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- W2912583339 endingPage "G719" @default.
- W2912583339 startingPage "G701" @default.
- W2912583339 abstract "Irritable bowel syndrome (IBS) is one of the commonest gastrointestinal disorders. Although long-time considered a pure functional disorder, intense research in past years has rendered a very complex and varied array of observations indicating the presence of structural and molecular abnormalities underlying characteristic motor and sensitive changes and clinical manifestations. Analysis of gene and protein expression in the intestinal mucosa has shed light on the molecular mechanisms implicated in IBS physiopathology. This analysis uncovers constitutive and inductive genetic and epigenetic marks in the small and large intestine that highlight the role of epithelial barrier, immune activation, and mucosal processing of foods and toxins and several new molecular pathways in the origin of IBS. The incorporation of innovative high-throughput techniques into IBS research is beginning to provide new insights into highly structured and interconnected molecular mechanisms modulating gene and protein expression at tissue level. Integration and correlation of these molecular mechanisms with clinical and environmental data applying systems biology/medicine and data mining tools emerge as crucial steps that will allow us to get meaningful and more definitive comprehension of IBS-detailed development and show the real mechanisms and causality of the disease and the way to identify more specific diagnostic biomarkers and effective treatments." @default.
- W2912583339 created "2019-02-21" @default.
- W2912583339 creator A5055112597 @default.
- W2912583339 creator A5071230889 @default.
- W2912583339 creator A5079090385 @default.
- W2912583339 creator A5091244822 @default.
- W2912583339 date "2019-06-01" @default.
- W2912583339 modified "2023-10-07" @default.
- W2912583339 title "Mucosal RNA and protein expression as the next frontier in IBS: abnormal function despite morphologically intact small intestinal mucosa" @default.
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