A
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.
Papers
More filters
Journal ArticleDOI
Experimental issues in assessment of G protein function in cardiac disease.
TL;DR: This communication will clarify some of the experimental issues relating to G proteins and cardiovascular research by discussing the strengths and weaknesses of two G proteins that have undergone extensive investigations.
Journal ArticleDOI
Detection of interleukin and interleukin-receptor mRNA in human heart by polymerase chain reaction.
TL;DR: While interleukin-1-receptor mRNA was present in samples from non-failing hearts and those with idiopathic myopathy, it was absent from patients with inflammatory myocarditis, suggesting receptor mRNA down-regulation.
Journal ArticleDOI
A1 Adenosine Receptor Upregulation Accompanies Decreasing Myocardial Adenosine Levels in Mice With Left Ventricular Dysfunction
Hajime Funakoshi,Lefteris C. Zacharia,Zhonghua Tang,Jin Zhang,Ling L. Lee,Julie C. Good,David E. Herrmann,Yoshihiro Higuchi,Walter J. Koch,Edwin K. Jackson,Tung O. Chan,Arthur M. Feldman +11 more
TL;DR: Modulation of the myocardial adenosine system and its signaling pathways may be a novel therapeutic target in patients with heart failure.
Journal ArticleDOI
Benefit and safety of enhanced external counterpulsation in treating coronary artery disease patients with a history of congestive heart failure.
William Lawson,Elizabeth D. Kennard,Richard Holubkov,Sheryl F. Kelsey,John E. Strobeck,Ozlem Soran,Arthur M. Feldman +6 more
TL;DR: Patients with congestive heart failure maintained their reduction in angina but were significantly more likely to have experienced a MACE end point at 6 months, while the angina class improved in 68%, with comparable quality of life benefit, in the heart failure cohort.
Journal ArticleDOI
Adenylyl cyclase: a new target for heart failure therapeutics.
TL;DR: With the use of transgenic overexpression and gene-targeted knockouts, investigators have demonstrated the potential utility of low levels of β2AR overexpressed or inhibition of βAR kinase (βARK) in improving cardiac contractile function without obvious cardiotoxicity.