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Background: Atrial fibrillation (AF) develops in the early postoperative period in each third patient undergoing coronary bypass surgery (CBPS). Multifactorial pathogenesis of postoperative AF is unclear. The concept of postoperative inflammation as a potential basic mechanism of this condition has been implied in many studies. Pre- and postoperative treatment with antiinflammatory statins proved beneficial as a means for reducing the frequency of AF., Materials and Methods: The meta-analysis is based on the results of 15 clinical studies carried out in the last 15 years. They included 9369 patients of whom 5598 (59.75%) used statins and 3771 (49.25%) did not receive them. The following endpoints were evaluated in the early postoperative periods: fiequency of AF, overall lethality, frequency of cerebral circulation disorders and myocardial infarction. Odds ratio (OR) and 95% CI were calculated, levels of inflammation markers before and after surgery and duration of hospitalization were determined., Results: Statins decreased the frequency of AF soon after CBPS (OR 0,481 at 95% CI 0,345-0,672; p = 0,000), they did not influence overall lethality (OR 0,837 at 95% CI 0,501-1,399: p = 0,497) and frequency of myocardial infarction (OR 1,001 at 95% CI 0,702-1,426; p = 0,997), but decreased frequency of cerebral circulation disorders (OR 0,067 at 95% Cl 0,037- 0,121; p = 0,000). Also, they reduced duration of hospitalization and serum levels of inflammation markers., Conclusion: Results of clinical studies available to date leave no doubt that statins produce anti-inflammatory and anti-arrhythmic effects. Meta-analysis of relevant studies confirmed on the whole the positive role of statin therapy prior to CBPS.

Aim: To estimate whether optimal antiplatelet therapy can be selected in terms of CYP2C19 polymorphism., Subjects and Methods: The prospective randomized trial included 124 patients (93 men and 31 women) who were to undergo percutaneous coronary intervention. They initially received dual antiplatelet therapy: clopidogrel 75 mg + acetylsalicylic acid (ASA) 300 mg. Genetic testing was performed in all the patients to reveal the carriage of allelic variants of the genes of cytochrome P-450 isoenzymes and the efficiency of antiplatelet therapy was evaluated. The carriers of one allele (CYP2C19*2/*1) were randomized into 3 subgroups according to further antiplatelet therapy. The therapy was not changed in Subgroup 1. The dose of clopidogrel was increased up to 150 mg/day and that of ASA remained unchanged in Subgroup 2. In Subgroup 3, the therapy was completely changed to the regimen: ASA 300 mg + ticagrelor 90 mg twice daily. Three days later, platelet aggregation was reinvestigated in all the three subgroups., Results: In our investigation, the prevalence of carriage of at least one of the CYP2C19*2 alleles was about 35%. Comparison of the baseline platelet aggregation levels during the same platelet therapy showed statistically significant differences between the carriers and non-carriers: 32.7±11.6 and 44.8±12.9 (p=0.0024). Compared with the baseline values, there was a drug therapy switching-induced reduction in platelet aggregation in Subgroups 2 and 3 (p=0.0001 and p=0.0056, respectively). No statistically significant differences were found in Subgroup 1., Conclusion: The determination of CYP2C19 gene polymorphism allows a personalized approach to be applied in antiplatelet therapy for all patients with coronary artery disease.

We studied the features of functional interaction between the subsystems of autonomic control of heart rate (HR) and arterial pressure (AP) giving rise to 0.1 Hz oscillations in R-R intervals (RRI) and photoplethysmogram (PPG). The study included 25 healthy subjects (6 women and 19 men) aged between 18 and 32 years. The signals of RRI, PPG and respiration were simultaneously recorded under breathing with a frequency linearly increasing from 0.05 Hz to 0.25 Hz within 25 minutes in a sitting position of a subject. The possibility of phase and frequency locking of 0.1 Hz oscillations in RRI and PPG by respiration is shown. We revealed that theses oscillations have different width and location of the intervals of phase and frequency locking by respiration. This distinction points to the functional independence between the mechanisms of autonomic control of 0.1 Hz oscillations in RRI and PPG.

