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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.
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Ectopic expression of S28A-mutated Histone H3 modulates longevity, stress resistance and cardiac function in Drosophila.
Julius P. Joos,Ali R. Saadatmand,Christian Schnabel,Ivana Viktorinová,Theresa Brand,Michael Kramer,Stanley Nattel,Dobromir Dobrev,Pavel Tomancak,Johannes Backs,Petra Kleinbongard,Gerd Heusch,Kristina Lorenz,Edmund Koch,Silvio Weber,Ali El-Armouche +15 more
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.
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Pharmacological elimination of motion artifacts during optical imaging of cardiac tissues: Is blebbistatin the answer?
Danshi Li,Stanley Nattel +1 more
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.
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Distinct genomic replacements from Lewis correct diastolic dysfunction, attenuate hypertension, and reduce left ventricular hypertrophy in Dahl salt-sensitive rats.
Alan Y. Deng,Stanley Nattel,Yanfen Shi,Nathalie L'Heureux,Sophie Cardin,Annie Ménard,Julie Roy,Jean-Claude Tardif +7 more
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.
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The Kv4.2 N-terminal restores fast inactivation and confers KChIP2 modulatory effects on N-terminal-deleted Kv1.4 channels
Marc Pourrier,Marc Pourrier,Daniel Herrera,Daniel Herrera,Ricardo Caballero,Ricardo Caballero,Gernot Schram,Zhiguo Wang,Stanley Nattel,Stanley Nattel +9 more
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.
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Demonstration of an Inward Na+‐Ca2+ Exchange Current in Adult Human Atrial Myocytes
Gui-Rong Li,Stanley Nattel +1 more
TL;DR: Whether an electrogenic INa.Ca is present in adult human atrial myocytes, and if so, whether it contributes to APD is determined.