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10.1097/MOG.0000000000000363 http://scihub22266oqcxt.onion/10.1097/MOG.0000000000000363 C5572460!5572460 !28402994     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28402994 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Curr+Opin+Gastroenterol 2017 ; 33 (4 ): 239-245 Nephropedia Template TP {{tp|p=28402994 |t=2017. Intestinal fibrosis: ready to be reversed |pdf=|usr=}}{{28402994 }} gab.com Text Intestinal fibrosis: ready to be reversed JO: Curr Opin Gastroenterol http://www.kidney.de/pget.php?&tw=1&pmid=28402994 #FOAvip PURPOSE OF REVIEW: Intestinal fibrosis is a common complication of several enteropathies, with inflammatory bowel disease (IBD) being the major cause. Intestinal fibrosis affects both ulcerative colitis and Crohn's disease, and no specific antifibrotic therapy exists. This review highlights recent developments in this area. RECENT FINDINGS: The pathophysiology of intestinal stricture formation includes inflammation-dependent and inflammation-independent mechanisms. A better understanding of the mechanisms of intestinal fibrogenesis and the availability of compounds for other nonintestinal fibrotic diseases bring clincial trials in stricturing Crohn's disease within reach. SUMMARY: Improved understanding of its mechanisms and ongoing development of clinical trial endpoints for intestinal fibrosis will allow the testing of novel antifibrotic compounds in IBD. Twit Text FOAVip Intestinal fibrosis: ready to be reversed ????Curr Opin Gastroenterol http://www.kidney.de/pget.php?&tw=1&pmid=28402994 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28402994 #FOAvip English Wikipedia <ref>{{Cite pmid|28402994 }}</ref> Intestinal fibrosis: ready to be reversed #MMPMID28402994 Latella G ; Rieder F Curr Opin Gastroenterol 2017[Jul]; 33 (4 ): 239-245 PMID28402994 show ga PURPOSE OF REVIEW: Intestinal fibrosis is a common complication of several enteropathies, with inflammatory bowel disease (IBD) being the major cause. Intestinal fibrosis affects both ulcerative colitis and Crohn's disease, and no specific antifibrotic therapy exists. This review highlights recent developments in this area. RECENT FINDINGS: The pathophysiology of intestinal stricture formation includes inflammation-dependent and inflammation-independent mechanisms. A better understanding of the mechanisms of intestinal fibrogenesis and the availability of compounds for other nonintestinal fibrotic diseases bring clincial trials in stricturing Crohn's disease within reach. SUMMARY: Improved understanding of its mechanisms and ongoing development of clinical trial endpoints for intestinal fibrosis will allow the testing of novel antifibrotic compounds in IBD. |*Antifibrinolytic Agents/pharmacology [MESH] |*Drug Discovery [MESH] |Constriction, Pathologic [MESH] |Disease Progression [MESH] |Extracellular Matrix/*drug effects [MESH] |Fibrosis/*drug therapy/etiology [MESH] |Humans [MESH] |Inflammatory Bowel Diseases/complications/*drug therapy/physiopathology [MESH]Intestinal fibrosis: ready to be reversed (epmc).pdf DeepDyve Pubget Overpricing