For clinical medicine the problem of complications associated with the metabolic syndrome is significant and requires a multidisciplinary approach, since the metabolic syndrome itself has long since moved from the sphere of interest of endocrinologists and cardiologists to general medical practice. Most commonly, the metabolic syndrome leads to cardiovascular and cerebrovascular complications. One of the topics currently under discussion is the question of the influence of the components of the metabolic syndrome on the condition of the respiratory system. An epidemiological association between visceral obesity and insulin resistance with chronic obstructive pulmonary disease, bronchial asthma, and obstructive sleep apnea/hypopnea syndrome has been established. Although respiratory disorders are common in patients with clinical equivalents of the metabolic syndrome, their pathogenesis is not well understood. Aim of the study was to analyze the role of individual most significant components (pathogenetic factors) of the metabolic syndrome in the pathogenesis of respiratory disorders. Conclusion . Clinical and laboratory equivalents of the metabolic syndrome, such as obesity, hyperglycemia, and hyperinsulinemia, contribute to respiratory function impairment. The most discussed process that combines the components of the metabolic syndrome and its associated complications is chronic systemic inflammation. The review presents a conceptual scheme of the pathogenesis of respiratory disease in the metabolic syndrome and highlights the role of its factors in the development of qualitative changes in the air-blood barrier and a decrease in the diffusion capacity of the lungs. The authors pointed out a number of unresolved issues in the pathogenesis of respiratory disorders in the metabolic syndrome and also emphasized the relevance of experimental studies of early mechanisms of lung disease development using animal models.

Purpose. The aim of the study was to investigate the subpopulation composition and prooxidant activity of adipose tissue cells in the big omentum of patients with metabolic syndrome.Material and Methods. A fragment of white adipose tissue obtained from the greater omentum during planned endoscopic cholecystectomy in 37 female patients aged 48 (34; 65) years was used as a material for the study. The main group was represented by patients with metabolic syndrome (n = 31) diagnosed according to current recommendations for management of patients with metabolic syndrome. Six patients without signs of metabolic syndrome, comparable with the main group in terms of age and gender, made up the comparison group. The subpopulation composition of the adipose tissue cells in the greater omentum was determined by immunohistochemical analysis. The content of reactive oxygen species in the isolated cell pools of adipocytes and mesenchymal stromal cells was identified using flow cytometry.Results. Comparison of the mean values in the groups showed a statistically significant prevalence in patients with metabolic syndrome only in the level of cells expressing CD68 (macrophage marker) on their surface (p < 0.05). Correlation analysis allowed to detect a positive relationship between morphometric indicators determining the severity of infiltrative changes of adipose tissue (the number of infiltrates) and the relative number of cells presenting CD3 (r = 0.357, p < 0.05), CD36 (r = 0.575, p < 0.05), and CD68 (r = 0.374, p < 0.05) on their surface, respectively. A comparative analysis of the level of reactive oxygen species in adipose tissue cells showed statistically significantly (p < 0.05) higher values of reactive oxygen species in patients with metabolic syndrome compared with the control group both in adipocytes and in mesenchymal stromal cells.Conclusion. The presence of a positive correlation between the relative numbers of cells presenting CD3, CD36, and CD68 markers and the morphometric parameters reflecting the severity of infiltrative manifestations suggested that the mentioned cell lymphocyte and macrophage populations were involved in the development of infiltration in the adipose tissue in metabolic syndrome. The pro-inflammatory phenotype of adipose tissue in metabolic syndrome was characterized not only by a number of morphological features, but also by enhanced prooxidant activity of the adipocytes and mesenchymal stromal cells.

