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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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Journal ArticleDOI
Phosphodiesterase 5 inhibition blocks pressure overload-induced cardiac hypertrophy independent of the calcineurin pathway
Steven Hsu,Takahiro Nagayama,Norimichi Koitabashi,Manling Zhang,Liye Zhou,Djahida Bedja,Kathleen L. Gabrielson,Jeffery D. Molkentin,David A. Kass,Eiki Takimoto +9 more
TL;DR: PDE5A inhibition and its accompanying PKG activation blunt hypertrophy and improve heart function even without Cn activation is found.
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Comparison of heart rate variability in patients with chronic fatigue syndrome and controls
TL;DR: In this article, a two-stage tilt-table test was performed on 19 patients with chronic fatigue syndrome (CFS) and 11 healthy controls, and the results showed that upright tilt resulted in a similar decrease in HF power, increase in LF power, and increase in the LH/HF ratio.
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Key pathways associated with heart failure development revealed by gene networks correlated with cardiac remodeling
Zhong Gao,Andreas S. Barth,Deborah DiSilvestre,Fadi G. Akar,Yanli Tian,Antti J. Tanskanen,David A. Kass,Raimond L. Winslow,Gordon F. Tomaselli +8 more
TL;DR: A well-controlled canine model of tachycardia-induced HF is used to examine global gene expression in left ventricular myocardium with Affymetrix canine oligonucleotide arrays, concluding that the majority of tachypacing-induced transcriptional changes occur early after initiation of rapid ventricular pacing.
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Biochemical and Mechanical Dysfunction in a Mouse Model of Desmin-Related Myopathy
Alina Maloyan,Hanna Osinska,Jan Lammerding,Jan Lammerding,Richard T. Lee,Richard T. Lee,Oscar H. Cingolani,David A. Kass,John N. Lorenz,Jeffrey Robbins +9 more
TL;DR: It is indicated that oxypurinol treatment largely prevented mitochondrial deficiency in DRM but that contractility was not improved because of mechanical deficits in passive cytoskeletal stiffness.
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Bi-modal Dose-dependent Cardiac Response to Tetrahydrobiopterin in Pressure-overload Induced Hypertrophy and Heart Failure
An L. Moens,Elizabeth A. Ketner,Eiki Takimoto,Tim S. Schmidt,Charles A. O'Neill,Michael S. Wolin,Nicholas J. Alp,Keith M. Channon,David A. Kass +8 more
TL;DR: The dose response of daily oral synthetic sapropterin dihydrochloride on pre-established pressure-overload cardiac disease exposes a potential limitation for the clinical use of BH4, as variability of cellular redox and perhaps heart disease could produce a variable therapeutic window among individuals.