scispace - formally typeset
S

Stanley Nattel

Researcher at Montreal Heart Institute

Publications -  802
Citations -  72437

Stanley Nattel is an academic researcher from Montreal Heart Institute. The author has contributed to research in topics: Atrial fibrillation & Heart failure. The author has an hindex of 132, co-authored 778 publications receiving 65700 citations. Previous affiliations of Stanley Nattel include Mayo Clinic & Brigham and Women's Hospital.

Papers
More filters
Journal ArticleDOI

Ectopic expression of S28A-mutated Histone H3 modulates longevity, stress resistance and cardiac function in Drosophila.

TL;DR: A critical role is established for H3S28 phosphorylation in vivo for life span, stress resistance, cardiac and mitochondrial function in Drosophila, and this findings may pave the way for H 3S28osphorylation as a putative target to treat stress-related disorders such as heart failure.
Journal ArticleDOI

Pharmacological elimination of motion artifacts during optical imaging of cardiac tissues: Is blebbistatin the answer?

TL;DR: High-resoluion optical mapping has become a common research tool in asic cardiac electrophysiology, especially in the investigaion of Electrophysiologic mechanisms by which convenional electrical recordings are hampered by inadequate reslution or by a lack of precise information on repolarization.
Journal ArticleDOI

Distinct genomic replacements from Lewis correct diastolic dysfunction, attenuate hypertension, and reduce left ventricular hypertrophy in Dahl salt-sensitive rats.

TL;DR: Novel prognostic, diagnostic and therapeutic strategies for hypertensive diastolic heart failure likely emerge from this work, as genes present in the replaced chromosome segments of the two positive congenic strains are not commonly known to affect blood pressure, diastolics function or left ventricular mass.
Journal ArticleDOI

The Kv4.2 N-terminal restores fast inactivation and confers KChIP2 modulatory effects on N-terminal-deleted Kv1.4 channels

TL;DR: Substitution of the Kv4.4 chimeric subunits significantly increased current expression and slowed inactivation without altering the rate of recovery from inactivation, indicating the ability of Kv1.4 subunits to display a variety of properties of K v4.2 N-terminal, including inactivation time-dependence, accelerated recovery from Inactivation and interaction with KChIP2, to Kv 1.4.
Journal ArticleDOI

Demonstration of an Inward Na+‐Ca2+ Exchange Current in Adult Human Atrial Myocytes

TL;DR: Whether an electrogenic INa.Ca is present in adult human atrial myocytes, and if so, whether it contributes to APD is determined.