Publications by authors named "Michael J Rovetto"

Increased cardiac myocyte contractility by the β-adrenergic system is an important mechanism to elevate cardiac output to meet hemodynamic demands and this process is depressed in failing hearts. While increased contractility involves augmented myoplasmic calcium transients, the myofilaments also adapt to boost the transduction of the calcium signal. Accordingly, ventricular contractility was found to be tightly correlated with PKA-mediated phosphorylation of two myofibrillar proteins, cardiac myosin binding protein-C (cMyBP-C) and cardiac troponin I (cTnI), implicating these two proteins as important transducers of hemodynamics to the cardiac sarcomere.

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The amount of work the heart can perform during ejection is governed by the inherent contractile properties of individual myocytes. One way to alter contractile properties is to alter contractile proteins such as myosin heavy chain (MyHC), which is known to demonstrate isoform plasticity in response to disease states. The purpose of this study was to examine myocyte functionality over the complete range of MyHC expression in heart, from 100% alpha-MyHC to 100% beta-MyHC, using euthyroid and hypothyroid rats.

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Fifty-eight investigators from the fields of biochemistry, physiology, cardiology, nuclear medicine, and physics met to discuss the development of metabolic imaging techniques for application to cardiovascular and pulmonary studies in health and disease. The workshop was sponsored by the Division of Heart and Vascular Diseases, National Heart, Lung, and Blood Institute and was held on September 16 to 18 in Bethesda, Maryland, in facilities provided by the American College of Cardiology. This report summarizes the presentations and discussions and presents recommendations for future studies.

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