The aim of the study was to identify the features of the cellular composition and cytokine profile of bronchoalveolar lavage fluid in rats in a model of diet-induced metabolic syndrome.Materials and methods. In an experiment on animals (rats), a model of metabolic syndrome (MS) induced by a high-fat and high-carbohydrate diet was reproduced. To assess the viability of the reproduced model, biochemical and morphometric methods were used, such as measurement of body weight, specific gravity of liver and visceral fat, and blood pressure, determination of glucose concentration in the blood (including a glucose tolerance test), as well as determination of blood lipid parameters. To assess the intensity of the inflammatory response in the blood, the concentration of total protein, the total number of leukocytes, and the levels of immunocytokines (interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)α, monocyte chemoattractant protein (MCP)-1) were determined. Open bronchoalveolar lavage was performed on the isolated heart – lung complex. The concentration of protein, immunocytokines (IL-6, IL-10, TNFα, MCP-1), the total number of leukocytes, and the ratio of their morphological types were determined in the bronchoalveolar lavage fluid (BALF).Results. In animals with MS, an increase in the total number of leukocytes in the blood due to granulocytes and a rise in the concentration of protein, TNFα, and IL-10 were revealed compared with the parameters in the controls. BALF analysis revealed an increase in the concentration of protein, the total number of leukocytes, and the absolute number of alveolar macrophages, neutrophil granulocytes, and lymphocytes. The levels of IL-6 and MCP-1 were more than 1.5 times higher.Conclusion. Changes in the qualitative and quantitative parameters of BALF are inflammatory in nature and are formed during a systemic inflammatory response accompanying metabolic disorders in modeling MS in rats in the experiment.

Aim of study: to examine the features of expression of CD-markers of blood mononuclear leukocytes and their functional activity in the metabolic syndrome. Conducted a cross-sectional (transverse) study of 76 patients with essential hypertension (EH) II stage (BP <180/110 mm Hg.) [10] in conjunction with the metabolic syndrome and 20 people, formed the control group. Along with a complete clinical, laboratory and instrumental examination taken in a specialized cardiological clinic was conducted determination of surface markers of lymphocytes CD4+, CD8+ and monocytes CD36+ and assessment of the level of spontaneous production of reactive oxygen blood mononuclear leukocytes. Found that in patients with the metabolic syndrome compared with the control group the proportion of CD4+ lymphocytes and the level of spontaneous ROS production by mononuclear leukocytes significantly higher. The positive correlated interconnection between these indicators and the number of CD36+ monocytes with the majority of clinical and metabolic markers of MS confirmes their participation in mechanism of immune inflammation and oxidative stress in this pathological process.

The aim of this study was to assess effects of the eight-week course of atorvastatin therapy upon the levels of spontaneous cytokine production by mononuclear blood leukocytes (MNBC) in metabolic syndrome. An open-label prospective study included 36 patients with stage II hypertension (blood pressure < 180/110 mm Hg.) accomplished by metabolic syndrome. Along with clinical surveys performed at a specialized cardiological clinics, we assessed spontaneous cytokine production by MNBC during treatment with atorvastatin. It was shown that the 8-week treatment of these patients with atorvaststin, at individually matched daily doses (20 to 40 mg) was associated with reduced serum concentration of acute phase proteins (C-reactive protein and neopterin), as well as decreased spontaneous production of proinflammatory cytokines (IL-1β, IL-6 and TNFα) by MNBCs. The latter finding is of great importance for pathogenesis of metabolic syndrome.

Objective: research gender features of relationship of hormonal activity of adipose tissue and proinflammatory status with essential hypertension (EH) in combination with metabolic syndrome (MS).Material and methods. Were examined 46 patients with essential hypertension stage (BP < 180/110 mm Hg.) in conjunction with the metabolic syndrome. Along with a complete clinical, laboratory and instrumental examination adopted in specialized cardiological clinic, were defined concentrations in serum leptin, adiponectin, resistin and visfatin and the level of markers of systemic inflammation (C-reactive protein, neopterin and fibrinogen), was assessed the level of spontaneous production of cytokines and active oxygen species and the expression level of CD4, CD8 and CD36 – blood mononuclear leukocytes markers.Results and conclusions. It was established that the hormonal status of adipose tissue have women with EH combined with MS are characterized by higher levels of leptin and adiponectin in blood serum than in men.It was established not only a significant role adipokin imbalance in mechanisms of MS and systemic inflammation in these patients category, but also were studied gender characteristics. While for men in the development of the above pathological manifestations hipoadiponektinemia has the most meaning, and for women – hyperleptinemia.

