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10.1016/j.jhep.2015.11.002 http://scihub22266oqcxt.onion/10.1016/j.jhep.2015.11.002 C4761314!4761314!26555271     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Hepatol 2016 ; 64 (3): 699-707 Nephropedia Template TP {{tp|p=26555271|t=2016. Liver Bid-suppression for treatment of fibrosis associated with nonalcoholic steatohepatitis |pdf=|usr=}}{{26555271}} gab.com Text Liver Bid-suppression for treatment of fibrosis associated with nonalcoholic steatohepatitis JO: J Hepatol http://www.kidney.de/pget.php?&tw=1&pmid=26555271 #FOAvip Background & Aims: Liver fibrosis is the most worrisome feature of Nonalcoholic Steatohepatitis (NASH). Growing evidence supports a link between hepatocyte apoptosis and liver fibrogenesis. Our aim was to determine the therapeutic efficacy and safety of liver Bid, a key pro-apoptotic molecule, suppression using RNA interference (RNAi) for the treatment of fibrosis. Methods: First, we optimized the delivery system for Bid siRNA in mice using ten different stealth RNAi siRNAs and two lipid formulations -Invivofectamine2.0 and a newly developed inviofectamine3.0 - that have been designed for high efficacy accumulation in the liver, assessed via real time PCR of Bid mRNA. Next, C57BL/6 mice were placed on a choline-deficient L-amino acid defined (CDAA) diet. After 19 wks of CDAA diet, a time-point that results in severe fibrotic-NASH, mice were injected with the selected Bid siRNA-Invivofectamine3.0 biweekly for three weeks. Additionally hepatocyte-specific Bid-deficient (Bid?hep) mice were placed on CDAA diet for 20 wks. Results: A maximum Bid knockdown was achieved at 1.5 mg/kg siRNA with inviofectamine3.0, whereas it was at 7 mg/kg with Invivofectamine2.0. In NASH mice, after 3 wks of treatment, BID protein was reduced to 10% and this was associated with an improvement in liver fibrosis and inflammation associated with a marked reduction in TUNEL-positive cells, caspase 3 activation, and a reduction in mitochondrial BAX and BAK. Bid?hep mice showed similar protection from fibrotic changes. Conclusion: Our data demonstrate that liver Bid suppression by RNAi technology, as well as hepatocyte-specific Bid-deficiency, improves liver fibrosis coupled with a reduction of inflammation in experimental NASH. These findings are consistent with existing evidence that hepatocyte apoptosis triggers HSC activation and liver fibrosis and suggest that Bid inhibition may be useful as an antifibrotic NASH therapy. Twit Text FOAVip Liver Bid-suppression for treatment of fibrosis associated with nonalcoholic steatohepatitis ????J Hepatol http://www.kidney.de/pget.php?&tw=1&pmid=26555271 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26555271 #FOAvip English Wikipedia <ref>{{Cite pmid|26555271}}</ref> Liver Bid-suppression for treatment of fibrosis associated with nonalcoholic steatohepatitis #MMPMID26555271 Eguchi A; Mollerat Du Jeu XD; Johnson CD; Nektaria A; Feldstein AE J Hepatol 2016[Mar]; 64 (3): 699-707 PMID26555271show ga Background & Aims: Liver fibrosis is the most worrisome feature of Nonalcoholic Steatohepatitis (NASH). Growing evidence supports a link between hepatocyte apoptosis and liver fibrogenesis. Our aim was to determine the therapeutic efficacy and safety of liver Bid, a key pro-apoptotic molecule, suppression using RNA interference (RNAi) for the treatment of fibrosis. Methods: First, we optimized the delivery system for Bid siRNA in mice using ten different stealth RNAi siRNAs and two lipid formulations -Invivofectamine2.0 and a newly developed inviofectamine3.0 - that have been designed for high efficacy accumulation in the liver, assessed via real time PCR of Bid mRNA. Next, C57BL/6 mice were placed on a choline-deficient L-amino acid defined (CDAA) diet. After 19 wks of CDAA diet, a time-point that results in severe fibrotic-NASH, mice were injected with the selected Bid siRNA-Invivofectamine3.0 biweekly for three weeks. Additionally hepatocyte-specific Bid-deficient (Bid?hep) mice were placed on CDAA diet for 20 wks. Results: A maximum Bid knockdown was achieved at 1.5 mg/kg siRNA with inviofectamine3.0, whereas it was at 7 mg/kg with Invivofectamine2.0. In NASH mice, after 3 wks of treatment, BID protein was reduced to 10% and this was associated with an improvement in liver fibrosis and inflammation associated with a marked reduction in TUNEL-positive cells, caspase 3 activation, and a reduction in mitochondrial BAX and BAK. Bid?hep mice showed similar protection from fibrotic changes. Conclusion: Our data demonstrate that liver Bid suppression by RNAi technology, as well as hepatocyte-specific Bid-deficiency, improves liver fibrosis coupled with a reduction of inflammation in experimental NASH. These findings are consistent with existing evidence that hepatocyte apoptosis triggers HSC activation and liver fibrosis and suggest that Bid inhibition may be useful as an antifibrotic NASH therapy. äLiver Bid-suppression for treatment of fibrosis associated with nonalc(epmc).pdf DeepDyve Pubget Overpricing