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David A. Kass
Researcher at Johns Hopkins University School of Medicine
Publications - 605
Citations - 63963
David A. Kass is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Heart failure & Cardiac resynchronization therapy. The author has an hindex of 127, co-authored 580 publications receiving 58747 citations. Previous affiliations of David A. Kass include University of Pittsburgh & Johns Hopkins University.
Papers
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Journal ArticleDOI
Precardiac deletion of Numb and Numblike reveals renewal of cardiac progenitors
Lincoln T. Shenje,Lincoln T. Shenje,Peter Andersen,Hideki Uosaki,Laviel Fernandez,Peter P. Rainer,Peter P. Rainer,Gun Sik Cho,Dong Ik Lee,Weimin Zhong,Richard P. Harvey,David A. Kass,Chulan Kwon +12 more
TL;DR: It is shown that deletion of the ancient cell-fate regulator Numb (Nb) and its homologue Numblike (Nbl) depletes CPCs in second pharyngeal arches (PA2s) and is associated with an atrophic heart.
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Pathological Cardiac Hypertrophy Alters Intracellular Targeting of Phosphodiesterase Type 5 From Nitric Oxide Synthase-3 to Natriuretic Peptide Signaling
Manling Zhang,Eiki Takimoto,Dong Ik Lee,Celio X.C. Santos,Taishi Nakamura,Steven Hsu,Aiyang Jiang,Takahiro Nagayama,Djahida Bedja,Yuan Yuan,Philip Eaton,Ajay M. Shah,David A. Kass +12 more
TL;DR: In this paper, the authors hypothesized that PDE5 substrate selectivity is retargeted to blunt natriuretic peptide (NP) stimulated guanylyl cyclase.
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Usefulness of Soluble Endoglin as a Noninvasive Measure of Left Ventricular Filling Pressure in Heart Failure
Navin K. Kapur,Kevin S. Heffernan,Adil A. Yunis,Peter Parpos,Michael S. Kiernan,Nikhil A. Sahasrabudhe,Carey Kimmelstiel,David A. Kass,Richard H. Karas,Michael E. Mendelsohn +9 more
TL;DR: In this paper, the authors measured the sEng levels in 82 consecutive patients with suspected left ventricular dysfunction referred for determination of left heart filling pressures using cardiac catheterization and found that the seng levels correlated with the LVEDP (R = 0.689; p < 0.0001), irrespective of the LV ejection fraction.
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Pacemaker-induced transient asynchrony suppresses heart failure progression.
Jonathan A. Kirk,Khalid Chakir,Kyounghwan Lee,Edward Karst,Ronald J. Holewinski,Gianluigi Pironti,Richard S. Tunin,Iraklis Pozios,Theodore P. Abraham,Pieter P. de Tombe,Howard A. Rockman,Jennifer E. Van Eyk,Jennifer E. Van Eyk,Roger Craig,Taraneh Ghaffari Farazi,David A. Kass +15 more
TL;DR: It is shown that heart failure with synchronous contraction is improved by inducing dyssynchrony for 6 hours daily by right ventricular pacing using an intracardiac pacing device, in a process called pacemaker-induced transient asynchrony (PITA), and suggested that PITA could bring the benefits of CRT to the many heart failure patients with synchronOUS contraction who are not CRT candidates.
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Role of Calcium-Sensitive K+ Channels and Nitric Oxide in In Vivo Coronary Vasodilation From Enhanced Perfusion Pulsatility
TL;DR: K+Ca activation and NO comodulate in vivo pulsatility-stimulated coronary flow, supporting an important role of a hyperpolarization pathway in enhanced mechanovascular signaling.