Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1097/SHK.0000000000000231 http://scihub22266oqcxt.onion/10.1097/SHK.0000000000000231 C4199874!4199874!25004066     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25004066&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 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 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\25004066.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Shock 2014 ; 42 (5): 424-31 Nephropedia Template TP {{tp|p=25004066|t=2014. Hepatocellular heme oxygenase-1: a potential mechanism of erythropoietin-mediated protection after liver ischemia-reperfusion injury |pdf=|usr=}}{{25004066}} gab.com Text Hepatocellular heme oxygenase-1: a potential mechanism of erythropoietin-mediated protection after liver ischemia-reperfusion injury JO: Shock http://www.kidney.de/pget.php?&tw=1&pmid=25004066 #FOAvip Hepatic ischemia-reperfusion (IR) results in progressive injury, initiated by oxidative stress during ischemia and compounded by cytokine-mediated inflammation during reperfusion. Recovery requires strict regulation of these events. Recombinant human erythropoietin (rhEPO) is thought to mitigate hepatocellular IR injury by altering the non-parenchymal liver microenvironment. This study sought to identify additional mechanisms whereby rhEPO is protective after liver IR injury.Methods: Mice were treated with rhEPO (4units/gm SQ) at the onset of partial liver ischemia and assessed for transaminase and histologic injury at intervals after reperfusion. Induction of cytokines, activation of signal transducers and activators of transcription (STATs), suppressors of cytokine signaling (Socs1, Socs3, Cis), caspase-3 activation, and heme oxygenase-1 (HO-1) expression were assessed in post-ischemic liver. Effects of rhEPO stimulation were further characterized in whole liver lysates from mice undergoing rhEPO injection alone and in cultured AML-12 hepatocytes. Results: rhEPO treatment at the onset of severe (90min) hepatic IR confirmed commensurate biochemical and histological protection without affecting tissue cytokine levels. Although Socs3 and STAT5 activation were induced in normal liver after in vivo rhEPO injection, this treatment did not augment expression beyond that seen with IR alone, and neither was induced in cultured hepatocytes treated with rhEPO. rhEPO inhibited caspase-3 activation in non-parenchymal cells, while hepatocellular HO-1 was rapidly induced both in vivo and in vitro with rhEPO treatment. Conclusion: These data suggest HO-1 as a potent mechanism of rhEPO-mediated protection after liver IR, which involves both direct hepatocellular and non-parenchymal mechanisms. Twit Text FOAVip Hepatocellular heme oxygenase-1: a potential mechanism of erythropoietin-mediated protection after liver ischemia-reperfusion injury ????Shock http://www.kidney.de/pget.php?&tw=1&pmid=25004066 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25004066 #FOAvip English Wikipedia <ref>{{Cite pmid|25004066}}</ref> Hepatocellular heme oxygenase-1: a potential mechanism of erythropoietin-mediated protection after liver ischemia-reperfusion injury #MMPMID25004066 Riehle KJ; Hoagland V; Benz W; Campbell JS; Liggitt DH; Langdale LA Shock 2014[Nov]; 42 (5): 424-31 PMID25004066show ga Hepatic ischemia-reperfusion (IR) results in progressive injury, initiated by oxidative stress during ischemia and compounded by cytokine-mediated inflammation during reperfusion. Recovery requires strict regulation of these events. Recombinant human erythropoietin (rhEPO) is thought to mitigate hepatocellular IR injury by altering the non-parenchymal liver microenvironment. This study sought to identify additional mechanisms whereby rhEPO is protective after liver IR injury.Methods: Mice were treated with rhEPO (4units/gm SQ) at the onset of partial liver ischemia and assessed for transaminase and histologic injury at intervals after reperfusion. Induction of cytokines, activation of signal transducers and activators of transcription (STATs), suppressors of cytokine signaling (Socs1, Socs3, Cis), caspase-3 activation, and heme oxygenase-1 (HO-1) expression were assessed in post-ischemic liver. Effects of rhEPO stimulation were further characterized in whole liver lysates from mice undergoing rhEPO injection alone and in cultured AML-12 hepatocytes. Results: rhEPO treatment at the onset of severe (90min) hepatic IR confirmed commensurate biochemical and histological protection without affecting tissue cytokine levels. Although Socs3 and STAT5 activation were induced in normal liver after in vivo rhEPO injection, this treatment did not augment expression beyond that seen with IR alone, and neither was induced in cultured hepatocytes treated with rhEPO. rhEPO inhibited caspase-3 activation in non-parenchymal cells, while hepatocellular HO-1 was rapidly induced both in vivo and in vitro with rhEPO treatment. Conclusion: These data suggest HO-1 as a potent mechanism of rhEPO-mediated protection after liver IR, which involves both direct hepatocellular and non-parenchymal mechanisms. äHepatocellular heme oxygenase-1: a potential mechanism of erythropoiet(epmc).pdf DeepDyve Pubget Overpricing