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Arthur M. Feldman
Researcher at Thomas Jefferson University
Publications - 296
Citations - 41891
Arthur M. Feldman is an academic researcher from Thomas Jefferson University. The author has contributed to research in topics: Heart failure & Tumor necrosis factor alpha. The author has an hindex of 79, co-authored 289 publications receiving 40355 citations. Previous affiliations of Arthur M. Feldman include Johns Hopkins University School of Medicine & Valley Hospital.
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Myocardial infarction associated with a myocardial bridge.
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Altered expression of α-subunits of G proteins in failing human hearts
TL;DR: The results suggest that alterations at the level of transcription as well as post-translational modifications can affect the activities of transmembrane signaling proteins in chronic congestive heart failure.
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Resistance of Akt kinases to dephosphorylation through ATP-dependent conformational plasticity
Tung O. Chan,Jin Zhang,Ulrich Rodeck,John M. Pascal,Roger S. Armen,Maureen Spring,Calin Dan Dumitru,Valerie D. Myers,Xue Li,Joseph Y. Cheung,Arthur M. Feldman +10 more
TL;DR: It is described that targeting Akt kinase to the cell membrane markedly reduced sensitivity of phosphorylated Akt to dephosphorylation by protein phosphatase 2A, providing an explanation for the “paradoxical” Akt hyperph phosphorylation induced by ATP-competitive inhibitor, A-443654.
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Impact of cardiac resynchronization therapy on exercise performance, functional capacity, and quality of life in systolic heart failure with QRS prolongation: COMPANION trial sub-study.
Teresa De Marco,Eugene E. Wolfel,Arthur M. Feldman,Brian D. Lowes,Michael B. Higginbotham,Jalal K. Ghali,Lynne E. Wagoner,Philip C. Kirlin,Jerry D. Kennett,Satish Goel,Leslie A. Saxon,John P. Boehmer,David E. Mann,Elizabeth Galle,Fred Ecklund,Patrick Yong,Michael R. Bristow +16 more
TL;DR: CRT patients with moderate to advanced symptoms of systolic heart failure and prolonged QRS intervals benefit from the addition of CRT to OPT in terms of exercise capacity, functional status, and QOL.
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MMP inhibition modulates TNF-α transgenic mouse phenotype early in the development of heart failure
TL;DR: The results suggest that MMP activation may play a critical role in changes of myocardial function through the remodeling of extracellular matrix, and MMP inhibition may serve as a potential therapeutic strategy for heart failure, albeit within a narrow window during the development of heart failure.