The development of new antinociceptive agents and new approaches to pain relief based on potent non-narcotic analgesics is one of the most in demand and urgent directions of modern pharmacology. This work substantiates the choice of the clinically most relevant representative of non-narcotic analgesics from the α 2 -adrenoreceptor agonist class - dexmedetomidine, which acts at low doses and demonstrates high therapeutic index for various modes of administration. An analgesic efficacy of dexmedetomidine in single intranasal administration of the original experimental pharmaceutical formulation was evaluated in models of acute thermal and visceral pain in laboratory animals (female outbred white mice). A pronounced dose-dependent analgesic effect of the dexmedetomidine preparation in the 10 and 50 μg/kg dosage was revealed in the test models of visceral pain. The analgesic effect of dexmedetomidine was accompanied by a dose-dependent sedative (but not anesthetic) effect in mice, with peak at 30 minutes for intranasal administration of 50 μg/kg of drug. In the doses used, dexmedetomidine did not exert any acute toxic effects in mice.

Panic disorder is a widespread socially significant disease which genetic nature is poorly known. Since panic-driving features of cholecystokinin had been discovered, the gene that encodes this polypeptide (CCK ) and its receptors (CCKAR, CCKBR), as well as the mutations within, have been extensively studied. The aim of the present research was to assess frequencies of occurrence of seven single nucleotide substitutions in genes CCK, CCKAR, and CCKBR in the sample of patients with diagnosed panic disorder, and in the control sample of unexamined Moscow citizens. Reliable increase in occurrence frequency of rs1805000:T single nucleotide substitution in CCKBR gene was eventually found in the sample of panic disorder patients compared to the control, which allow us to suspect the involvement of this SNP into panic disorder aetiology. We also found the association of allele combination CCK rs11571842:A + CCKAR rs1800908:T with panic disorder development.

RHOA protein, a member of small GTPases family, is implicated in cell morphogenesis, adhesion, and in cell cycle regulation. RHOA gene (3p21.31) exhibits cell transformation activity, and therefore gene is considered as a potential oncogene. The aim of this study was to investigate RHOA transcription and copy number changes in three epithelial tumors (breast, renal cell and epithelial ovarian carcinomas, 45 tumor/normal pairs altogether). EII, HhaI, AciI n Bsh1236I). Hypomethylation of the RHOA promoter region in tumor DNA was observed two times more frequently than increased methylation. Moreover, all (15) cancer cases with hypomethylation of the RHOA gene showed a 2-10 fold increased expression of RHOA. It was concluded that gene copy multiplication and demethylation of the RHOA promoter region can contribute to transcription activation of this gene in epithelial tumors.