Introduction. Congenital heart disease (CHD) is one of the most common fetal malformations resulting in high postnatal disability and mortality. Despite significant advances in the diagnosis and surgical correction of defects, the molecular genetic aspects of the pathogenesis of this disease are still not fully understood. TREM-1 key receptor for the innate immune response, inflammatory inducing and involved in the pathogenesis of acute and chronic diseases.

Purpose. To determine genotype frequencies of the TREM-1 gene in children with congenital heart disease.

Methods. 154 children with congenital heart disease were included in the study. Genomic DNA isolated from peripheral blood leukocytes was used as a material for the study. The genotyped were with RT-PCR by 8 loci (rs1817537, rs3804277, rs6910730, rs7768162, rs2234246, rs4711668, rs9471535, rs2234237).

Results and conclusions. The C/C genotype of the rs2234246 polymorphism was more frequently found in the group of patients with ductus-independent CHD compared with the ductus-dependent CHD (38.2 % vs. 15.4 %, p = 0,006). The T/T genotype of the rs4711668 was more frequently detected in the ductus-independent CHD (24 % vs. 8 % p = 0.02).

The study did not establish differences in the distribution of alleles and genotypes of the TREM-1 gene in patients with CHD and healthy children. At the same time, statistically significant differences in the distribution of genotypes of polymorphic rs2234246 and rs4711668 variants in groups of patients with ductus-dependent and ductus-independent blood circulation were obtained.

Management of thoracoabdominal aortic dissection (DeBakey III type) is still a controversial subject because of the individual features each patient, nonspecific complains and symptoms, and severe complications associated with disease progression, such as aortic rupture, visceral malperfusion syndrome, retrograde dissection, refractory hypertension and pain.

This article reports the clinical case of staged endovascular treatment of 78-year-old female with chronic thoracoabdominal aortic dissection (DeBakey type III) affected by uncontrollable hypertension. Endovascular treatment is proving to be an affective and safety tool for treatment this complex group of patients including nontolerant to open surgery.

Background. Insulin therapy is associated with the risk of hypoglycemia, high variability of glycemia. Therefore, therapy with analogues GLP1 becomes relevant for patients with myocardial infarction and diabetes mellitus type 2. These drugs can reduce glycemic variability and risk of hypoglycemia.

Objective. The effects of combination therapy analogue GLP1 and insulin should be studied in rats with experimental myocardial infarction and the impact of such therapy should be studied on the level of markers of myocardial damage, BNP, dynamics of the echocardiographic parameters and level of glycemia in patients with diabetes mellitus type 2 and myocardial infarction.

Design and methods. Neonatal streptozotocin diabetes mellitus was modeled in an experiment in rats. Groups of animals were formed depending on the time of the beginning of insulin therapy, analogue GLP1(exenatide) or a combination of these drugs — before or after experimental myocardial infarction. Morphological assessment of ischemia and necrosis areas was carried out and glycemic variability was assessed. Two groups of patients with type 2 diabetes mellitus and myocardial infarction were formed in the clinical part. The first group received standard insulin therapy, the second group received combination therapy with insulin and exenatide. Parameters of glycemia, markers of myocardial damage, BNP, dynamics of echocardiography were evaluated.

Results. The decrease of the area of necrosis, was observed in the combination therapy group in the experiment. Troponin I and CPK MV levels did not differ initially in all groups of patients. Reducing glycemic variability, a positive trend of level BNP, and EF was noted in patients with exenatide.

Conclusion. Exenatide has the most pronounced positive effect on the course of myocardial infarction at the introduction before the start of reperfusion. Exenatide had no effect on the dynamics of markers of myocardial damage, but reduced the glycemic variability, improved the dynamics of laboratory parameters in patients.

For a long time it was believed that hereditary tubulopathies, manifested by a wide range of peculiar disorders of ionic and acid-base homeostasis, are exclusively the prerogative of pediatricians. However, modern ideas about the pathogenesis of hereditary tubulopathies, methods of their diagnosis and treatment, have led to the fact that the meeting of an “adult” nephrologist with this pathology is not so rarely observed. On the one hand, the survival rate of patients whose hereditary tubulopathies were diagnosed in children, and even in antenatal age, has sharply increased. On the other hand, there are more and more clinical data on the possibility of manifestation of hereditary tubulopathies in young and even old age. One way or another, “adult” nephrologists more and more often began to observe patients with the hereditary tubulopathies described above. However, it should be recognized that most of us (Russian “adult” nephrologists) turned out to be unprepared for the current situation due to insufficient acquaintance with this rather rare, but very interesting pathology. It seems that the following description of clinical observation can to some extent fill this gap.

Background. Metabolic syndrome (MS) is characterized by a number of pathogenetic factors that adversely affect the function of the central nervous system (CNS). The study of early stages of ultrastructural damages in the CNS in the conditions of MS is important for compensation and prevention of pathological states leading to the brain hypoxia and cognitive disorders.

Objective. The aim was to investigate the morphological characteristics of the brain tissue and the cerebral capillaries in neocortex (the I-VI layers) sensorimotor region of rats with MS induced by a long-term (15 weeks) high-carbohydrate/high-fat (HC/HF) diet.

Design and methods. The neocortex ultrastructure was investigated using an electron microscopy.

Results. The moderate destructive changes in the components of the neurovascular units of the sensorimotor region of the cerebral cortex were detected in MS rats. Regardless of the functional response of brain capillaries (vasodilatation / vasoconstriction) to systemic insulin resistance and hyperglycemia, the signs of blood-brain barrier (BBB) dysfunctions were detected in MS-rats, such as an increase in the thickness and the impaired integrity of the basement membrane, endothelial microclasmosis, edema, and the estruction of perivascular glia. The destructive changes in cerebral capillaries were combined with neuro-vasal contacts increased 2,3 times, the proportion of apoptotic neurons increased 5 times and the proportion of normochromic neurons accurately reduced by 13 %.

Conclusion. In neocortex sensorimotor region of rats with MS induced by the HC/HF diet, the moderate dysfunction of the BBB and the reactive changes in neurons and neuro-vasal contacts were shown, and the cause of which may be hyperglycemia, dyslipidemia, and systemic insulin resistance typical for MS.

Background. Antipsoriatic medicines that have been successfully tested by imiquimod-induced psoriasislike skin inflammation in BALB/c mice may be used for therapy of psoriasis induced by the immune response as inflammatory cascade into skin layers.

Objective. Imiquimod-induced psoriasis-like skin inflammation approbation in BALB/c mice and search of more informative method of pathologic progress assessment for further extrapolating data to clinical cases.

Design and methods. Psoriasis-like skin inflammation in mice was induced by topical applying of the Aldara® cream (5 % imiquimod) to back skin for 7 days. Psoriasis Area and Severity Index (PASI), histological study, calculation of relative spleen and thymus mass to the body weight, hematological analysis and skin disease area determination were used for registration of pathologic building.

Results. During the study, was detected the increase of PASI score of animals with pathology to 18 with the formation of psoriasis-like plaques, significantly decrease body weight and relative thymus mass, significantly increase relative spleen mass, leukocytosis and leukocytic blood profile change, significant increase epidermal thickness, hyperkeratosis and inflammatory infiltration different degree.

Conclusion. Results of approbation studied pathologic model with using of hematological analysis and skin disease area determination consistent with similar studies’ data and partly clinical sings in patient with psoriasis.