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10.1371/journal.pone.0068393 http://scihub22266oqcxt.onion/10.1371/journal.pone.0068393 23840852!3695896!23840852     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 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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\23840852.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       PLoS+One 2013 ; 8 (6): e68393 Nephropedia Template TP {{tp|p=23840852|t=2013. Exacerbating effects of human parvovirus B19 NS1 on liver fibrosis in NZB/W F1 mice |pdf=|usr=}}{{23840852}} gab.com Text Exacerbating effects of human parvovirus B19 NS1 on liver fibrosis in NZB/W F1 mice JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=23840852 #FOAvip Systemic lupus erythematosus (SLE) is an autoimmune disorder with unknown etiology that impacts various organs including liver. Recently, human parvovirus B19 (B19) is recognized to exacerbate SLE. However, the effects of B19 on liver in SLE are still unclear. Herein we aimed to investigate the effects of B19 on liver in NZB/W F1 mice by injecting subcutaneously with PBS, recombinant B19 NS1, VP1u or VP2, respectively. Our experimental results revealed that B19 NS1 protein significantly enhanced the TGF-beta/Smad fibrotic signaling by increasing the expressions of TGF-beta, Smad2/3, phosphorylated Smad2/3, Smad4 and Sp1. The consequent fibrosis-related proteins, PAI-1 and alpha-SMA, were also significantly induced in livers of NZB/W F1 mice receiving B19 NS1 protein. Accordingly, markedly increased collagen deposition was also observed in livers of NZB/W F1 mice receiving B19 NS1 protein. However, no significant difference was observed in livers of NZB/W F1 mice receiving B19 VP1u or VP2 as compared to the controls. These findings indicate that B19 NS1 plays a crucial role in exacerbating liver fibrosis in NZB/W F1 mice through enhancing the TGF-a/Smad fibrotic signaling. Twit Text FOAVip Exacerbating effects of human parvovirus B19 NS1 on liver fibrosis in NZB/W F1 mice ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=23840852 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23840852 #FOAvip English Wikipedia <ref>{{Cite pmid|23840852}}</ref> Exacerbating effects of human parvovirus B19 NS1 on liver fibrosis in NZB/W F1 mice #MMPMID23840852 Hsu TC; Tsai CC; Chiu CC; Hsu JD; Tzang BS PLoS One 2013[]; 8 (6): e68393 PMID23840852show ga Systemic lupus erythematosus (SLE) is an autoimmune disorder with unknown etiology that impacts various organs including liver. Recently, human parvovirus B19 (B19) is recognized to exacerbate SLE. However, the effects of B19 on liver in SLE are still unclear. Herein we aimed to investigate the effects of B19 on liver in NZB/W F1 mice by injecting subcutaneously with PBS, recombinant B19 NS1, VP1u or VP2, respectively. Our experimental results revealed that B19 NS1 protein significantly enhanced the TGF-beta/Smad fibrotic signaling by increasing the expressions of TGF-beta, Smad2/3, phosphorylated Smad2/3, Smad4 and Sp1. The consequent fibrosis-related proteins, PAI-1 and alpha-SMA, were also significantly induced in livers of NZB/W F1 mice receiving B19 NS1 protein. Accordingly, markedly increased collagen deposition was also observed in livers of NZB/W F1 mice receiving B19 NS1 protein. However, no significant difference was observed in livers of NZB/W F1 mice receiving B19 VP1u or VP2 as compared to the controls. These findings indicate that B19 NS1 plays a crucial role in exacerbating liver fibrosis in NZB/W F1 mice through enhancing the TGF-a/Smad fibrotic signaling. |Actins/genetics/metabolism[MESH] |Animals[MESH] |Collagen/genetics/metabolism[MESH] |ErbB Receptors/genetics/metabolism[MESH] |Female[MESH] |Humans[MESH] |Liver Cirrhosis/*genetics/metabolism/*virology[MESH] |Liver/metabolism/*pathology/virology[MESH] |Mice[MESH] |Mice, Inbred NZB[MESH] |Parvovirus B19, Human/*genetics/*metabolism[MESH] |Phosphorylation/genetics[MESH] |Plasminogen Activator Inhibitor 1/genetics/metabolism[MESH] |Signal Transduction/genetics[MESH] |Smad Proteins/genetics/metabolism[MESH]Exacerbating effects of human parvovirus B19 NS1 on liver fibrosis in (epmc).pdf DeepDyve Pubget Overpricing