So little source, so much sink: requirements for afterdepolarizations to propagate in tissue. - Wikidata - awgldk - TriplyDB

So little source, so much sink: requirements for afterdepolarizations to propagate in tissue.

So little source, so much sink: requirements for afterdepolarizations to propagate in tissue.

http://www.wikidata.org/entity/Q34099038

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Na⁺ transport in the normal and failing heart - remember the balance Computational Representations of Myocardial Infarct Scars and Implications for Arrhythmogenesis The infrahisian conduction system and endocavitary cardiac structures: relevance for the invasive electrophysiologist Mechanisms of ventricular arrhythmias: from molecular fluctuations to electrical turbulence Stochastic spontaneous calcium release events trigger premature ventricular complexes by overcoming electrotonic load Pacemaker Created in Human Ventricle by Depressing Inward-Rectifier K⁺ Current: A Simulation Study A Computational Study of the Factors Influencing the PVC-Triggering Ability of a Cluster of Early Afterdepolarization-Capable Myocytes Role of sodium and calcium dysregulation in tachyarrhythmias in sudden cardiac death.Light-based Approaches to Cardiac Arrhythmia Research: From Basic Science to Translational Applications Ionic mechanisms of arrhythmogenesis Perspective: a dynamics-based classification of ventricular arrhythmias Calsequestrin mutations and catecholaminergic polymorphic ventricular tachycardia Microdomain-Specific Modulation of L-Type Calcium Channels Leads to Triggered Ventricular Arrhythmia in Heart Failure.Mechanisms Underlying the Emergence of Post-acidosis Arrhythmia at the Tissue Level: A Theoretical Study.Inflammatory dilated cardiomyopathy in Abcg5-deficient mice.Local Gradients in Electrotonic Loading Modulate the Local Effective Refractory Period: Implications for Arrhythmogenesis in the Infarct Border Zone.The Electrogenic Na+/K+ Pump Is a Key Determinant of Repolarization Abnormality Susceptibility in Human Ventricular Cardiomyocytes: A Population-Based Simulation Study.Dynamic conduction and repolarisation changes in early arrhythmogenic right ventricular cardiomyopathy versus benign outflow tract ectopy demonstrated by high density mapping & paced surface ECG analysis.A multiscale computational modelling approach predicts mechanisms of female sex risk in the setting of arousal-induced arrhythmias.Depolarization of cardiac membrane potential synchronizes calcium sparks and waves in tissue Nonlinear and Stochastic Dynamics in the Heart Cardiac arrhythmia induced by genetic silencing of 'funny' (f) channels is rescued by GIRK4 inactivation The timing statistics of spontaneous calcium release in cardiac myocytes.Complex excitation dynamics underlie polymorphic ventricular tachycardia in a transgenic rabbit model of long QT syndrome type 1 Variations in local calcium signaling in adjacent cardiac myocytes of the intact mouse heart detected with two-dimensional confocal microscopy.Cardiac fibrosis as a determinant of ventricular tachyarrhythmias.SR calcium handling dysfunction, stress-response signaling pathways, and atrial fibrillation.Spontaneous atrial fibrillation initiated by tyramine in canine atria with increased sympathetic nerve sprouting Neuronal Na+ channel blockade suppresses arrhythmogenic diastolic Ca2+ release.Structural heterogeneity modulates effective refractory period: a mechanism of focal arrhythmia initiation Targeting the late component of the cardiac L-type Ca2+ current to suppress early afterdepolarizations Arrhythmogenic consequences of myofibroblast-myocyte coupling The statistics of calcium-mediated focal excitations on a one-dimensional cable Glycolytic inhibition causes spontaneous ventricular fibrillation in aged hearts.Optogenetic determination of the myocardial requirements for extrasystoles by cell type-specific targeting of ChannelRhodopsin-2.Criticality in intracellular calcium signaling in cardiac myocytes Enhanced sensitivity of aged fibrotic hearts to angiotensin II- and hypokalemia-induced early afterdepolarization-mediated ventricular arrhythmias.Fibrosis in Atrial Fibrillation - Role of Reactive Species and MPO.Delayed afterdepolarizations generate both triggers and a vulnerable substrate promoting reentry in cardiac tissue Synchronization of early afterdepolarizations and arrhythmogenesis in heterogeneous cardiac tissue models.

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P2860

So little source, so much sink: requirements for afterdepolarizations to propagate in tissue.

http://www.wikidata.org/entity/Q34099038

description

2010 nî lūn-bûn

@nan

2010 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի սեպտեմբերին հրատարակված գիտական հոդված

@hy

2010年の論文

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2010年論文

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2010年論文

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2010年論文

@zh-hk

2010年論文

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2010年論文

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2010年论文

@wuu

name

So little source, so much sink ...... ations to propagate in tissue.

@ast

So little source, so much sink ...... ations to propagate in tissue.

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So little source, so much sink ...... ations to propagate in tissue.

@nl

type

label

So little source, so much sink ...... ations to propagate in tissue.

@ast

So little source, so much sink ...... ations to propagate in tissue.

@en

So little source, so much sink ...... ations to propagate in tissue.

@nl

prefLabel

So little source, so much sink ...... ations to propagate in tissue.

@ast

So little source, so much sink ...... ations to propagate in tissue.

@en

So little source, so much sink ...... ations to propagate in tissue.

@nl

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J.BPJ.2010.06.042

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Biophysical Journal

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So little source, so much sink ...... ations to propagate in tissue.

@en

P2093

Alan Garfinkel

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Daisuke Sato

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James N Weiss

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Yuanfang Xie

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Zhilin Qu

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P2860

Genesis of ectopic waves: role of coupling, automaticity, and heterogeneity

Synchronization of chaotic early afterdepolarizations in the genesis of cardiac arrhythmias.

Diastolic intracellular calcium-membrane voltage coupling gain and postshock arrhythmias: role of purkinje fibers and triggered activity.

Unidirectional block between isolated rabbit ventricular cells coupled by a variable resistance.

Regulation of cardiac sarcoplasmic reticulum Ca release by luminal [Ca] and altered gating assessed with a mathematical model.

A condition for setting off ectopic waves in computational models of excitable cells.

A rabbit ventricular action potential model replicating cardiac dynamics at rapid heart rates

Cardiac alternans induced by fibroblast-myocyte coupling: mechanistic insights from computational models.

Spontaneous calcium release in tissue from the failing canine heart.

Microfibrosis produces electrical load variations due to loss of side-to-side cell connections: a major mechanism of structural heart disease arrhythmias.

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5

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2010-09-01T00:00:00Z

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46147415

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20816052

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2931729

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