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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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Journal ArticleDOI

Decreased bioactivity of the guanine nucleotide-binding protein that stimulates adenylate cyclase in hearts from cardiomyopathic Syrian hamsters

P D Kessler, +3 more
- 01 Jul 1989 - 
TL;DR: It is concluded that a functional defect in alpha Gs may contribute to a contractile abnormalities in the cardiomyopathic BIO 14.6 hamster, however, the etiology of thealpha Gs defect remains obscure.
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Usefulness of OPC-8212, a quinolinone derivative, for chronic congestive heart failure in patients with ischemic heart disease or idiopathic dilated cardiomyopathy.

Arthur M. Feldman, +13 more
- 01 Nov 1991 - 
TL;DR: It is suggested that OPC-8212 is beneficial in treating patients with congestive heart failure and that further evaluation of this new inotropic agent is warranted.
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Regulated Overexpression of the A1-Adenosine Receptor in Mice Results in Adverse but Reversible Changes in Cardiac Morphology and Function

Hajime Funakoshi, +16 more
- 21 Nov 2006 - 
TL;DR: The inducible A1-AR transgenic mouse model provides novel insights into the role of adenosine signaling in heart failure and illustrates the potentially deleterious consequences of selective versus nonselective activation of adenoine-signaling pathways in the heart.
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Immunodetectable levels of the inhibitory guanine nucleotide-binding regulatory proteins in failing human heart: discordance with measurements of adenylate cyclase activity and levels of pertussis toxin substrate.

Arthur M. Feldman, +4 more
- 01 Apr 1991 - 
TL;DR: Although functional activity of alpha Gi was increased in the particulate fractions of the failing heart as measured by inhibition of guanine nucleotide-stimulated adenylate cyclase activity, there were not associated changes in the levels of immunodetectable Gi.
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Effects of soluble TNF receptor treatment on lipopolysaccharide-induced myocardial cytokine expression

Toshiaki Kadokami, +7 more
- 01 May 2001 - 
TL;DR: Inability to block myocardial expression of IL-6 and MCP-1 suggests a possible mechanism for the failure of anti-TNF therapies in the treatment of endotoxin shock, and differentially altered the cytokine expression in the plasma and myocardium during endotoxemia.