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Relationship between intrinsic pathway of cardiomyocyte apoptosis and morphological changes of the myocardium in acute focal ischemia

The role of heat shock proteins in the pathogenesis of heart failure (Review)) is of great importance, since they play a major role in the implementation of compensatory and adaptive

Beclin-1-Dependent Autophagy of Left Ventricular Cardiomyocytes in SHR and Wistar-Kyoto Rats with Type 1 Diabetes MellitusAutophagy is considered as a mechanism of progression of heart failure, but under certain

Features of Allostatic Load in Patients with Essential Hypertension without Metabolic Syndrome Depending on the Nature of Nighttime Decreases in Blood PressureChanges in the activity of the renin–angiotensin–aldosterone system are responsible for a stable

Expression of Bax and Bcl-2 Proteins in Left-Ventricular Cardiomyocytes in Wistar-Kyoto and SHR Rats with Insulin-Dependent Diabetes Mellitus, and a combination of these pathologies. Insulin-dependent diabetes mellitus was modelled by a single

Small Heat Shock Proteins HSP10 and HSP27 in the Left Ventricular Myocardium in Rats with Arterial Hypertension and Insulin-Dependent Diabetes Mellitus of 38-week arterial hypertension and a combination of arterial hypertension with diabetes mellitus

Myocardial Glutathione Synthase and TRXIP Expression Are Significantly Elevated in Hypertension and Diabetes: Influence of Stress on Antioxidant Pathways-dependent diabetes mellitus (DM) induced by streptozotocin, on 38- and 57-week-old hypertensive SHR rats and on a

Heat Shock Protein HSP60 in Left Ventricular Cardiomyocytes of Hypertensive Rats with and without Insulin-Dependent Diabetes Mellitus-57 weeks. Insulin-dependent diabetes mellitus was modeled by a single parenteral administration of 65 mg

BCL2-regulated apoptotic process in myocardial ischemia-reperfusion injury (Review), are the most significant for contemporary research due to their reversibility. BCL2 is a key anti

THE DEVELOPMENT FEATURES OF DEPRESSION IN LABORATORY ANIMALS WITH INDUCED MONOAMINES DEFICIENCY

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