We prospectively examined whether two physiological parameters, ictal peak HR and postictal suppression in ictal EEG, during every session, including those with abortive seizure, predicted ECT efficacy. Ictal peak HR and postictal suppression index were analyzed in 53 consecutive inpatients with depression using generalized estimating equations analysis, which corrects for the repeated nature of the observations. The peak HR and postictal suppression index were associated with therapeutic efficacy in remitters during sessions with adequate seizure. The physiological characteristics

check details of the remitters included lower peak HR, lower stimulus energy, and higher postictal suppression index. However, these results could not be generalized, and are limited to non-atropine

conditions and bilateral ECT. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“The this website complex pathophysiological interactions between heart and kidney diseases are collectively known as cardiorenal syndrome. The renin angiotensin system (RAS) may have a pivotal role in the development of cardiorenal syndrome. The aim of this study was to elucidate the RAS activity responsible for adverse post-infarction remodeling and prognosis in mice with renal failure. To establish the type IV cardiorenal syndrome model, 5/6 nephrectonny (NIX) was performed in a surgical procedure, followed by the induction of myocardial ischemia (MI) by a coronary artery

ligation 4 weeks later. NTX and MI resulted in deteriorated left ventricular remodeling and RAS activation, which was improved by an aliskiren that appeared to be independent of renal function and blood pressure (BP). Moreover, MI induced in renin and angiotensinogen double-transgenic (Tg) mice showed comparable effects to MI plus NTX mice, including advanced ventricular remodeling and enhancement of RAS, oxidative stress, and monocytes Rebamipide chemoattractant protein (MCP)-1. Aliskiren suppressed these changes in the MI-induced Tg mice. In in vitro study, Nox2 expression was elevated by the stimulation of plasma from NTX mice in isolated neonatal cardiomyocytes. However, Nox2 upregulation was negated when we administered plasma from aliskiren-treated-NTX mice or isolated cardiomyocytes from AT1-deficient mice. Primary mononuclear cells also showed an upregulation in the expression of Nox2 and MCP-1 by stimulation with plasma from NIX mice. Our data suggest that renal disorder results in ventricular dysfunction and deteriorates remodeling after MI through excessive RAS activation. Moreover, renin inhibition improved the changes caused by cardiorenal syndrome. Laboratory Investigation (2012) 92, 1766-1776; doi:10.1038/labinvest.2012.