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Full-Text Articles in Medicine and Health Sciences
Prevalence Of The Hypervirulent Nap1/Bi/027 Strain Of C. Difficile In Southwestern Virginia And Risk Factors Associated With Infection, Andrew O. Hanna, Anthony Baffoe-Bonnie, Shikha Vasudeva
Prevalence Of The Hypervirulent Nap1/Bi/027 Strain Of C. Difficile In Southwestern Virginia And Risk Factors Associated With Infection, Andrew O. Hanna, Anthony Baffoe-Bonnie, Shikha Vasudeva
Graduate Medical Education (GME) Resident and Fellow Research Day Posters
C. difficile infection (CDI) incidence has increased over the last several decades. The BI/NAP1/027 ribotype was discovered in 2005 and has since been responsible for multiple outbreaks in the US and Canada. This subtype of C. Difficile is known to be more virulent in vivo and produce more severe disease. Limited regional data of the prevalence of this ribotype is available, which could help guide treatment. Using infection control data from a large regional hospital and a VA medical center, this study documented the prevalence of the 027 ribotype in Southwest Virginia. Patients were included if they were tested at …
Epigenetic Silencing Of Socs3 Expression Contributes To Fibrosis In Crohn’S Disease, Emily T. Marshall, Chao Li, John K. Kuemmerle
Epigenetic Silencing Of Socs3 Expression Contributes To Fibrosis In Crohn’S Disease, Emily T. Marshall, Chao Li, John K. Kuemmerle
MD Student Summer Research Fellowship Program Posters
Identified risk polymorphisms affecting the Jak-STAT3 pathway in patients with Crohn’s disease could affect TGF-β1 and collagen I expression and in the pathway’s negative regulator, SOCS3. Genetic factors, however, account for only ~25% of disease. Epigenetic events also shape gene expression. Recent experiments showed that autocrine IL-6 production in mesenchymal cells, subepithelial myofibroblasts (SEMF) and muscle cells, of patients with fibrostenotic Crohn’s disease causes sustained Jak-STAT3 activity, excess TGF-β1 and Collagen I production and fibrosis. SOCS3 paradoxically decreased in these cells. We now identify epigenetic mechanisms that silence SOCS3 expression in SEMF of patients with fibrostenotic Crohn’s disease. In a …