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You-Tang Shen

Researcher at University of Medicine and Dentistry of New Jersey

Publications -  62
Citations -  3289

You-Tang Shen is an academic researcher from University of Medicine and Dentistry of New Jersey. The author has contributed to research in topics: Hemodynamics & Blood flow. The author has an hindex of 27, co-authored 62 publications receiving 3186 citations. Previous affiliations of You-Tang Shen include Harvard University & Pennsylvania State University.

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Recombinant Glucagon-Like Peptide-1 Increases Myocardial Glucose Uptake and Improves Left Ventricular Performance in Conscious Dogs With Pacing-Induced Dilated Cardiomyopathy

TL;DR: rGLP-1 dramatically improved LV and systemic hemodynamics in conscious dogs with advanced DCM induced by rapid pacing and may be a useful metabolic adjuvant in decompensated heart failure.
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Direct Effects of Glucagon-Like Peptide-1 on Myocardial Contractility and Glucose Uptake in Normal and Postischemic Isolated Rat Hearts

TL;DR: GLP-1 has direct effects on the normal heart, reducing contractility, but increasing myocardial glucose uptake through a non-Akt-1-dependent mechanism, distinct from the actions of insulin.
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Active metabolite of GLP-1 mediates myocardial glucose uptake and improves left ventricular performance in conscious dogs with dilated cardiomyopathy

TL;DR: In DCM, GLP-1-(9-36) mimics the effects ofGLP- 1-36 in stimulating myocardial glucose uptake and improving left ventricular (LV) and systemic hemodynamics through insulinomimetic as opposed to insulinotropic effects.
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Mechanism of Impaired Myocardial Function During Progressive Coronary Stenosis in Conscious Pigs Hibernation Versus Stunning

TL;DR: The data suggest that the reduced function during ameroid-induced coronary stenosis reflected cumulative myocardial stunning rather than a primary deficit in coronary blood flow or "hibernating myocardium."
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Peripheral Vascular Endothelial Dysfunction and Apoptosis in Old Monkeys

TL;DR: Vascular endothelial dysfunction was present in old monkeys without evidence of atherosclerosis, which may be due to endothelial apoptosis and reduced endothelial cell density.