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To measure drug sensitivity, we used the decrease in the release of the inflammatory cytokine TNF from the fresh IBD tissues in the presence or absence of test drugs to pharmacologically assess patient response to IBD therapy. As a measure of drug equivance, we used the decrease in the release of TNF from the fresh IBD tissues in the presence or absence of test drugs. Our results showed differences in prescription among patients in our cohort of IBD patients with differences in gender, age, or disease, as well as new genetic polymorphisms, which were attributed to a variety in reaction to the anti-inflammatory drug BIRB796.
Source link: https://www.ncbi.nlm.nih.gov/bioproject/794529
In physiological hypoxia, intestinal epithelial cells of the intestinal epithelial cells are present, resulting in hypoxia-inducible factor activation and supporting barrier function and cell metabolism. According to gene set enrichment analysis, both undifferentiated and differentiated Caco-2 cells treatment, as well as Cobalt chloride and oxyquinoline treatment of both undifferentiated and differentiated Caco-2 cells, stimulate the HIF-signaling pathway. Patients with IBD-confirmed HIF-1 signaling pathway activation in the sigmoid colon of patients with ulcerative colitis and terminal ileum of patients with Crohn's disease, according to a publicly available RNA sequence set of the intestinal epithelial cells of patients with Crohn's disease. In IBD samples, the core gene set from the gut hypoxia model was discovered. Expression activation of ITGA5 and PLAUR genes encoding integrin 5 and urokinase-type plasminogen activator receptor was detected in IBD samples. The proposed role of HIF1A and NFATC1 in the regulation of ITGA5 and PLAUR gene expression was shown by a transcription factor analysis with the previously developed miRGTF system, which revealed the potential involvement of HIF1A and NFATC1 in the regulation of gene expression in ITGA5 and PLAUR gene expression.
Source link: https://www.ncbi.nlm.nih.gov/bioproject/773242
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