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Bulletin of Experimental Biology and Medicine - The psychopharmacological effects of a stimulator of functions of progenitor cells of the nervous tissue STAT3 inhibitor (STAT3 Inhibitor XIV, LLL12)...  相似文献   
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Bulletin of Experimental Biology and Medicine - The role of signaling molecules in synthesis of humoral regulators of granulocytopoiesis by the hematopoietic microenvironmental cells during stress...  相似文献   
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Bulletin of Experimental Biology and Medicine - The study focuses on the development of principally novel priority-oriented healthcare strategy — targeted therapy in regenerative medicine...  相似文献   
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Bulletin of Experimental Biology and Medicine - We studied the expression of ARID1A, prostaglandin E2 synthase, and prostaglandin E2 receptor in the endometrium and ovarian, peritoneal, and...  相似文献   
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We modeled acute disruption of the brain blood circulation (ADBC) by bilateral ligature of the common carotids in white outbred rats. This resulted in the formation of endothelial dysfunction of capillary network in the IV–V layers of the cortex and the vessels of the pia mater, choroids plexuses, and the branches of the middle cerebral and ophthalmic arteries, which was seen as a considerable decrease in the density of nuclei of endotheliocytes, a decrease in the RNA concentration in them, expression of vascular endothelial growth factor (VEGF), and a substantial decrease in the index of the proliferative activity of endotheliocytes. Intraperitoneal treatment of rats with ADBC with lysinium for 21 days at a dose of 50 mg/kg led on the 4th day to an increase in the density of endotheliocytes in the capillary network of the brain cortex and the walls of cerebral vessels and an increase in the RNA content in endothelial nuclei. At the end of the lysinium treatment, we observed an increase in the density of endotheliocytes in the capillary network of the brain cortex and the walls of cerebral vessels, an increase in the RNA content in nuclei of endotheliocytes, and an increase in the density of proliferating endotheliocytes in these vessels, which was associated with increased VEGF concentration. Administration of the control drug piracetam had no endothelium-protective effect.  相似文献   
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OBJECTIVE: Helicobacter pylori-associated atrophic gastritis is known to be a significant risk factor for gastric cancer. Among the well-known parameters of atrophic gastritis are the levels of serum gastrin-17 (G-17) and pepsinogen I (PG1), which are biomarkers of gastric antral and corpus mucosal activity, respectively. The aim of study was to compare the production of G-17 and PG1 in patients with or without stomach mucosal atrophy and to investigate the utility of serum PG1 and/or G-17 concentrations for the objective evaluation of atrophic gastritis. MATERIAL AND METHODS: A total of 178 dyspeptic Helicobacter pylori-positive patients underwent diagnostic upper gastrointestinal endoscopy with biopsy. The degree of histologic gastric mucosal atrophy was compared with the fasting levels of PG1, and to the postprandial levels of G-17 detected by enzyme immunoassay. RESULTS: A decrease in serum G-17 levels along with worsening of the antral atrophy was observed; the serum levels of PG1 were reduced during progression of the corpus atrophy. In the multifocal atrophic gastritis, values for PG1 and G-17 serum concentrations were significantly lower than the respective cut-off values. Statistical analysis revealed statistically significant differences between the serum levels of PG1 and G-17 measured at different stages of stomach mucosal atrophy. CONCLUSIONS: A strong reverse correlation was found between histologic/ endoscopic antral atrophy and serum G-17 levels, and between corpus atrophy and serum PG1 levels.  相似文献   
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The first congenital defect of hypoxia-sensing homozygosity for VHL 598C>T mutation was recently identified in Chuvash polycythemia. Subsequently, we found this mutation in 11 unrelated individuals of diverse ethnic backgrounds. To address the question of whether the VHL 598C>T substitution occurred in a single founder or resulted from recurrent mutational events in human evolution, we performed haplotype analysis of 8 polymorphic markers covering 340 kb spanning the VHL gene on 101 subjects bearing the VHL 598C>T mutation, including 72 homozygotes (61 Chuvash and 11 non-Chuvash) and 29 heterozygotes (11 Chuvash and 18 non-Chuvash), and 447 healthy unrelated individuals from Chuvash and other ethnic groups. The differences in allele frequencies for each of the 8 markers between 447 healthy controls (598C) and 101 subjects bearing the 598T allele (P < 10(-7)) showed strong linkage disequilibrium. Haplotype analysis indicated a founder effect. We conclude that the VHL 598C>T mutation, the most common defect of congenital polycythemia yet found, was spread from a single founder 1,000 to 62,000 years ago.  相似文献   
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