Publications by authors named "A S Tikhonenko"

The experience of solcoseryl application in 70 patients, operated on for an acute hemorrhage from gastroduodenal ulcer, was summarized. The preparation was injected intravenously in the dose of 10 ml in 5% solution of glucose every other day during 6 days and then in the dose of 5 ml intramuscularly during 4-5 days. High efficacy of solcoseryl, manifesting by more earlier elimination of pain and oedema, healing of mucosa by first intention, shortening of the treatment duration in stationary by 3-5 days, was established.

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We are interested in identifying the transcriptional targets of the Myc oncoproteins. To this end, we have fused Myc of the MC29 retrovirus with the rat glucocorticoid receptor. This chimeric protein requires dexamethasone to undergo nuclear translocation and achieve an active conformation.

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The v-myc-containing retrovirus MC29 induces neoplastic transformation of avian embryo cells. To determine which traits of the transformed phenotype are directly controlled by v-Myc, we engineered a conditional MC29 mutant (GRIM) expressing v-Myc as a fusion protein with the glucocorticoid receptor and the retroviral Gag polyprotein. Only in the presence of glucocorticoids such as dexamethasone is GRIM capable of transforming embryo cells, from which six stable GRIM-lines have been derived.

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It was shown by electron microscopy, that the native molecule of glutamate decarboxylase is a hexamer with dihedral symmetry; the subunits are situated at the apices of an octahedron. Apoenzyme at pH 6.0 is dissociated form.

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Isolated human metaphase chromosomes treated with formamide and prepared for electron microscopy by protein monolayer technique have an appearance of loop-shaped chromatin fibers coming off the central scaffold-like structures, such chromosomes having approximately the same histone content as those before treatment. The morphology of scaffold-like structures at different formamide concentrations is described. It is shown that during formamide treatment the protein-protein and/or protein-DNA interactions are weakened because of disruption of hydrogen bonds.

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