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10.1172/JCI86802 http://scihub22266oqcxt.onion/10.1172/JCI86802 C4811146!4811146 !26999598     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26999598 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26999598 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Clin+Invest 2016 ; 126 (4 ): 1245-7 Nephropedia Template TP {{tp|p=26999598 |t=2016. Influenza leaves a TRAIL to pulmonary edema |pdf=|usr=}}{{26999598 }} gab.com Text Influenza leaves a TRAIL to pulmonary edema JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=26999598 #FOAvip Influenza infection can cause acute respiratory distress syndrome (ARDS), leading to poor disease outcome with high mortality. One of the driving features in the pathogenesis of ARDS is the accumulation of fluid in the alveoli, which causes severe pulmonary edema and impaired oxygen uptake. In this issue of the JCI, Peteranderl and colleagues define a paracrine communication between macrophages and type II alveolar epithelial cells during influenza infection where IFN? induces macrophage secretion of TRAIL that causes endocytosis of Na,K-ATPase by the alveolar epithelium. This reduction of Na,K-ATPase expression decreases alveolar fluid clearance, which in turn leads to pulmonary edema. Inhibition of the TRAIL signaling pathway has been shown to improve lung injury after influenza infection, and future studies will be needed to determine if blocking this pathway is a viable option in the treatment of ARDS. Twit Text FOAVip Influenza leaves a TRAIL to pulmonary edema ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=26999598 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26999598 #FOAvip English Wikipedia <ref>{{Cite pmid|26999598 }}</ref> Influenza leaves a TRAIL to pulmonary edema #MMPMID26999598 Brauer R ; Chen P J Clin Invest 2016[Apr]; 126 (4 ): 1245-7 PMID26999598 show ga Influenza infection can cause acute respiratory distress syndrome (ARDS), leading to poor disease outcome with high mortality. One of the driving features in the pathogenesis of ARDS is the accumulation of fluid in the alveoli, which causes severe pulmonary edema and impaired oxygen uptake. In this issue of the JCI, Peteranderl and colleagues define a paracrine communication between macrophages and type II alveolar epithelial cells during influenza infection where IFN? induces macrophage secretion of TRAIL that causes endocytosis of Na,K-ATPase by the alveolar epithelium. This reduction of Na,K-ATPase expression decreases alveolar fluid clearance, which in turn leads to pulmonary edema. Inhibition of the TRAIL signaling pathway has been shown to improve lung injury after influenza infection, and future studies will be needed to determine if blocking this pathway is a viable option in the treatment of ARDS. |Animals [MESH] |Humans [MESH] |Influenza A virus/*immunology [MESH] |Interferon Type I/*immunology [MESH] |Macrophages, Alveolar/*immunology [MESH] |Orthomyxoviridae Infections/*immunology [MESH] |Paracrine Communication/*immunology [MESH] |Pulmonary Edema/*immunology [MESH] |Respiratory Mucosa/*immunology [MESH]Influenza leaves a TRAIL to pulmonary edema (epmc).pdf DeepDyve Pubget Overpricing