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Direct preconditioning of cardiac myocytes via opioid receptors and [K.
The description of our automated cardiac myocyte imaging assay illustrates an elegant and sophisticated approach for the use of these primary cells in a relatively high throughput lead optimization effort.
A matter of life and death: cardiac myocyte apoptosis and regeneration," also appears in the same issue of the Journal.
Hajjar's laboratory has focused on targeting signaling pathways in cardiac myocytes to improve contractile function in heart failure and to block signaling pathways resulting in cell death.
The new data confirms that in the in vitro cardiac myocyte model, Cytopia's specific molecules are more effective than the molecules tested in previous work at SUNY.
In the second presentation, entitled "Caspase Inhibition Reduces Cardiac Myocyte Apoptosis and Preserves Myocardial Mass During Peripartum Cardiomyopathy in G alpha q Transgenic Mice," it was shown that continuous administration of a caspase inhibitor led to an almost four-fold reduction in heart muscle cell death via apoptosis, improvement in heart function, and complete prevention of mortality in a mouse model of pregnancy-induced heart failure.
2+]-ATPase, SERCA2a, are key features of cardiac myocyte dysfunction in both experimental and human heartfailure (8,9).
Other major topics of the program include atherosclerosis, acute coronary syndromes, congestive heart failure, cardiomyopathy, electrophysiology, vascular medicine, venous thromboembolism, valvular heart disease, stem cell research, and cardiac myocyte regeneration.
After 21 days in culture, the cells differentiated towards a cardiac myocyte phenotype, which was demonstrated by expression of morphological changes (appearance of binuclear cells with striated fibers and ramifications), detection of cardiospecific markers through inmunofluorescence, and the presence of cardiac muscle-related genes that were analysed through RT-PCR; and finally, by expression of reverse transcription.
Hence, alterations in gene expression of cardiac potassium and calcium channels may dramatically affect the capability of a cardiac myocyte to repolarize.
The protein disulfide isomerase family and thiol-disulfide oxidoreductases are likely enzymes involved in cardiac myocyte disulfide bond formation.
Cytokinetics' scientists have demonstrated in animal models that cardiac myosin activators increase cardiac contractility without stimulating beta-adrenergic receptors or inhibiting phosphodiesterase activity, and consequently, without increasing cardiac myocyte intracellular calcium, which may be arrhythmogenic and has been associated with other adverse clinical effects.