Autoimmune hepatitis (AH) is a chronic inflammatory immunodependent disease of the liver. Women are affected more frequently than men. The patients show clinical and morphological signs of chronic hepatitis, extrahepatic manifestations of immune disorders (autoimmune thyroiditis, non-specific ulcerative colitis, vitiligo, diabetes mellitus, etc.), readily respond to glucocorticoid therapy have elevated levels of ALA, gamma-globulins (especially IgG), serum ANA, SMA, LKM or SLA antibodies. Untreated AH promotes rapid development of liver cirrhosis with 90% 10-year lethality. AH is diagnosed by exclusion and is of primary importance for clinical practice. The treatment is based on the use of immunosuppressors as a rule prescribed in addition to steroid therapy. It results in complete remission and normal life expectancy in 80% of the cases.

We studied biophysical features of interaction between 0.1 Hz oscillations in heart rate variability (HRV) and distal blood flow (DBF) variability in healthy subjects and patients after acute myocardial infarction (MI). 125 patients after acute MI (72 male and 53 female) aged between 30 and 83 years and 33 healthy subjects (23 male and 10 female) aged between 20 and 46 years were included in the study. The duration of prospective study of MI patients was one year. We estimated the delay in coupling between 0.1 Hz oscillations in H RV and DBF variability. It is found out that in healthy subjects the delay in coupling from heart rate to DBF is less than delay in coupling from DBF to heart rate. Acute MI results mainly in disruption of coupling from heart rate to DBF. This coupling is partially restored in one year after acute MI, but the delay in coupling remains significantly smaller than in healthy subjects. The features of coupling from DBF to heart rate are restored in MI patients within three weeks after infarction. After this period the delay in this coupling in MI patients is approximately the same as it is in healthy subjects.

Aim: To compare clinical efficacy of standard outpatient follow-up of hypertensive patients with efficacy of such follow-up with application of internet techniques and mobile telephone systems (ITMTS)., Material and Methods: Two groups of hypertensive patients were examined: group 1 (n=97, 45% females, age 49 +/- 11 years) on one-year ITMTS follow-up; group 2 (n=102, 50% females, age 51 +/- 11 years) on standard one-year follow-up. Clinical efficacy was assessed by the rate of achievement and maintenance of target blood pressure, dynamics of modifiable risk factors (smoking, obesity) for a year., Results: Withdrawal in group 1 was 36%, target blood pressure was achieved in 77% patients vs. 12% in group 2 (p < 0.001)., Conclusion: Introduction of ITMTS technologies into outpatient clinics activity considerably raises efficacy of outpatient treatment of hypertensive patients.

The data of TLR-4 and TLR-2 existance in adipose tissue cells is presented in the review, their signal pathway is described, and an idea of physiological and pathological role of innate immune system receptors is given proof. TLRs activation leads to insulin resistance of adipose, hepatic and muscle cells, which increases glucose and lipids level in blood. This reaction is defined as a condition of physiological insulin resistance, which role is in providing immune processes with energetic and plastic substances. Ligands of TLRs are components of microorganisms: bacterial lipoproteins and liopolysacharides, as well as nonsaturated fatty acids. Inadequate uptake of the latter with food activates TLR-4 and R-2, acting as a mechanism for pathological alterations. Under the conditions of innate imunity receptors excessive activation, there is an adipose tissue inflammation, overproduction of cytokines, along with insulin resistance. It promotes the progress of obesity, diabetes and atherosclerosis.

Obesity is a factor contributing to the development of atherosclerosis and cardiovasular diseases. A key pathogenetic mechanism of obesity-associated atherosclerosis is inflammation of the adipose tissue concomitant with mild systemic inflammation, altered secretion of adipokines and cytokines, and insulin resistance. This review is focused on the role of hypoadiponectinemia, enhanced secretion of leptin, resistin, TNF-alpha, IL-1, IL-6, interferon-gamma, and activation of renin-angiotensin system in pathogenesis of atherosclerosis. The stimulatory action of insulin resistance accompanying inflammation of the adipose tissue on evolution of atherosclerosis is mediated through the development of dyslipidemia, hyperglycemia, and arterial hypertension. Other important factors involved in pathogenetic mechanisms of atherosclerosis are inflammation of perivascular fatty tissue and paracrine activity of cytokines and chemokines it releases.

