Investigating the role of interleukin-1 beta and glutamate in inflammatory bowel disease and epilepsy using discovery browsing
Abstract Background Structured electronic health records are a rich resource for identifying novel correlations, such as co-morbidities and adverse drug reactions. For drug development and better understanding of biomedical phenomena, such correlations need to be supported by viable hypotheses about...
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doaj-3c109e83d23f49d5b864ec0908d7c91b2020-11-25T02:09:36ZengBMCJournal of Biomedical Semantics2041-14802018-12-019111410.1186/s13326-018-0192-yInvestigating the role of interleukin-1 beta and glutamate in inflammatory bowel disease and epilepsy using discovery browsingThomas C. Rindflesch0Catherine L. Blake1Michael J. Cairelli2Marcelo Fiszman3Caroline J. Zeiss4Halil Kilicoglu5RetiredSchool of Information Sciences, University of Illinois at Urbana-ChampaignKaiser Permanente Southern CaliforniaIndependent researcherDepartment of Comparative Medicine, Yale School of MedicineLister Hill National Center for Biomedical Communications, U.S. National Library of MedicineAbstract Background Structured electronic health records are a rich resource for identifying novel correlations, such as co-morbidities and adverse drug reactions. For drug development and better understanding of biomedical phenomena, such correlations need to be supported by viable hypotheses about the mechanisms involved, which can then form the basis of experimental investigations. Methods In this study, we demonstrate the use of discovery browsing, a literature-based discovery method, to generate plausible hypotheses elucidating correlations identified from structured clinical data. The method is supported by Semantic MEDLINE web application, which pinpoints interesting concepts and relevant MEDLINE citations, which are used to build a coherent hypothesis. Results Discovery browsing revealed a plausible explanation for the correlation between epilepsy and inflammatory bowel disease that was found in an earlier population study. The generated hypothesis involves interleukin-1 beta (IL-1 beta) and glutamate, and suggests that IL-1 beta influence on glutamate levels is involved in the etiology of both epilepsy and inflammatory bowel disease. Conclusions The approach presented in this paper can supplement population-based correlation studies by enabling the scientist to identify literature that may justify the novel patterns identified in such studies and can underpin basic biomedical research that can lead to improved treatments and better healthcare outcomes.http://link.springer.com/article/10.1186/s13326-018-0192-yLiterature-based discoveryDiscovery browsingEpilepsyInflammatory bowel diseaseInterleukin-1 betaGlutamate |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Thomas C. Rindflesch Catherine L. Blake Michael J. Cairelli Marcelo Fiszman Caroline J. Zeiss Halil Kilicoglu |
spellingShingle |
Thomas C. Rindflesch Catherine L. Blake Michael J. Cairelli Marcelo Fiszman Caroline J. Zeiss Halil Kilicoglu Investigating the role of interleukin-1 beta and glutamate in inflammatory bowel disease and epilepsy using discovery browsing Journal of Biomedical Semantics Literature-based discovery Discovery browsing Epilepsy Inflammatory bowel disease Interleukin-1 beta Glutamate |
author_facet |
Thomas C. Rindflesch Catherine L. Blake Michael J. Cairelli Marcelo Fiszman Caroline J. Zeiss Halil Kilicoglu |
author_sort |
Thomas C. Rindflesch |
title |
Investigating the role of interleukin-1 beta and glutamate in inflammatory bowel disease and epilepsy using discovery browsing |
title_short |
Investigating the role of interleukin-1 beta and glutamate in inflammatory bowel disease and epilepsy using discovery browsing |
title_full |
Investigating the role of interleukin-1 beta and glutamate in inflammatory bowel disease and epilepsy using discovery browsing |
title_fullStr |
Investigating the role of interleukin-1 beta and glutamate in inflammatory bowel disease and epilepsy using discovery browsing |
title_full_unstemmed |
Investigating the role of interleukin-1 beta and glutamate in inflammatory bowel disease and epilepsy using discovery browsing |
title_sort |
investigating the role of interleukin-1 beta and glutamate in inflammatory bowel disease and epilepsy using discovery browsing |
publisher |
BMC |
series |
Journal of Biomedical Semantics |
issn |
2041-1480 |
publishDate |
2018-12-01 |
description |
Abstract Background Structured electronic health records are a rich resource for identifying novel correlations, such as co-morbidities and adverse drug reactions. For drug development and better understanding of biomedical phenomena, such correlations need to be supported by viable hypotheses about the mechanisms involved, which can then form the basis of experimental investigations. Methods In this study, we demonstrate the use of discovery browsing, a literature-based discovery method, to generate plausible hypotheses elucidating correlations identified from structured clinical data. The method is supported by Semantic MEDLINE web application, which pinpoints interesting concepts and relevant MEDLINE citations, which are used to build a coherent hypothesis. Results Discovery browsing revealed a plausible explanation for the correlation between epilepsy and inflammatory bowel disease that was found in an earlier population study. The generated hypothesis involves interleukin-1 beta (IL-1 beta) and glutamate, and suggests that IL-1 beta influence on glutamate levels is involved in the etiology of both epilepsy and inflammatory bowel disease. Conclusions The approach presented in this paper can supplement population-based correlation studies by enabling the scientist to identify literature that may justify the novel patterns identified in such studies and can underpin basic biomedical research that can lead to improved treatments and better healthcare outcomes. |
topic |
Literature-based discovery Discovery browsing Epilepsy Inflammatory bowel disease Interleukin-1 beta Glutamate |
url |
http://link.springer.com/article/10.1186/s13326-018-0192-y |
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