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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.
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Cortisol-mediated synchrinization of circadian rhythm in urinary potassium excretion.
TL;DR: Results indicate that the cirdacian rhythm of plasma cortisol concentration acts as an internal mediator in the circadian timing system, synchronizing a potentially autonomous oscillation in renal potassium excretion to environmental time cues and to other circadian rhythms within the animal.
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Leveraging Signaling Pathways to Treat Heart Failure With Reduced Ejection Fraction.
TL;DR: A review of existing approaches for the treatment of heart failure with reduced ejection fraction due to systolic dysfunction can be found in this article, where the focus is on signaling pathways that are tractable for therapeutic manipulation.
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Force-frequency relation in patients with left ventricular hypertrophy and failure
TL;DR: Patients with genetic and acquired left ventricular hypertrophy have reduced chamber compliance, delayed relaxation, and small and often deformed cavities all conspire to limit pump performance and reserve capacity while raising pulmonary venous pressures.
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Role of calcitonin gene-related peptide (CGRP) in chronic hypoxia-induced pulmonary hypertension in the mouse. Influence of gene transfer in vivo.
Trinity J. Bivalacqua,Albert L. Hyman,Philip J. Kadowitz,Nazareno Paolocci,David A. Kass,Hunter C. Champion +5 more
TL;DR: In this paper, an adenoviral vector encoding CGRP (AdRSVCGRP) was used to examine the effects of in vivo gene transfer to the lung on increases in PVR, right ventricular mass, and pulmonary vascular remodeling that occurs in chronic hypoxia in the mouse.
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Dual Labeling Biotin Switch Assay to Reduce Bias Derived From Different Cysteine Subpopulations: A Method to Maximize S-Nitrosylation Detection.
Heaseung Sophia Chung,Heaseung Sophia Chung,Christopher I. Murray,Christopher I. Murray,Vidya Venkatraman,Vidya Venkatraman,Erin L. Crowgey,Peter P. Rainer,Robert N. Cole,Ryan Bomgarden,John C. Rogers,Wayne Balkan,Joshua M. Hare,David A. Kass,Jennifer E. Van Eyk +14 more
TL;DR: In this paper, the authors investigated potential labeling bias in the existing methods with a single tag to detect SNO, explore if there are distinct cysteine subpopulations, and then, develop a strategy to maximize the coverage of SNO proteome.