Mechanisms of enhanced beta-adrenergic reserve from cardiac resynchronization therapy. - Wikidata - awgldk - TriplyDB

Mechanisms of enhanced beta-adrenergic reserve from cardiac resynchronization therapy.

Mechanisms of enhanced beta-adrenergic reserve from cardiac resynchronization therapy.

http://www.wikidata.org/entity/Q33771680

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The "missing" link between acute hemodynamic effect and clinical response Metabolic remodeling in moderate synchronous versus dyssynchronous pacing-induced heart failure: integrated metabolomics and proteomics study RGS2 is a primary terminator of β₂-adrenergic receptor-mediated G(i) signaling A computational approach to understanding the cardiac electromechanical activation sequence in the normal and failing heart, with translation to the clinical practice of CRT Electromechanical dyssynchrony and resynchronization of the failing heart Dysautonomia due to reduced cholinergic neurotransmission causes cardiac remodeling and heart failure.Electrical remodeling in the failing heart.β-Adrenergic receptor subtype signaling in heart: from bench to bedside.Regulation of GPCR signaling in hypertension.Improvement of left ventricular function under cardiac resynchronization therapy goes along with a reduced incidence of ventricular arrhythmia.Increased beta2-adrenoceptors in doxorubicin-induced cardiomyopathy in rat.Pathobiology of cardiac dyssynchrony and resynchronization.Assessment of distribution and evolution of mechanical dyssynchrony in a porcine model of myocardial infarction by cardiovascular magnetic resonance.Galphas-biased beta2-adrenergic receptor signaling from restoring synchronous contraction in the failing heart.A finer tuning of G-protein signaling through regulated control of RGS proteins.Basic science of cardiac resynchronization therapy: molecular and electrophysiological mechanisms Practical applicability of landiolol, an ultra-short-acting β1-selective blocker, for rapid atrial and ventricular tachyarrhythmias with left ventricular dysfunction Spatial control of the βAR system in heart failure: the transverse tubule and beyond.The zebrafish as a novel animal model to study the molecular mechanisms of mechano-electrical feedback in the heart.Pacemaker-induced transient asynchrony suppresses heart failure progression Mechanistic insight into prolonged electromechanical delay in dyssynchronous heart failure: a computational study Pathological ventricular remodeling: therapies: part 2 of 2.Cardiac resynchronization sensitizes the sarcomere to calcium by reactivating GSK-3β.Functional role, mechanisms of regulation, and therapeutic potential of regulator of G protein signaling 2 in the heart.The molecular fingerprint of cardiac dyssynchrony and cardiac resynchronization therapy.Biventricular pacing: current trends and future strategies.Animal models of dyssynchrony.Cellular electrophysiological abnormalities in dyssynchronous hearts and during CRT.Electrical remodeling in dyssynchrony and resynchronization.Transcriptome, proteome, and metabolome in dyssynchronous heart failure and CRT.Cardiac resynchronization therapy: a breakthrough in heart failure management.Strategies to improve cardiac resynchronization therapy.Cardiac resynchronization therapy: history, present status, and future directions.Cellular and Molecular Aspects of Dyssynchrony and Resynchronization.Cardiac dyssynchrony and response to cardiac resynchronisation therapy in heart failure: can genetic predisposition play a role?Heart rate and dyssynchrony in patients with cardiac resynchronization therapy: a pilot study.Cardiac resynchronization therapy update: evolving indications, expanding benefit?Cardiac resynchronization therapy restores sympathovagal balance in the failing heart by differential remodeling of cholinergic signaling.Measurement of Strain in Cardiac Myocytes at Micrometer Scale Based on Rapid Scanning Confocal Microscopy and Non-Rigid Image Registration.Cardiac resynchronization therapy corrects dyssynchrony-induced regional gene expression changes on a genomic level.

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P2860

Mechanisms of enhanced beta-adrenergic reserve from cardiac resynchronization therapy.

http://www.wikidata.org/entity/Q33771680

description

2009 nî lūn-bûn

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2009 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2009 թվականի փետրվարին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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name

Mechanisms of enhanced beta-adrenergic reserve from cardiac resynchronization therapy.

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Mechanisms of enhanced beta-adrenergic reserve from cardiac resynchronization therapy.

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Mechanisms of enhanced beta-adrenergic reserve from cardiac resynchronization therapy.

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Mechanisms of enhanced beta-adrenergic reserve from cardiac resynchronization therapy.

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Mechanisms of enhanced beta-adrenergic reserve from cardiac resynchronization therapy.

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Mechanisms of enhanced beta-adrenergic reserve from cardiac resynchronization therapy.

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Mechanisms of enhanced beta-adrenergic reserve from cardiac resynchronization therapy.

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David A Kass

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Edwin W Lai

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Gordon F Tomaselli

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Kathryn M Jaques-Robinson

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Khalid Chakir

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Richard S Tunin

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Rui-ping Xiao

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Samantapudi K Daya

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Takeshi Aiba

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Theodore P Abraham

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P2860

Heart Disease and Stroke Statistics--2008 Update: A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee

Opposing effects of beta(1)- and beta(2)-adrenergic receptors on cardiac myocyte apoptosis : role of a pertussis toxin-sensitive G protein

Cardioprotection specific for the G protein Gi2 in chronic adrenergic signaling through beta 2-adrenoceptors.

Myocardial beta-adrenergic receptor function during the development of pacing-induced heart failure

Expression of ten RGS proteins in human myocardium: functional characterization of an upregulation of RGS4 in heart failure.

Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure.

The effect of cardiac resynchronization on morbidity and mortality in heart failure.

The beta-adrenergic receptor kinase in heart failure.

What is the role of beta-adrenergic signaling in heart failure?

Inhibitory G-proteins and their role in desensitization of the adenylyl cyclase pathway in heart failure.

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