AIM:To study effect of atorvastatin on spontaneous production of cytokines and reactive oxygen species by mononuclear leukocytes of blood of hypertensive patients with metabolic syndrome in vivo and in vitro.MATERIAL AND METHODS:We conducted an 8-week open prospective study on 36 patients with essential stage II hypertension associated with metabolic syndrome. Along with examination made in specialized cardiological clinic we assessed spontaneous production of cytokines and reactive oxygen species by blood mononuclear leukocytes during therapy with atorvastatin (in vivo). Dynamics of these parameters under the influence of atorvastatin on suspension of mononuclear leukocytes was also assessed in vitro.RESULTS:Therapy with atorvastatin (20 to 40 mg/day) facilitated reduction of serum concentration of acute phase proteins (C-reactive protein and neopterin) and decrease of spontaneous production by blood mononuclear leukocytes of proinflammatory cytokines (interleukin [IL]-1β, IL-6 and tumor necrosis factor [TNF]-α) and reactive oxygen species. Dynamics of cytokine concentrations in supernatants of mononuclear leukocytes obtained after incubation of the cells with atorvastatin in vitro confirmed the assumption of direct inhibitory effect of this drug on spontaneous production of some proinflammatory cytokines (IL-6 and monocyte chemotactic protein-1). Absence of significant lowering of concentrations of other proinflammatory cytokines (IL-1β and TNF-α) and expression of reactive oxygen species in vitro evidenced for complex indirect effect of therapy with atorvastatin on their production.

Objective. To study interconnection between hyperleptinemia, the quality of life (QOL) and the severity of metabolic disorders in patients with essential hypertension with metabolic syndrome (MS). Design and methods.We have examined 46 patients with essential hypertension (blood pressure < 180/110 mm Hg), accompanied by MS. Along with complete clinical, laboratory and instrumental examination, customary in a specialized cardiologic clinic, the QOL research was carried out using MOS SF-36questionnaire. Besides, the concentration of leptin in blood serum was determined.Results and conclusions. Patients with essential hypertension with hyperleptinemia show higher intensity of clinical and laboratory markers of MS, higher activity of the systemic inlammatory response and increased QOL. A statistically signiicant inverse correlation between serum leptin level and QOL scales (SF-36) was detected.

Due to the fact that nowadays mechanisms of syntropy of pathological conditions and nosological units, united within the metabolic syndrome, remain unclear, the scientific review attempts to summarize data on the role of fatty tissue inflammation in pathogenesis of this symptom complex. The results of recent major foreign studies on evaluation of pro-inflammatory activity of adipocytes and macrophages of the fatty tissue, as well as the data on peculiarities of their interactions in abdominal obesity, which is the main component of the metabolic syndrome, were analyzed. Studing pathogenesis of fatty tissue inflammation from the perspective of evaluation of disorders in cell cooperation will allow to more deeply understand cellular and molecular mechanisms of this process as well as open new avenues for developing new pathogenetically justified approaches to metabolic syndrome treatment.

Aim. To comprehensively study hemostasis pathology and its association with the laboratory markers and mediators of inflammation in patients with metabolic syndrome (MS).Subjects and methods. One hundred and eleven patients with type 2 diabetes mellitus, who were diagnosed as having MS, were examined. Vascular-platelet and secondary hemostases and anticoagulant and fibrinolytic systems were evaluated, by performing the complete clinical, laboratory, and instrumental study accepted in a specialized endocrinology clinic. The blood concentrations of high-sensitivity C-reactive protein and proinflammatory cytokines were determined in all the patients with MS and control persons (n=50).Results. It was found that in patients with MS, hemostasis pathology that might be classified as the combined form of a prethrombotic state, which was caused by different types of a constellation of vascular-platelet and plasma hemostases, as well as physiological anticoagulant deficiency, was linked to the laboratory markers and mediators of subclinical inflammation.Conclusion. In the patients with MS, subclinical systemic inflammation is of substantial importance for the mechanisms of a prethrombotic state.

AIM:To study pleiotropic effects of atorvastatin during 8-week therapy of metabolic syndrome and estimate their relationship with dynamics of quality of life characteristics (QLC).MATERIAL AND METHODS:This 8-week study included 36 patients with stage II hypertensive disease associated with metabolic syndrome (MS). Comprehensive clinical, laboratory and instrumental examination was supplemented by QLC assessment using the MOS SF-36 questionnaire.RESULTS:8-week therapy of stage II hypertensive disease associated with metabolic syndrome using individually selected doses of atorvastatin (20 to 40 mg/d) significantly reduced atherogenic cholesterol fraction and serum leptin levels; it had positive effect on carbohydrate and purine metabolism and safely maintained positive dynamics of subjective assessment of most points of the MOS SF-36 questionnaire.

