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http://scihub22266oqcxt.onion/ C5489887!5489887!28670375     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Transl+Res 2017 ; 9 (6): 2865-77 Nephropedia Template TP {{tp|p=28670375|t=2017. Lyn kinase enhanced hepatic fibrosis by modulating the activation of hepatic stellate cells |pdf=|usr=}}{{28670375}} gab.com Text Lyn kinase enhanced hepatic fibrosis by modulating the activation of hepatic stellate cells JO: Am J Transl Res http://www.kidney.de/pget.php?&tw=1&pmid=28670375 #FOAvip The non-selectivity of tyrosine kinase inhibitors is the leading cause of drug withdrawals, and limits their application in anti-fibrosis. The role of Src tyrosine kinase Lyn in hepatic fibrosis remains elusive. In this study, we aimed to elucidate the role of Lyn kinase in the pathogenesis of hepatic fibrosis. Through examining Lyn-transgenic (Lyn TG) mice treated with CCl4 (carbon tetrachloride), we determined whether Lyn kinase is involved in the pathogenesis of hepatic fibrosis. On top of that, we also investigated the role of Lyn in the activation of hepatic stellate cells (HSCs) in vitro. Here, we showed that Lyn kinase was highly expressed in liver fibrosis upon CCl4 treatment. Meanwhile, Lyn TG mice showed that perivascular infiltration of mononuclear cells, and the markers of liver injury and hepatocytes apoptosis were significantly increased in liver tissue after CCl4 treatment. In comparison with wild-type (WT) mice after CCl4 treatment, we found that the ?brotic score in liver tissues of Lyn TG mice with the same treatment went up dramatically, so did the gene expression of fibrotic markers. In addition, over-expression of Lyn kinase drastically promoted the expression of HSCs activation markers in vivo or in vitro. Additionally, the Src-specific inhibitor PP2 significantly suppressed the increased expression of integrin ?v?3 in TGF-?1-induced HSCs, and PP2 further induced HSC apoptosis in TGF-?1-treated cells. These results collectively indicated that Lyn kinase is implicated in the pathogenesis of hepatic fibrosis through the modulating of HSC activation. Twit Text FOAVip Lyn kinase enhanced hepatic fibrosis by modulating the activation of hepatic stellate cells ????Am J Transl Res http://www.kidney.de/pget.php?&tw=1&pmid=28670375 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28670375 #FOAvip English Wikipedia <ref>{{Cite pmid|28670375}}</ref> Lyn kinase enhanced hepatic fibrosis by modulating the activation of hepatic stellate cells #MMPMID28670375 Li Y; Xiong L; Gong J Am J Transl Res 2017[]; 9 (6): 2865-77 PMID28670375show ga The non-selectivity of tyrosine kinase inhibitors is the leading cause of drug withdrawals, and limits their application in anti-fibrosis. The role of Src tyrosine kinase Lyn in hepatic fibrosis remains elusive. In this study, we aimed to elucidate the role of Lyn kinase in the pathogenesis of hepatic fibrosis. Through examining Lyn-transgenic (Lyn TG) mice treated with CCl4 (carbon tetrachloride), we determined whether Lyn kinase is involved in the pathogenesis of hepatic fibrosis. On top of that, we also investigated the role of Lyn in the activation of hepatic stellate cells (HSCs) in vitro. Here, we showed that Lyn kinase was highly expressed in liver fibrosis upon CCl4 treatment. Meanwhile, Lyn TG mice showed that perivascular infiltration of mononuclear cells, and the markers of liver injury and hepatocytes apoptosis were significantly increased in liver tissue after CCl4 treatment. In comparison with wild-type (WT) mice after CCl4 treatment, we found that the ?brotic score in liver tissues of Lyn TG mice with the same treatment went up dramatically, so did the gene expression of fibrotic markers. In addition, over-expression of Lyn kinase drastically promoted the expression of HSCs activation markers in vivo or in vitro. Additionally, the Src-specific inhibitor PP2 significantly suppressed the increased expression of integrin ?v?3 in TGF-?1-induced HSCs, and PP2 further induced HSC apoptosis in TGF-?1-treated cells. These results collectively indicated that Lyn kinase is implicated in the pathogenesis of hepatic fibrosis through the modulating of HSC activation. äLyn kinase enhanced hepatic fibrosis by modulating the activation of h(epmc).pdf DeepDyve Pubget Overpricing