Ischemic postconditioning (IPostC) of brain is a method of endogenous neuroprotection provided in the form of short episodes of ischemia-reperfusion made in the reperfusion period after damaging ischemia. The review considered the effects IPostC of brain and signaling systems involved in the mechanisms of neuroprotection. The information about the impact IPostC on the energy metabolism of neurons is presented in this review.

Background. Search and development of new regulators of functional activity of the hypothalamic- pituitary-thyroid axis is one of actual problems in endocrinology and pharmacology. We have previously shown that palmitoylated peptide 612-627 (Pal) structurally corresponding to the third intracellular loop of receptor of thyroid-stimulating hormone (TSH) activates the adenylyl cyclase signaling system in thyroidal membranes in vitro and stimulates the production of thyroxine by the thyroid gland in vivo. Objective. The aim of this work was to study a dose-dependency of the stimulating effect of peptide 612-627 (Pal) on the level of thyroid hormones in its intranasal and intramuscular administration into rats. Design and methods. The peptide was administered once to Wistar male rats at the doses from 45 to 900 pg/kg when administered intranasally and at the doses from 150 to 1350 pg/kg when administered intramuscularly. Prior to administration and for 6 h after administration the changes of the levels of free (fT₄) and total thyroxine (tT₄) and total triiodothyronine (tT₃) were evaluated. Results. It is shown that peptide 612-627 (Pal) in both routes of administration in a dose- dependent manner increased the levels of fT₄ and tT₃ At the same time, the intranasal route was more effective as ED₅₀ value and the maximal stimulating effect on fT₄ production when peptide administered intranasally was 87 pg/kg and 38 %, while in the case of intramuscular route - 275 pg/kg and 25 %, respectively. Conclusion. These findings indicate the ability of peptide 612-627 (Pal) to effectively stimulate hormone-producing function of the thyroid gland when peptide administered intranasally into rats at the range of the doses 225-450 pg/kg.

This article is a review of current literature regarding the association of sensorineural hearing loss with type 2 diabetes mellitus. We discuss theories of development of sensorineural hearing loss in patients with diabetes.

Nonspecific systemic biological reaction of arterial blood pressure (AP) from the entire body level, vasomotor center and proximal arterial bed compensates metabolic and microcirculation disorders in the distal arterial bed. This occurs when a) primary local metabolic disorders at the autocrine level, physiological or nonphysiological cell death, and “littering” of extracellular medium cause microcirculation disorders in paracrine cell communities (PCC) and impair the biological functions of homeostasis, trophology, endoecology and adaptation, and b) local compensation of impaired perfusion in PCC by peripheral peristaltic pumps and redistribution of local circulation in the biological reaction of endothelium-dependent vasodilation cannot improve realization of biological function. Systemic AP elevation without symptomatic arterial hypertension (AH) is an indicator of impaired homeostasis, trophology, endoecology and adaptation. All types of AH develop according to a universal algorithm irrespective of causes of impaired blood flow and microcirculation in distal arterial bed. Nonspecific systemic compensation of metabolic disorders from the entire body level in the proximal arterial bed is always the same and always leads to nonphysiological changes in target organs. We believe that specific etiologic features of the universal AH pathogenesis can be elucidated using complex technological metabolonomics approaches the validity of which so far has not been tested for differential diagnostics of impaired functions.

Background. The abnormalities of micro- and macrocirculation in obesity are associated with the changes in the activity of NO-synthases, the enzymes catalyzing synthesis of endogenous NO. However, in experimental obesity they are not well understood. There are no data on the influence of long-term treatment with intranasally administered insulin (I-I) that is used for the treatment of pre-diabetic states on NO-synthase activity. Objective. The aim of this work was to study the activity of NO-synthases in the tissues of rats with obesity induced by high- fat diet and the influence of long-term I-I treatment on them. Design and methods. To induce the obesity, Wistar male rats received a high-fat diet during 4 months. The I-I treatment was started on the 60^th day of the diet, and carried out for two months at a daily dose 0.48 IU/rat. The activity of total, neuronal and endothelial isoforms of NO-synthase in the brain, myocardium and skeletal muscles was evaluated. Results. It was shown that in the myocardium and skeletal muscles of obese rats the activity of total and endothelial NO-synthases was decreased, and in the brain it has not significantly changed. The treatment of obese rats with II resulted in partial or complete restoration of the activity of total and endothelial NO-synthases in the myocardium and skeletal muscles, and caused an increase of NO-synthase activity in the brain above this level in control. Conclusion. Summing up, long-term I-I treatment restores insulin signaling system in the brain and positively affect the NO-synthase system in CNS and periphery, attenuated in the obesity, which can lead to improved blood circulation and to prevent the development of dysfunctions of the nervous, the cardiovascular and other systems.

