoding failed.") - except Exception as e: - print(f"An unexpected error occurred: {e}") - - -def write_data(json_path: str, writer: csv.writer): - with open(json_path, 'r', encoding='utf-8-sig') as json_file: - data = json.load(json_file) - for item in data: - segments = item['p']['segments'][0] - - subject_data = segments['end']['properties'] - object_data = segments['start']['properties'] - predicate_data = segments['relationship']['properties'] - - subject_name = subject_data['name'] - object_name = object_data['name'] - predicate = predicate_data['predicate'].split('biolink:', 1)[1].replace('_', ' ') - sentence = subject_data['description'] - publications = object_data['publications'][0] if 'publications' in object_data else '' - sentence_id = segments['end']['identity'] - - triple = generate_triple(subject_name, predicate, object_name) - question = generate_question(triple, sentence) - - writer.writerow([ - predicate_data['id'], - triple, - sentence_id, - sentence, - question, - "True", - publications - ]) - - -def generate_triple(subject_name: str, predicate: str, object_name: str): - return f"{subject_name} {predicate} {object_name}" - - -def generate_question(triple: str, sentence: str): - return f"Is the triple {triple} supported by the sentence {sentence}" \ No newline at end of file diff --git a/util/chembl/semmed_triple_mapping.py b/util/chembl/semmed_triple_mapping.py deleted file mode 100644 index 99c8347..0000000 --- a/util/chembl/semmed_triple_mapping.py +++ /dev/null @@ -1,52 +0,0 @@ -# This code processes the data from the semmed_triple_data.csv file, -# creates a new 'TRIPLE' column from this data, and then filters this data -# to select only those triples that match the predicates specified in the predicate-remap.yaml file. -# As a result, only those triples from SemMedDB that match the predicates from the yaml file are displayed, -# and are also written to the filtered_triple_data.csv file in the project data folder -# yaml from https://github.com/RTXteam/RTX-KG2/blob/master/predicate-remap.yaml - -import os -import sys -import pandas as pd -import yaml -from src.triple_processing import process_triple_row - -sys.path.append(os.path.join(os.path.dirname(os.path.abspath(__file__)), '..', '..')) - -current_dir = os.path.dirname(os.path.realpath(__file__)) - -predicate_file_path = os.path.join(current_dir, '..', '..', 'data', 'predicate-remap.yaml') - -with open(predicate_file_path, 'r') as file: - predicate_mapping_raw = yaml.safe_load(file) - - -predicate_mapping = {key.replace('_', ' '): value if key != "isa" else "is a" for key, value in - predicate_mapping_raw.items()} - -data_file_path = os.path.join(current_dir, '..', '..', 'data', 'semmed_triple_data.csv') -semmed_data = pd.read_csv(data_file_path) - -semmed_data.columns = [ - "PREDICATION_ID", "SENTENCE_ID", "PMID", "PREDICATE", "SUBJECT_CUI", "SUBJECT_NAME", - "SUBJECT_SEMTYPE", "SUBJECT_NOVELTY", "OBJECT_CUI", "OBJECT_NAME", "OBJECT_SEMTYPE", - "OBJECT_NOVELTY", "Column", "Column", "Column" -] - -semmed_data['PREDICATE'] = semmed_data['PREDICATE'].str.replace('_', ' ').str.lower() -semmed_data['PREDICATE'] = semmed_data['PREDICATE'].apply(lambda x: "is a" if x == "isa" else x) - -semmed_data['TRIPLE'] = semmed_data.apply(lambda row: process_triple_row(row)[2], axis=1) - -new_predicate_mapping = {key.split(':')[1]: value for key, value in predicate_mapping.items()} - -filtered_data = semmed_data[semmed_data['PREDICATE'].isin(new_predicate_mapping.keys())] - -print(filtered_data.head()) - -filtered_data = (filtered_data[['PREDICATION_ID', 'SENTENCE_ID', 'TRIPLE']].rename - (columns={'PREDICATION_ID': 'Predicate ID', 'SENTENCE_ID': 'Sentence ID', 'TRIPLE': 'Triple'})) - -filtered_data = filtered_data.reindex(columns=['Predicate ID', 'Triple', 'Sentence ID']) - -filtered_data.to_csv(os.path.join('..', '..', 'data', 'filtered_triple_data.csv'), index=False) diff --git a/util/model_accuracy/accuracy.py b/util/model_accuracy/accuracy.py deleted file mode 100644 index 43b23bc..0000000 --- a/util/model_accuracy/accuracy.py +++ /dev/null @@ -1,127 +0,0 @@ -import argparse -import os -import pandas as pd -import matplotlib.pyplot as plt -import numpy as np - -IS_CORRECT_COLUMN = 'Is Correct' -PREDICATE_ID_COLUMN = 'Predicate ID' - - -def calculate_accuracy(test_df_path, result_path): - # Load test data - test_df = pd.read_csv(test_df_path) - result_data = pd.read_csv(result_path) - - print(f"Rows in test_df: {len(test_df)}") - print(f"Rows in result_data: {len(result_data)}") - - # Data preprocessing - test_df['Label'] = test_df['Label'].replace({'True': True, 'False': False, 'Undefined': np.nan}) - result_data[IS_CORRECT_COLUMN] = ( - result_data[IS_CORRECT_COLUMN].replace({'True': True, 'False': False, 'Undefined': np.nan})) - - # Merging dataframes - merged_data = pd.merge(test_df, result_data, on=PREDICATE_ID_COLUMN, how='inner', validate='one_to_one') - - print(f"Rows in merged_data: {len(merged_data)}") - - test_ids = set(test_df[PREDICATE_ID_COLUMN]) - result_ids = set(result_data[PREDICATE_ID_COLUMN]) - unmatched_result_count = len(result_ids - test_ids) - - print(f"Unmatched {PREDICATE_ID_COLUMN} in result_data: {unmatched_result_count}") - if unmatched_result_count > 0: - print("Unmatched Predicate IDs may be due to missing entries in either test or result datasets and it's ok ;) ") - - # Extracting relevant columns - test_labels = merged_data['Label'] - results = merged_data[IS_CORRECT_COLUMN] - - # Calculating accuracy and statistics - correct_predictions = np.sum(results == test_labels) - incorrect_predictions = np.sum(results != test_labels) - true_results = np.sum(results is True) - false_results = np.sum(results is False) - undefined_results = np.sum(pd.isna(results)) - - accuracy = correct_predictions / (correct_predictions + incorrect_predictions) - - stats = { - 'total_results': len(merged_data), - 'correct': correct_predictions, - 'incorrect': incorrect_predictions, - 'true_results': true_results, - 'false_results': false_results, - 'undefined_results': undefined_results - } - - return accuracy, stats - - -def plot_accuracy(accuracy, stats, title): - incorrect = 1.0 - accuracy - - # Customizing the style - plt.style.use('ggplot') - - font = {'family': 'serif', 'color': 'darkgrey', 'weight': 'normal', 'size': 16} - - # Creating a pie chart - _, ax = plt.subplots(figsize=(12, 12)) - ax.pie([accuracy, incorrect], labels=['Correct', 'Incorrect'], - colors=['#4CAF50', 'lightgrey'], autopct='%1.1f%%', startangle=140) - ax.set_title(title, fontdict=font) - - # Displaying model accuracy and additional statistics - plt.figtext(0.5, 0.95, f"**{title} Model Accuracy: {accuracy:.2f}**", - ha='center', fontsize=14, weight='bold', color='purple') - - # Adjusted positions of the text, with styling - plt.figtext(0.25, 0.08, f"Total results: {stats['total_results']}", ha='left') - plt.figtext(0.25, 0.05, f"Correct predictions: {stats['correct']}", ha='left') - plt.figtext(0.25, 0.02, f"Incorrect predictions: {stats['incorrect']}", ha='left') - plt.figtext(0.65, 0.08, f"True results: {stats['true_results']}", ha='left') - plt.figtext(0.65, 0.05, f"False results: {stats['false_results']}", ha='left') - plt.figtext(0.65, 0.02, f"Undefined results: {stats['undefined_results']}", ha='left') - - plt.show() - - -def main(): - parser = argparse.ArgumentParser(description='Calculate and plot model accuracy.') - parser.add_argument('--model', required=True, help='Name of the model') - parser.add_argument('--icl', action='store_true', help='Flag to indicate in-context learning') - parser.add_argument('--test_df_file', required=True, help='Name of the test dataframe file') - parser.add_argument('--result_file', required=True, help='Name of the result file') - - args = parser.parse_args() - - # Define the path to the data directory - base_dir = os.path.dirname(os.path.dirname(os.path.dirname(os.path.abspath(__file__)))) - data_dir = os.path.join(base_dir, 'data') - result_dir = os.path.join(base_dir, 'result') - - # Construct the file paths - if args.icl: - # For models with ICL, use the specified test dataframe file - test_df_file = os.path.join(data_dir, f"{args.test_df_file}_{args.model}_icl.csv") - else: - # For models without ICL, use the human_labeled_semmed.csv file - test_df_file = os.path.join(data_dir, 'human_labeled_semmed.csv') - # Uncomment the line below this annotation (and comment, pls, line on top) - # to use the specified test dataframe file for standart model too. - # test_df_file = os.path.join(data_dir, f"{args.test_df_file}_{args.model}_icl.csv") - - result_file = os.path.join(result_dir, f"{args.model}{'_icl' if args.icl else ''}_{args.result_file}.csv") - - accuracy, total_results = calculate_accuracy(test_df_file, result_file) - print(f"**{args.model} Model Accuracy: {accuracy:.2f}**") - print(f"Total test results: {total_results}") - - model_title = f'{args.model} {"(with ICL)" if args.icl else ""}' - plot_accuracy(accuracy, total_results, f'{model_title} Model Accuracy') - - -if __name__ == "__main__": - main() From 7b5514a5813c8e4e981a615519d2d2b9d821a031 Mon Sep 17 00:00:00 2001 From: mfl15 <144844529+mfl15@users.noreply.github.com> Date: Wed, 22 Jan 2025 19:15:20 +0000 Subject: [PATCH 2/2] env example --- env.example | 15 +++++++++++++++ 1 file changed, 15 insertions(+) create mode 100644 env.example diff --git a/env.example b/env.example new file mode 100644 index 0000000..e978188 --- /dev/null +++ b/env.example @@ -0,0 +1,15 @@ + + +OPENAI_API_KEY= + +LANGFUSE_PUBLIC_KEY= +LANGFUSE_SECRET_KEY= +LANGFUSE_HOST= + + +DB_USERNAME= +DB_PASSWORD= +DB_NAME= +DB_HOST= +DB_PORT= +