The feasibility of using molecular genetic markers associated with thyroid neoplasms and more aggressive course of the disease is now actively studied. We analyzed the diagnostic value of somatic mutations in the hot spots of BRAF, KRAS, KRAS, EIF1AX, and TERT genes in histological material from 153 patients with thyroid gland neoplasms. BRAF mutations (exon 15, codon area 600-601) were found in 54 patients, NRAS mutations (exon 3, codon 61) were detected in 12 patients; mutations KRAS, TERT, and EIF1AX genes were not detected.Immunohistochemical reaction to glial fibrillar acid protein (GFAP) is widely used for identification of activated satellite cells in sensory ganglia. We used this marker in studies of satellite cells activation in dorsal root ganglia during aging and under conditions of experimental systemic inflammation in young (4 months) and aged (18-19 months) rats and animals with experimental LPS-induced systemic inflammation. The number of GFAP+ satellite cells increased significantly after parenteral injection of LPS and during aging, which can indicate similarity of mechanisms of reactive glial changes during aging and systemic inflammation.The immunolocalization of apoptotic factors in rat neocortex was studied on the model of permanent occlusion of the middle cerebral artery with administration of exogenous BDNF. We revealed heterogeneous distribution of pro- and anti-apoptotic factors in the stroke area and in the surrounding penumbra, where caspase-3+ and p53+ cells were found. Their number was maximum on day 3 of ischemia. The number of neurons containing anti-apoptotic factors was relatively decreased. Injection of BDNF changed the distribution of apoptotic factors. In the penumbra area, BDNF enhanced the expression of Mdm2 primarily in the pyramid cells of layers V/VI and Bcl-2 in interneurons of layers II and III. Localization of p53 and caspase-3 varied at different terms of the ischemic period and showed an inverse dependence. Considering the selective neuroprotective effect of BDNF, various mechanisms of the formation of ischemic tolerance in neurons are proposed.In male rats, acute renal failure was simulated by clamping the vascular pedicle of the left kidney for 60 or 90 min and right-sided nephrectomy. In the control series, no therapy was performed. In the experimental series, the animals were daily injected subcutaneously with Cellex, a protein-peptide complex (PPC) chromatographically isolated from the brain tissue of pig embryos with a molecular weight of its components from 10 to 250 kDa. PPC was administered 5 times a week (10 injections) in a dose of 0.1 ml/kg (0.1 mg active substance per 1 kg body weight). Ischemia of a single kidney led to the development of acute renal failure, more severe after 90-min ischemia. PPC therapy reduced the severity of functional disorders mainly at the early stages (3 and 7 days) with normalization of blood concentrations of urea and creatinine, creatinine clearance, tubular reabsorption of sodium and calcium, including the cases with 90-min ischemia, which did not occur in the control series. https://www.selleckchem.com/TGF-beta.html PPC therapy also contributed to hypertrophy of many glomeruli, prevented the development of glomerulosclerosis, and reduced damage to the epithelium of the renal tubules. At the same time, neither pronounced lymphohistiocytic infiltration, nor focal nephrosclerosis typical of control series were observed.The study examined the effect of α2-adrenoreceptor (α2-AR) activation against the background of preliminary blockage of If on the performance of Langerndorff-isolated rat heart. Stimulation of α2-AR in isolated rat hearts against the background of ZD7288 in concentrations of 10-9 M and 3×10-5 M changed the negative dynamics of myocardial inotropy to positive (by 25 and 38%; p less then 0.05). Activation of α2-AR produced opposite effects on HR. If blockade abolished tachycardia caused by activation of α2-AR; HR deceleration in response to α2-AR agonist against the background of If blocker in a concentration 10-9 M was 41% (p less then 0.05). We observed negative dynamics of coronary flow (by 38%; p less then 0.05) in isolated adult rat hearts after application of α2-AR agonist against the background of If blockade (10-9 M).We studied the expression of C9orf72 gene in pathologies associated with hexanucleotide repeats expansion in this gene frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). The study included 7 patients with hexanucleotide repeats expansion in the C9orf72 gene and 9 patients of the control group. The expression of C9orf72 mRNA was evaluated in blood leukocytes by real-time PCR. Methylation of CpG-sites in C9orf72 promotor region was evaluated by DNA sequencing after bisulfite conversion. A 2-fold decrease in the C9orf72 gene expression was found in patients with hexanucleotide repeats expansion in comparison with controls, though the difference did not reach statistical significance due to small sample size. The highest expression was shown for ALS in comparison with FTD and FTD-ALS phenotype. A trend to inverse correlation between C9orf72 mRNA level and promoter methylation of this gene as well as between mRNA level and age of disease onset was demonstrated. Acute coronary syndrome (ACS) indicates the serious clinical manifestation of coronary artery disease (CAD) and is closely associated with cardiovascular prognosis in patients with ACS. This study was aimed to study the prevalence of type 2 diabetes mellitus (T2DM) and the relation of HbA1c with the severity of CAD in patients presenting as non-diabetic ACS. Diabetic status of the patients was assessed with fasting blood sugar (FBS) and HbA1c levels, and coronary artery disease burden was assessed by coronary angiography. Out of 208 patients, 85.1% were males, and 14.9% were females; 73.56% cases were hypertensive. 80.77% of cases had STEMI, 17.79% had NSTEMI, and 1.44% had unstable angina. Out of 168 STEMI patients, 64.3% were thrombolysed, 21.42% presented late, 2.38% had contraindications to thrombolysis, and 11.9% underwent primary PCI. FBS in diabetic range was found in 44.23% of cases, impaired FBS in 36.54%, and 19.23% of patients had FBS in non-diabetic range. According to HbA1c, 41.8% were diabetic, 39.