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Victor A. Maltsev

Researcher at National Institutes of Health

Publications -  127
Citations -  7919

Victor A. Maltsev is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Diastolic depolarization & Sinoatrial node. The author has an hindex of 46, co-authored 119 publications receiving 7231 citations. Previous affiliations of Victor A. Maltsev include Henry Ford Hospital & Ford Motor Company.

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A Coupled SYSTEM of Intracellular Ca2+ Clocks and Surface Membrane Voltage Clocks Controls the Timekeeping Mechanism of the Heart’s Pacemaker

TL;DR: Evidence is examined that forms the basis of this coupled-clock system concept in cardiac SANCs, where G protein-coupled receptors signaling creates pacemaker flexibility, ie, effects changes in the rhythmic action potential firing rate, by impacting on these very same factors that regulate robust basal coupled- clock system function.
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Embryonic stem cells differentiate in vitro into cardiomyocytes representing sinusnodal, atrial and ventricular cell types

TL;DR: The presented ES cell differentiation system permits the investigation of commitment and differentiation of embryonic cells into the cardiomyogenic lineage in vitro.
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Cardiomyocytes differentiated in vitro from embryonic stem cells developmentally express cardiac-specific genes and ionic currents.

TL;DR: The data demonstrate that ES cell-derived cardiomyocytes represent a unique model to investigate the early cardiac development and permit pharmacological/toxicological studies in vitro.
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Embryonic stem cells: a model to study structural and functional properties in cardiomyogenesis

TL;DR: Progress in this field is hampered by the inability to study cardiomyocytes from early, embryonal hearts because of their very small size and because of the lack of cardiac cell lines that mimic various stages of cardiac development.
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Novel, Ultraslow Inactivating Sodium Current in Human Ventricular Cardiomyocytes

TL;DR: Cardiomyocytes isolated from normal and explanted failing human hearts express INaL characterized by an ultraslow voltage-independent inactivation and reactivation, which is independent of the peak transient Na+ current.