Results 251 to 260 of about 100,632 (325)

A model of β‐adrenergic stimulation in human ventricular cells for tissue‐scale simulations of sympathetically modulated tachycardias

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Modelling β‐adrenergic stimulation in sympathetically remodelled ventricular substrates. Myocardial infarction could result in sympathetic remodelling in ventricular tissues, which affects arrhythmia dynamics. However sympathetic remodelling is challenging to control experimentally; therefore we created an ionic model that ...
Kelly Zhang   +3 more
wiley   +1 more source

Mechanistic insights into sex differences in atrial electrophysiology and arrhythmia vulnerability through sex‐specific computational models

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Sex‐specific models of the human atrial myocyte in normal sinus rhythm (nSR) and chronic atrial fibrillation (cAF) revealed increased alternans susceptibility in cAF males and DADs in females, driven primarily by ICaL and ryanodine receptor remodelling.
Nathaniel T. Herrera   +6 more
wiley   +1 more source

Energetic microdomains and the vascular control of neuronal and muscle excitability: Toward a unified model

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend The capillary–mitochondria–ion channel (CMIC) axis scales structural resources to match functional workload. (Left) In settings of restricted energetic capacity (e.g. cortical neurons), sparse capillary networks and modest mitochondrial pools set a lower energetic ceiling, sufficient to support phasic, low‐workload excitability. (
L. Fernando Santana, Scott Earley
wiley   +1 more source

Small‐conductance Ca2⁺‐activated K⁺ channels in cardiac excitation–contraction coupling: Bridging mitochondria, sarcolemma and antiarrhythmic therapy

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Mitochondrial SK channel enhancement reduces cardiac arrhythmia trigger. Spontaneous sarcoplasmic reticulum (SR) Ca2+ release via hyperactive RyR2s underlies an increased arrhythmia trigger, promoting early and delayed afterdepolarizations during stress. Hyperactive RyR2s causes rise in cytosolic [Ca2+] during diastole. Clearance
Dmitry Terentyev   +7 more
wiley   +1 more source

Caenorhabditis elegans as an in vivo model system for human inherited primary arrhythmia syndromes

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Most genes involved in inherited primary arrhythmia syndromes (IPAS) are conserved in Caenorhabditis elegans, where genetic manipulation enables functional characterization of variants, identification of regulatory proteins, and in vivo drug testing.
Antoine Delinière   +6 more
wiley   +1 more source

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