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V S Repin

Publications and source records attributed to V S Repin.

At least 181 records · Page 10Linked to original sources
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[Embryonic stem cells (from fundamental biology to medicine)].

The recent achievements in isolation, primary and long term culturing, cell Immunophenotyping, SAGE--mRNA--profiling, the clonogenic growth parameters of embryonic stem cells and mesenchymal stem cells have been outlined in connection with cell pluripotency and restricted differentiation, mediated by signals both in culture and in situ. Multidisciplinary data obtained by cell biologists, embryologists with recent functional genomic data give the new way for practical implementation of bioimplants derived from embryonic stem cell for cell-replacement therapy.

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[Embryonic stem cells: from fundamental studies--to clinical application].

A short history of embryonic stem cell (ESC) discovery, cell line isolation, phenotyping and cell behavior both in situ and in vitro is outlined. The path of ESC differentiation into restricted specialized cell types mediated by signal network in culture and by grafting cell into recipient tissues is considered. Potentialities of ESC as the generator of spare parts of organs for regenerative medicine and related bioethical issues are briefly outlined.

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[The source of the iron binding with nitric oxide in activated macrophages].

No decrease in iron-sulphur centers was found in cultured macrophage cells (J774) after the treatment with nitric oxide (10(-7) M NO/10(7) cells) during 5 min. The center content was controlled by the electron spin resonance (ESR) method. The macrophages pretreated with dithionite + methyl viologen showed the formation of dinitrosyl iron complexes (DNIC) with a characteristic ESR signal at g approximately 2.03. The data suggest that loosely bound nonheme iron (free iron) mostly contributes to the formation of these complexes. Iron from iron-containing proteins does not release from these centers under the direct action of nitric oxide. The iron-sulphur centers can be destroyed by the products of nitric oxide oxidation (NO2, N2O3, etc.) as oxidizing and acid agents.

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[Protein composition and synthesis in islands of Langerhans isolated from normal rats and rats with alloxan diabetes].

Protein fractions with dissimilar electrophoretic mobility were identified in Langerhans, islands. In solitory islands, isolated from pancreas of rats with alloxan diabetes as compared with normal rats the protein composition varied distinctly: fractions of "constant" proteins and, specifically, the insulin fraction disappeared completely, total amount of identified fractions was decreased with relative alteration in their mobility. The total protein-synthesizing activity of Langerhans' islands from diabetic animals was 3-4-fold decreased as compared with that of control animals. An effect of "glucose repression" of protein synthesis was observed in isolated Langerhans' islands.

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[Inhibition of thrombocyte spreading and the formation of thrombus-like aggregates bound with substrate by the anti-anginal agent trapidil].

Effects of trapidil (rocornal) on interaction of human thrombocytes, purified by gel filtration, and the surface covered with fibrillar collagen from calf skin (CCS) were studied using scanning electron microscopy. When the soluble inductors were absent, trapidil did not affect the thrombocyte adhesion. At the same time, trapidil inhibited the shape alterations of laminated thrombocytes, induced by CCS-substrate with simultaneous increase in the ratio of disc-shaped cells and a decrease in laminated thrombocytes. Soluble inductors of the thrombocyte activity (arachidonic acid, stable derivative of prostaglandin endoperoxides U46619 and thrombin) stimulated the cells mass-scale lamination as well as formation of thrombus-like aggregates bound with CCS-substrate. Trapidil prevented completely the effects of exogenous arachidonic acid and of U46619 on interaction of thrombocytes and the substrate but inhibited only by 40-50% the synthesis of thromboxane A2 in the cells induced by arachidonic acid. The drug blocked also an aggregation of thrombocytes in suspension, lamination and formation of aggregates bound with the surface, induced by low but not by high concentrations of thrombin. Possible use of trapidil is discussed.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
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[Quantitative analysis of lesions of the aortic and carotid artery endothelium in experimental diabetes in rabbits by scanning electron microscopy].

A significant increase in the number and zone area of argyrophil cells, craters and stomata of the intracellular formations were seen in the aortic and carotid pectoral and peritoneal regions of rabbits with 5-week alloxan diabetes. The number and zone area of vascular de-endothelization did not increase. Cell polymorphism, apart from maintenance of pronounced argyrophilia and micro-injuries, occurred to diabetes of 5-month standing. Deranged properties of the macrovascular endothelial integument may be of great importance in the pathogenesis of atheromatosis in diabetes mellitus.

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[The effect of dimethyl-(imidazol-1-yl) methanesulfonic acid on experimental atherogenesis in rabbits].

The hypocholesterolemic and antiatherosclerotic activities of the new imidazole derivative dimethyl-(imidazole-1-yl) methanesulfonic acid (1273) were investigated in rabbits fed through a probe either cholesterol, 200 mg/kg body weight, suspended in sunflower seed oil or that supplemented by imidazole, 15 mg/kg body weight, or its derivative 1273, 30 mg/kg body weight. Total cholesterol showed an 8-fold increase in all rabbit groups as compared to that in the animals fed a routine laboratory chow. In the agent 1273-given animals, the aortic atherosclerotic lesion index (ALI) was 7.8%, which was 2.4 times lower that in hypercholesterolemic animals untreated with this agent or treated with imidazole. Concurrently with a decrease in the aortic ALI, the agent 1273 lowered the rabbit hepatic levels of free and esterified cholesterol. The experimental findings of cultured rabbit hepatocytes suggest that the agent 1273 reduces hepatic cholesterol levels by inhibiting the de novo cholesterol synthesis. In vitro studies on murine J774 macrophages have demonstrated that inhibition of cholesterol esterification in the vascular wall macrophages is one of the possible mechanisms responsible for the antiatherosclerotic activity of this derivative of imidazole.

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