This review deals with the role of adipose tissue inflammation (ATI) in the development of type 2 diabetes mellitus (DM2). ATI is regarded as a link between obesity and DM2. The review illustrates the involvement of main adipokines in pathogenesis of DM2 and provides a detailed description of such factors as impaired adiponectin and stimulation of cytokine production responsible for metabolic disorders, activation of lipolysis, in adipocytes, increased fatty acid and triglyceride levels, suppression of insulin activity at the receptor and intracellular levels. Adipokines, in the first place cytokines, act on the insulin signal pathway and affect the intracellular inflammatory kinase cascade. At the intercellular level, ATI stimulates JNK and IKK-beta/kB responsible for the development of insulin resistance via such mechanisms as activation of cytokine secretion in the adipose tissue, oxidative stress, and induction of endoplasmic reticulum enzymes. The key role of JNK and IKK-beta/kB in the inhibition of the insulin signal pathway is mediated through inactivation of insulin receptor substrate 1. Also, it is shown that ATI modulates B-cell function and promotes progressive reduction of insulin secretion.

The review describes a new pathomorphological phenomenon: adipose tissue inflammation (ATI) that develops in obesity and is characterized by cell infiltration, fibrosis, microcirculatory changes, a shift in adipokine secretion and adipose tissue metabolism, as well as blood accumulation of nonspecific inflammatory markers, such as C-reactive protein, fibrinogen, leukocytes, the level of which reflects the degree of the process. The changes in adipokine secretion and shifts in fat and carbohydrate metabolism, which are typical of ATI, favor the development of atherosclerosis, essential hypertension, type 2 diabetes, and the metabolic syndrome. ATI shows up as a connecting link between these diseases and obesity. The definition of obesity as a chronic inflammatory disease is justified.

The concept of adipose tissue as an inactive organ, which serves only for the accumulation and storage of energy substrates and triglycerides, has finally remained in the past. Studies of recent decades have shown that adipose tissue is very active in the metabolic aspect, and also produces many hormone-like substances, mediators, cytokines, chemokines that act at the local and systemic level, i.e., para- and endocrine. Regulatory substances produced in adipose tissue have received the general name adipokines or adipocytokines. Their study is the most actively developing area of ​​modern endocrinology. Adipokines made it possible to explain the pathophysiology of the long-known clinical phenomena of the close relationship between obesity, diabetes mellitus (DM), arteriosclerosis and insulin resistance. The list of adipokines produced in adipose tissue is very impressive and will undoubtedly be supplemented. By the beginning of 2008, the following adipokines were described: leptin, adiponectin, resistin, tumor necrosis factor a (TNF-a), interleukin-6 (IL-6), visfatin, apelin, omentine, vaspin, retinol-binding protein-4 (RBP-4) and other factors, including lipoprotein lipase, apolipoprotein E, complement factors, tissue factor, plasminogen activation inhibitor-1 (IAP-1), proteins of the renin angiotensin system (RAS). In addition, adipocytes express chemokines such as MCP-1 and RANTES.This review schematically presents the basic physiological and pathophysiological actions of known adipokines.

The aim of this clinico-epidemiological study was to elucidate the role of postprandial hyperglycemia (PH) and high glucose level 2 hours after glucose load in the development of cardiovascular disorders (CDD) in patients with type 2 diabetes mellitus and in the general population. Medical interventions to reduce PH decrease the risk of CDD. Pathophysiological studies show the involvement of oxidative stress in pathogenesis of CDD in cases with PH. Acute hyperglycemia increases heart rate and arterial pressure, disturbs myocardial perfusion and contractility, causes endothelial dysfuncton and atherosclerosis. The following preparations are recommended to subjects with DM2 and PH: alpha-glucosidase inhibitors, glynides, ultrashort-acting insulin analogs, dipeptidylpeptidase-4 inhibitors, exenatide (incretin mimetic).

