Stephanie Allo

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Three processes that have been implicated in ischemic injury are impaired Ca2+ movement, altered osmoregulation, and membrane remodeling. Because the amino acid, taurine, affects all three processes, it seemed logical that changes in the myocardial content of taurine might affect ischemic injury. To test this hypothesis, infarct size and areas at risk were(More)
OBJECTIVES Depression in Na+/Ca2+ exchanger activity is an important factor in the development of the diabetic cardiomyopathy. Since the mechanism underlying this depression remains unknown, the aim of this study was to determine the contribution of hyperglycemia and insulinopenia towards the observed impairment in Na+/Ca2+ exchanger activity. METHODS(More)
Noninsulin-dependent diabetes is associated with a decrease in the activity of sarcolemmal phosphatase 1, but no change in the activities of phosphatase 2A, 2B, or 2C. Also unaffected by diabetes were the activities of protein kinase C, cAMP-dependent protein kinase and calcium-calmodulin protein kinase. Because of the decrease in phosphatase 1 activity,(More)
Phorbol 12-myristate 13-acetate (PMA), norepinephrine (NE), and contraction stimulate cardiomyocyte growth (increased protein content). Differences exist in the time course and extent of protein and RNA accumulation. Cells plated at 4 x 10(6) cells/60-mm dish and arrested with 50 mM KCl demonstrated no significant growth. Treatment with PMA stimulated(More)
Drug-induced taurine depletion of rat heart led to the accumulation of free CoA, free carnitine and long-chain acylcarnitine, but a small decrease in long-chain fatty acyl-CoA. Although elevations in total tissue long-chain acylcarnitine levels have been linked to defective membrane function and the association of long-chain acylcarnitines with(More)
Non-insulin-dependent diabetic (NIDD) male Wistar rats develop a cardiomyopathy approximately 9 mo after the onset of the diabetic condition. This cardiomyopathy is characterized by reduced contractility, relaxation, cardiac work, and diastolic compliance. Although the basis for these defects is not completely understood, altered cellular Ca2+ regulation(More)
The mechanism by which phorbol esters induce hypertrophic growth of cardiomyocytes was investigated. Control and 4 alpha-phorbol 12,13-didecanoate-treated myocytes demonstrated a slow rate of growth as measured by the protein/DNA ratio and cell area. In contrast, treatment with phorbol 12-myristate 13-acetate (PMA) stimulated protein accumulation by 34%,(More)
The mechanism(s) by which rRNA accumulates during the growth of cardiac myocytes was investigated. The rates of rDNA transcription were measured in contracting myocytes and compared with nonbeating myocytes depolarized with 50 mM KCl. After 3 days of contraction the absolute rate of rDNA transcription was accelerated by 2-fold as measured by incorporation(More)