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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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Anti–Tumor Necrosis Factor-α Antibody Limits Heart Failure in a Transgenic Model

TL;DR: Blockade of TNF-&agr; bioactivity by antibody therapy may both preserve cardiac function and partially reverse pathological changes in congestive heart failure.
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Effects of Tumor Necrosis Factor Gene Polymorphisms on Patients With Congestive Heart Failure

TL;DR: The prevalence of TNF gene polymorphisms in CHF patients and the correlation of genotypes to in vivo TNF-α levels were studied and there were no differences in the TNF allele frequencies between CHF and control subjects.
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Interleukin-1β Inhibits Phospholamban Gene Expression in Cultured Cardiomyocytes

TL;DR: It is demonstrated that IL-1 beta alters the expression of phospholamban, a key regulator of cardiac contractility, at both the transcript and protein levels, which suggest novel mechanisms by which IL- 1 beta may modify cardiac function.
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Aldosterone Synthase Promoter Polymorphism Predicts Outcome in African Americans With Heart Failure : Results From the A-HeFT Trial

TL;DR: The aldosterone synthase promoter -344C allele linked to higher ald testosterone levels is associated with poorer event-free survival in blacks with heart failure, and the role of a Aldosterone receptor antagonists in diminishing this apparent genetic risk remains to be explored.
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Coxsackievirus B3 Induces T Regulatory Cells, Which Inhibit Cardiomyopathy in Tumor Necrosis Factor-α Transgenic Mice

TL;DR: The low TNF-α response during H310A1 infections is likely responsible for the T regulatory cell response in these animals, which reduces heart size and cardiac inflammation corresponding to the activation of CD4+CD25+FoxP3+ (T regulatory cells).