Pharmaceutical products reviewed in this paper markedly extend possibilities for the management of DM-2 and create prerequisites for diferential therapy of this disease. Exenatide and DPP-4 inhibitors do not cause hypoglycemia and may be prescribed to subjects in whom this condition may affect the ability to drive or operate machinery (drivers, pilots, etc.). The mechanism of action of DPP-4 inhibitors make them especially suitable for the treatment of early stages of DM-2 when B-cells are still capable of insulin secretion. They can be used at a dose of 100 mg once daily both for monotherapy and in combination with other oral hypoglycemic agents. These drugs are well tolerated by the patients but contraindicated to those with severe renal insuficiency. Exenatid is more eficacious than DPP-4 inhibitors and has advantages over insulin therapy because it does not increase body weight and do not require as frequent blood glucose monitoring. However, it produces side effects. Therefore, the treatment should be started with a low dose of the drug (5 mg subcutaneously twice daily) that can be doubled in 4 weeks. Bearing in mind the mechanism of action of exanatide, it is indicated largely to patients with DM-2 associated with obesity and a moderately elevated HbAlc level. Rimonabant is especially efficient due to its effect on the endocannabioid system of DM-2 patients with obesity, however it has a drawback of frequently producing adverse affects.

Having analyzed the data base of All-Army register contained information about 35,970 rescuers it was determined that 45.5% of them during works in dangerous radiative conditions complained of the health change for the worse characterized by the state of irritation of mucous membrane of superior respiratory and gastrointestinal tracts. The direct correlation between value of irradiation dose and frequency of complaints, and also degree of lowering of there physical performance have been defined.

The dynamics of hormonal secretion was studied in relation with the development of an ulcer defect in rats with acetate-induced gastroduodenal ulcer after Okabe. The formation of the ulcer was accompanied by increased gastrin, glucagon, cortisol, growth hormone, and histamine secretion and reduced glucose tolerance. The level of intragastric pH reduced, the activity of proteolytic enzymes in the gastrointestinal tract increased. Correlation analysis bore evidence for the contribution of gastroenteropancreatic hormones to the compensatory-adaptational responses, whereas with a higher blood cortisol level the surface of the ulcer defect was larger. Oral mineral water (Essentuki No. 17) promoted the secretion of gastrin, glucagon, and insulin and the experimental ulcers grew smaller in this case. The involvement of the hormonal factors in the mechanisms of the development of experimental acetate-induced ulcer is discussed.

Ultrasonic scanning following a course of mud therapy found out a stimulatory effect of the treatment on gallbladder motility. The bile composition reflected an anti-inflammatory action of mud applications which also enhanced bile lithogenesis.

Basing on literature reports and original investigations, the author considers recovery of normal gastrointestinal function as one of the mechanisms of mineral water action. Curing effect is realized by normalizing the function of the affected organ rather than gastric secretion and is due to a beneficial effect of the water on the regulatory gastrointestinal systems.

Hypersecretion of hydrocortisone, that of insulin, triiodothyronine, thyroxin reflecting phases of stress response and persistence were recorded in early and late postcholecystectomy terms, respectively. As intake of mineral water stimulates secretion of anabolic hormones (insulin, triiodothyronine and thyroxin) and inhibits secretion of catabolic hormone hydrocortisone, drinking of mineral water can be helpful in activation and adjustment of compensatory and adaptive responses after cholecystectomy.

The enthalpy effect of hydrate envelope deformation was first taken into consideration for estimating the influence of aqueous medium on the stability of RNA duplexes. In addition two rarely used parameters (macroscopic value of dielectric water permeability and entropy effect of dehydration) were employed. According to the energy model described the contribution of the free energy of dehydration to the RNA duplexes stability is significant even in comparison with that of the interstrand stacking.