Introduction. Microcirculatory disorders are the cornerstone of a large number of diseases, therefore during the treatment restoration of functions of microvessels using various ways is necessary. Nowadays, the research of non invasive, physiotherapeutic and effective methods of influence is being actual. Materials and methods. Observation of vital microcirculation under the influence of a local abdominal decompression was made on a mesentery of rats. Changes of length of mesentery vessels and width of their gleam was registered and estimated with curvimeter. Results and discussions. Established that sessions of a local abdominal decompression increase in number of open vessels in mesentery, and also to increase in width of a gleam of microvessels: right after LNP (local negative pressure) session length of microvessels of mesentery was increased twice, in 30 minutes after the session of LNP length of microvessels was increased by 1,6 times, in 2 hours - by 1,5 times. Width of gleam of mesentery vessels also changed during and after LNP: right after LOD session width of vascular gleams was increased by 2,3 times, after 30 minutes - by 1,9 times, after 2 hours - by 1,8 times. Conclusion. Local negative pressure influence upon abdominal area is an effective and physiologic method of toxins removal from an organism, decreasing the severity of intoxication. The method can be applied both independently and in a complex with other medical actions.

This article discusses the worldwide adopted recommendations for appointment of vitamin D during pregnancy: a minimal need for pregnant and lactating women is 600 IU per day, however, a daily dose may need to be increased to 1500-2000 IU to maintain a 25- (OH)D at a sufficient level (i. e. above 30 ng/ml). According to a study carried out in St. Petersburg in 2013-2014 years, after 20-25 weeks from the beginning of cholecalciferol supplementation in a group of pregnant women who received 500 IU of vitamin D, the number of women with a deficit almost halved. Applying vitamin D 1200 IU per dose for one month increased the concentration of 25- (OH)D in the blood serum by only 6,8 ± 0,5 ng/ml, and 25 % of pregnant women had a vitamin D deficiency even receiving it. However, the appointment of a daily dose of cholecalciferol 2000 IU during pregnancy showed higher levels of saturation of the body with vitamin D.

Syndrome r (18) - ring 18 chromosome cytogenetically is characterized by a complete or mosaic forms a ring chromosome 18 with the absence of the distal portions of the long and short arm of the chromosome. The clinical picture includes multiple dysmorphia, combined with varying degrees of mental retardation. Committal involvement of cardiovascular system and congenital heart defects typically are not described in cases of r (18). We observed 18-year-old patient with mental retardation, multiple facial dysmorphia, and subaortic stenosis. During standard karyotyping by PHA-stimulated lymphocytes patient revealed 46, XY, r (18) karyotype. Since congenital heart defects are not common feature of r (18) we hypothesized mosaic chromosomal aberrations and performed additional FISH analysis on blood smears using Aneu Vision (CEP 18) and To Tell Mix 11, Mix 12 probes. The study revealed three signals of chromosome 18 centromere and subtelomeric deletion of chromosome 18 in 15 % of the cells, contained two signals from the centromere of chromosome 18 with subtelomeric deletion to form a ring in 80 % of cells, 5 % of the uncultured cells in blood smear contained two signals from the centromere of chromosome 18 without subtelomeric deletion. In conclusion we describe clinical case of somatic mosaicism in patients with r (18) in combination with 18 trisomy in 15 % of blood cells, leading to combined phenotype of mental retardation and congenital heart defect.

Hypoxia recognized as the major etiologic factor of perinatal pathology of the nervous system. Changes of central hemodynamics in patients with congenital heart defects affect the cerebral blood flow and cause acute and chronic hypoxic-ischemic brain damage. The aim of the study was to investigate the characteristics of hemostasis and functional activity of endothelium with congenital heart defects in newborns with hypoxic central nervous system. We observed of varying degrees of gestation infants with hypoxic central nervous system and congenital heart disease. In the study of nervous and mental development of infants with hypoxic central nervous system during the first year of life was revealed declines quantify motor, speech and mental functions in all groups of observations. It is noted that in neonates with hypoxic encephalopathy and congenital heart disease, a change of hemostatic function, characterized by hypercoagulability, against endothelial dysfunction.