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.

10.1016/j.jtcvs.2015.11.031 http://scihub22266oqcxt.onion/10.1016/j.jtcvs.2015.11.031 C4805528!4805528!26769537     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26769537&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 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Thorac+Cardiovasc+Surg 2016 ; 151 (4): 1191-1200.e3 Nephropedia Template TP {{tp|p=26769537|t=2016. Mitigation of Myocardial Fibrosis by Molecular Cardiac Surgery Mediated Gene Overexpression |pdf=|usr=}}{{26769537}} gab.com Text Mitigation of Myocardial Fibrosis by Molecular Cardiac Surgery Mediated Gene Overexpression JO: J Thorac Cardiovasc Surg http://www.kidney.de/pget.php?&tw=1&pmid=26769537 #FOAvip Objective: Heart failure is accompanied by upregulation of transforming growth factor beta signaling, accumulation of collagen and dysregulation of sarcoplasmic reticulum calcium ATPase cardiac isoform 2a (SERCA2a). We examined the fibrotic response in small and large myocardial infarct and the effect of overexpressing the SERCA2a gene. Methods: Ischemic cardiomyopathy was induced via creation of large infarct or small infarct in 26 sheep. All animals were divided into four groups: small infarct; large infarct with heart failure; gene treated (large infarct with heart failure followed by AAV1.SERCA2a gene construct transfer by molecular cardiac surgery with recirculating delivery); and control group. Results: Heart failure was significantly less pronounced in the gene treated and small infarct groups than in the large infarct group. Expression of transforming growth factor beta signaling components was significantly higher in large infarct compared to small infarct or gene treated. Further, both the angiotensin II type 1 receptor and angiotensin II were significantly elevated in small and large infarcts, while gene treatment diminished this effect. Active fibrosis with de novo collagen synthesis was evident in large infarct, while small infarct and gene treatment groups showed less fibrosis with a lower ratio of de novo to mature collagen. Conclusions: The data presented supports that the progression of fibrosis is mediated through increased transforming growth factor beta and angiotensin II signaling, which is mitigated by increased SERCA2a gene expression. Twit Text FOAVip Mitigation of Myocardial Fibrosis by Molecular Cardiac Surgery Mediated Gene Overexpression ????J Thorac Cardiovasc Surg http://www.kidney.de/pget.php?&tw=1&pmid=26769537 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26769537 #FOAvip English Wikipedia <ref>{{Cite pmid|26769537}}</ref> Mitigation of Myocardial Fibrosis by Molecular Cardiac Surgery Mediated Gene Overexpression #MMPMID26769537 Katz MG; Brandon-Warner E; Fargnoli AS; Williams RD; Kendle AP; Hajjar RJ; Schrum LW; Bridges CR J Thorac Cardiovasc Surg 2016[Apr]; 151 (4): 1191-1200.e3 PMID26769537show ga Objective: Heart failure is accompanied by upregulation of transforming growth factor beta signaling, accumulation of collagen and dysregulation of sarcoplasmic reticulum calcium ATPase cardiac isoform 2a (SERCA2a). We examined the fibrotic response in small and large myocardial infarct and the effect of overexpressing the SERCA2a gene. Methods: Ischemic cardiomyopathy was induced via creation of large infarct or small infarct in 26 sheep. All animals were divided into four groups: small infarct; large infarct with heart failure; gene treated (large infarct with heart failure followed by AAV1.SERCA2a gene construct transfer by molecular cardiac surgery with recirculating delivery); and control group. Results: Heart failure was significantly less pronounced in the gene treated and small infarct groups than in the large infarct group. Expression of transforming growth factor beta signaling components was significantly higher in large infarct compared to small infarct or gene treated. Further, both the angiotensin II type 1 receptor and angiotensin II were significantly elevated in small and large infarcts, while gene treatment diminished this effect. Active fibrosis with de novo collagen synthesis was evident in large infarct, while small infarct and gene treatment groups showed less fibrosis with a lower ratio of de novo to mature collagen. Conclusions: The data presented supports that the progression of fibrosis is mediated through increased transforming growth factor beta and angiotensin II signaling, which is mitigated by increased SERCA2a gene expression. äMitigation of Myocardial Fibrosis by Molecular Cardiac Surgery Mediate(epmc).pdf DeepDyve Pubget Overpricing