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10.1016/j.hrthm.2017.01.027 http://scihub22266oqcxt.onion/10.1016/j.hrthm.2017.01.027 C5403568!5403568!28111350     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28111350&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 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Heart+Rhythm 2017 ; 14 (5): 727-36 Nephropedia Template TP {{tp|p=28111350|t=2017. Anti-arrhythmic effects of interleukin-1 inhibition following myocardial infarction |pdf=|usr=}}{{28111350}} gab.com Text Anti-arrhythmic effects of interleukin-1 inhibition following myocardial infarction JO: Heart Rhythm http://www.kidney.de/pget.php?&tw=1&pmid=28111350 #FOAvip Background: Interleukin-1 beta (IL-1?) is a key regulator of the inflammatory response following myocardial infarction (MI), by modulating immune cell recruitment, cytokine production, and extracellular matrix turnover. Elevated levels of IL-1? are associated with adverse remodeling, and inhibition of IL-1 signaling following MI results in improved contractile function. Objective: The goal of this study was to determine if IL-1 signaling also contributes to post-MI arrhythmogenesis. Methods: MI was created in two murine models of elevated inflammation: atherosclerotic on Western diet or wild-type with a sub-septic dose of lipopolysaccharide. The role of IL-1? was assessed with the IL-1 receptor antagonist, anakinra (10mg/kg/day, starting 24h post-MI). Results: In vivo and ex vivo molecular imaging showed reduced myocardial inflammation following a 4-day course of anakinra treatment, despite no change in infarct size. At day 5 post-MI, high-speed optical mapping of transmembrane potential (Vm) and intracellular Ca2+ in isolated hearts revealed that IL-1? inhibition improved conduction velocity, reduced action potential duration dispersion, improved intracellular Ca2+ handling, decreased Vm and Ca2+ alternans magnitude, and reduced spontaneous and inducible ventricular arrhythmias. These functional improvements were linked to increased expression of connexin43 and sarcoplasmic reticulum Ca2+-ATPase (SERCA). Conclusions: This study revealed a novel mechanism for IL-1? in contributing to defective excitation-contraction coupling and arrhythmogenesis in the post-MI heart. Our results suggest that inhibition of IL-1 signaling post-MI may represent a novel anti-arrhythmic therapy. Twit Text FOAVip Anti-arrhythmic effects of interleukin-1 inhibition following myocardial infarction ????Heart Rhythm http://www.kidney.de/pget.php?&tw=1&pmid=28111350 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28111350 #FOAvip English Wikipedia <ref>{{Cite pmid|28111350}}</ref> Anti-arrhythmic effects of interleukin-1 inhibition following myocardial infarction #MMPMID28111350 De Jesus NM; Wang L; Lai J; Rigor RR; Francis Stuart SD; Bers DM; Lindsey ML; Ripplinger CM Heart Rhythm 2017[May]; 14 (5): 727-36 PMID28111350show ga Background: Interleukin-1 beta (IL-1?) is a key regulator of the inflammatory response following myocardial infarction (MI), by modulating immune cell recruitment, cytokine production, and extracellular matrix turnover. Elevated levels of IL-1? are associated with adverse remodeling, and inhibition of IL-1 signaling following MI results in improved contractile function. Objective: The goal of this study was to determine if IL-1 signaling also contributes to post-MI arrhythmogenesis. Methods: MI was created in two murine models of elevated inflammation: atherosclerotic on Western diet or wild-type with a sub-septic dose of lipopolysaccharide. The role of IL-1? was assessed with the IL-1 receptor antagonist, anakinra (10mg/kg/day, starting 24h post-MI). Results: In vivo and ex vivo molecular imaging showed reduced myocardial inflammation following a 4-day course of anakinra treatment, despite no change in infarct size. At day 5 post-MI, high-speed optical mapping of transmembrane potential (Vm) and intracellular Ca2+ in isolated hearts revealed that IL-1? inhibition improved conduction velocity, reduced action potential duration dispersion, improved intracellular Ca2+ handling, decreased Vm and Ca2+ alternans magnitude, and reduced spontaneous and inducible ventricular arrhythmias. These functional improvements were linked to increased expression of connexin43 and sarcoplasmic reticulum Ca2+-ATPase (SERCA). Conclusions: This study revealed a novel mechanism for IL-1? in contributing to defective excitation-contraction coupling and arrhythmogenesis in the post-MI heart. Our results suggest that inhibition of IL-1 signaling post-MI may represent a novel anti-arrhythmic therapy. äAnti-arrhythmic effects of interleukin-1 inhibition following myocardi(epmc).pdf DeepDyve Pubget Overpricing