J. Randall Moorman

J. Randall Moorman

Professor of Medicine, Biomedical Engineering and Molecular Physiology and Biological Physics

M.D., University of Mississippi Medical Center, 1978

PO Box 800158
Charlottesville, VA 22908
Phone: 434-924-9605
FAX 434-982-1998

rm3h@virginia.edu

   

Research Interests

We study regulation of the heartbeat in health and disease.

Our major clinical research effort centers on sepsis, a life-threatening infection of the bloodstream and a major cause of morbidity and mortality in premature newborn infants. Currently, the diagnosis is often not suspected until late in the course of the illness when the infant is very ill indeed. We have developed a new strategy for early diagnosis based on the finding that signs of illness are preceded by abnormal heart rate characteristics (HRC) of reduced variability and transient decelerations. Using a validated predictive algorithm for continuous HRC monitoring, we have recently diagnosed and treated sepsis in infants who never became ill. We are conducting a randomized clinical trial to test the hypothesis that HRC monitoring improves the outcomes of infants in the neonatal intensive care unit. The techniques involve clinical neonatology and mathematical biostatistics.

Our major basic science research effort centers on the FXYD family of single transmembrane proteins that modulate membrane ion transport processes. Of particular interest is FXYD 1, or phospholemman (PLM), a major substrate for diverse protein kinases in heart that modulates Na,K-ATPase, Na-Ca exchanger, and to form osmolyte-selective channels. We utilize reagents and models ranging from highly purified wild-type and mutant protein to the knock-out mouse using most imaginable techniques of animal and cellular cardiac physiology, electrophysiology, structural biology, biochemistry, molecular biology, and cell imaging. Our goal is to understand the physiological role of PLM in heart, where it is the major substrate for phosphorylation by PKA (activated by beta adrenergic receptors) and PKC (activated by angiotensin-II receptors and a-adrenergic receptors). Since the major interventions to prolong life in congestive heart failure, which affects millions of Americans, are blockade of beta-adrenergic receptors and angiotensin-II receptors, the potential clinical importance of understanding PLM function is enormous.

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