Objective. To assess the quality of life (QOL) in hypertensive patients and to study the interrelation between the QOL indicators and the metabolic syndrome (MS) components. Design and methods. We examined 46 patients with stage II hypertension and 18 healthy subjects. Standard full clinical, laboratory and instrumental examination as well as QOL by MOS SF-36® questionnaire were performed in all subjects. Results and conclusions. Hypertensive patients and healthy subjects differed by the scale of general health (GH), physical functioning (PF), pain intensity (BP) and vitality (VT). We detected reverse correlation between the QOL indicators and all the components of MS, such as abdominal obesity, hyperglycemia, dislipoproteinemia, degree of arterial hypertension, as well as with fibrinogen level.

Object of research: to study the interrelation of activity of systemic inflammatory response and quality of life (QOL) and evidence of metabolic disorders in hypertensive patients with metabolic syndrome (MS).Material and methods. We carried out a study of 86 patients with hypertensive disease of II stage in combination with MS and 18 volunteers, who formed the control group. Along with a complete clinical, laboratory and instrumental examination, taken in a specialized cardiology clinic, the study of QOL using the MOS SF-36 questionnaire was carried out, as well as the research of activity of systemic inflammatory response.Results. We determined the reverse correlative interrelation of QOL indicators with all MS components, such as abdominal obesity, hyperglycemia, hypertriglyceridemia, the degree of arterial hypertension, but also with the level of markers of systemic inflammation (C-reactive protein, neopterin and fibrinogen), hyperinsulinemia and hyperleptinemia. It was found out that physical functioning (PF) has the strongest interrelations with the maximum number of clinical and laboratory indicators of MS and all the studied markers of systemic inflammation.

In this paper we investigated p38-dependent mechanisms of gaseous transmitters nitric oxide and hydrogen sulfide influence on XIAP and AVEN genes expression in Jurkat cells. Using the method of real-time PCR, XIAP and AVEN genes expression in cancer Jurkat cells was shown. Donors of gases of nitric oxide and hydrogen sulfide were negative regulators of the XIAP and AVEN gene expression in the cells of T-lymphoblast leukemia. Changes in the expression of above mentioned genes under NO and H2S influence occurred with the involvement of p38 MAP kinase

In this paper, participation of gases, nitric oxide, carbon monoxide and hydrogen sulfide, in cell apoptosis regulation has been analyzed according to the literature data and our own findings. Different mechanisms of nitric oxide influence on apoptotic reaction including modulation of transcription factors activity and increase in mitochondrion membrane permeabilisation are described. Brief description of the generation and signal transduction pathways of carbon monoxide is presented. Pro- and antiapoptotic mechanisms of hydrogen sulfide influence on cell fate are analyzed.

Investigation of influence of gases nitric oxide and hydrogen sulfide on apoptotic cell death of Jurlat cells and mononuclear leucocytes of healthy donors was conducted. It was shown that 100 mmol sodium nitroprussidi increased the apoptosis of T lymphoblast leukemia cells after 15’ incubation. 10 and 100 mmol donor of hydrogen sulfide caused apoptotic death of Jurkat cells after 15’ incubation. 15’ exposure of nitric oxide and hydrogen sulfide donors did not lead to the changes of cell death of mononuclear leucocytes. Gaseous transmitters NO and H2S increased necrosis of Jurkat cells and mononuclear leucocytes after 24 h incubation with the appropriate gase’s donor.

To study CD1a+ Langerhans cells and their extensions in epidermis and values of IL-4, IL-10, IL-17 and IFN-g in cell-free skin exudate there have been examined 40 patients of atopic dermatitis depending on phase pathological process. There have been found an increase in both CD1a+ dendritic extensions in medium layer of the epidermis and IL-4 and IL-10 in skin exudates. IFN-g exudate’s value has been decreased.