The main target for the action of mineral water in gastrointestinal diseases is the gastroenteropancreatic neuroendocrine system. The effect of oral mineral water is attributed both to physicochemical properties and the intelligence signal of mineral water.

Experiments with 40 dogs have demonstrated that overexercise of the maxillodental system for 30 days results in reduction of the bioenergy potential of the periodontal bone tissue of the overloaded teeth. When the traumatic overload was eliminated for the next 30 days, the functional parameters gradually recovered, but the biochemical characteristics of the regenerated bone did not fully normalize.

Examinations of different patients with duodenal ulcer performed during one year revealed seasonal changes in the function of the regulatory systems. Secretion of histamine, serotonin, insulin, and hydrocortisone was increased in spring and reduced in autumn. Secretion of adrenalin, noradrenalin and acetylcholinesterase activity were high in summer and low in autumn. The acid-producing function of the stomach did not depend on the season. It is suggested that deviations in the activity of the regulatory systems in spring and autumn may cause seasonal exacerbations of duodenal ulcer.

It has been demonstrated that the basal gastrin level in the blood of patients with peptic ulcer of the duodenum is similar to that in normal subjects. Food stimulation raises blood gastrin in normal subjects and patients. However, in patients, the peak of the blood hormone rise is higher, with this rise lasting for a longer time. Besides, the total output of the hormone is greater. These changes are most marked during an incomplete disease remission, being less remarkable when exacerbation gets attenuated and during a complete remission. A correlation has been noticed between the acid-forming function of the stomach and basal blood gastrin level that increases as the acid content in gastric juice descends. In patients experiencing a complete remission and in those in the stage of an incomplete remission and attenuated exacerbation, a direct correlation was ascertained between the stimulated hypergastrinemia and duration of the intragastral pH elevation in response to food intake. It is suggested that in peptic ulcer of the duodenum, hypergastrinemia occurs as a defence reaction aimed at the activation of trophic processes in the mucous membrane of the gastroduodenal zone.

The basal and food-stimulated gastrin secretion after selective proximal vagotomy, selective gastric vagotomy and truncular vagotomy was found to be elevated. Hypergastrinemia increased as gastric secretion was inhibited, thus attesting to the role of acid formation inhibition in the origin of the postvagotomy increase in the hormonal secretion. However the values of the intragastral pH being equal, the blood gastrin level was higher after vagotomy as compared to that seen in unoperated peptic ulcer patients. After vagotomy coupled with antrumectomy gastrin secretion remained at the level seen in the unoperated patients, indirect evidence for increased function of extraantral G cells. Inhibition of gastric secretion is no single cause of the postvagotomy hypergastrinemia, since the latter was essentially increased in the early postoperative times and in the presence of the vagotomy-induced disorders. It is concluded that increased secretion of gastrin after vagotomy secures trophic and compensatory-adaptation processes.

The paper presents a review of the data obtained on the shifts in alimentary function and in relevant regulatory hormonal system in response to a single and course intake of mineral water. It is established that mineral water is a load for alimentary tract, and brings about adaptive reactions when administered in courses. The author infers on the underlying factors contributing to therapeutic effect of crenotherapy. These factors are training effects, adaptive response, activation of repair processes.

Drug and spa conservative treatment of postvagotomy aftereffects has been reviewed. The analysis covers the use of enzymes, cholinergic blocking agents, cyproheptadine hydrochloride, amitriptyline hydrochloride, L-Dopa, diphenoxylic acids and opioids in dumping syndrome; benzohexonium and metoclopramide in gastrostasis; diphenoacids and opioids in postvagotomy diarrhea. Oral and external use of mineral water and mud applications proved most beneficial spa treatment modalities.

Correlation between a degree of activation of hormonal secretion and the expression of a pathological process in the gastroduodenal area was established in patients with peptic ulcer, chronic gastroduodenitis with raised secretory gastric function and in patients after vagotomy. A sequence of involvement in the reaction to disease of the regulatory systems of the local (gastrin, serotonin and histamine mechanisms), systemic (enteroinsular axis) and organic (glucocorticoid and adrenal function of the adrenal glands) levels was revealed.