Therefore, it seems plausible that fine tuning, in contrast to approaches that would completely abrogate TLR signaling, may have a future in efforts to translate TLR pathophysiology into clinical practice in human liver diseases. “
“Diverticular disease of the colon is one of the most common medical conditions affecting people in industrialized nations. The majority of patients with colonic diverticular disease will remain asymptomatic, while approximately 30% will suffer from inflammatory or bleeding complications. Management of uncomplicated diverticulitis is with bowel

rest and broad-spectrum antibiotics. Diverticulitis complicated by generalized Galunisertib peritonitis, abscess, or fistula formation usually requires surgical intervention. Mild, self-limited diverticular bleeding can be managed conservatively while angiographic and surgical interventions are reserved for severe or recurrent bleeding. Chronic symptoms from diverticular disease can mimic irritable bowel syndrome and inflammatory bowel disease.

Current studies are examining the use of probiotics and anti-inflammatory AZD9291 medications in the management of chronic diverticular disease. “
“Biliary atresia (BA), the most common cause of end-stage liver disease and the leading indication for pediatric liver transplantation, is associated with intrahepatic ductular reactions within regions of rapidly expanding periportal biliary fibrosis. Whereas the extent of such biliary 上海皓元 fibrosis is a negative predictor of long-term transplant-free survival, the cellular phenotypes involved in the fibrosis are not well established. Using a rhesus rotavirus-induced mouse model of BA, we demonstrate significant expansion of a cell population expressing the putative stem/progenitor cell marker,

PROMININ-1 (PROM1), adjacent to ductular reactions within regions of periportal fibrosis. PROM1positive (pos) cells express Collagen-1α1. Subsets of PROM1pos cells coexpress progenitor cell marker CD49f, epithelial marker E-CADHERIN, biliary marker CYTOKERATIN-19, and mesenchymal markers VIMENTIN and alpha-SMOOTH MUSCLE ACTIN (αSMA). Expansion of the PROM1pos cell population is associated with activation of Fibroblast Growth Factor (FGF) and Transforming Growth Factor-beta (TGFβ) signaling. In vitro cotreatment of PROM1-expressing Mat1a−/− hepatic progenitor cells with recombinant human FGF10 and TGFβ1 promotes morphologic transformation toward a myofibroblastic cell phenotype with increased expression of myofibroblastic genes Collagen-1α1, Fibronectin, and α-Sma.