[Characteristics of Inferior Myocardial Infarction With a Special Electrocardiographic Pattern (Aslanger) in Metabolic Syndrome].

AIM: To evaluate the features of ST-segment elevation myocardial infarction with the Aslanger pattern in comparison with traditional forms of inferior myocardial infarction in metabolic syndrome. MATERIAL AND METHODS: This study included 30 patients with inferior myocardial infarction in the presence of metabolic syndrome: 9 patients with the Aslanger electrocardiographic pattern (group 1, age 59.7 [58.4; 63.1] years) and the rest with one of the traditional forms (control group, 59.9 [57.2; 63.8] years, matched by all criteria of metabolic syndrome). All patients underwent primary percutaneous intervention with assessment of the angiographic picture. The magnitude of ST-segment elevation was measured in lead III at the J point and following 0.06 seconds, and the optimal threshold value of this indicator was determined for a new picture of myocardial infarction. RESULTS: The infarct-related artery in the Aslanger pattern was more often the circumflex artery (p=0.0099), and coronary thrombosis was characterized by a lower TIMI thrombus grade (p=0.014). SYNTAX values for the Aslanger pattern and for the traditional picture of inferior infarction with ST elevation in lead II≥III were higher than for a similar picture with ST elevation in lead III>II. The level of cTnI at admission (p=0.013) and after 24 hours (p=0.0017), the platelet count (p=0.0011) and mean volume (p=0.0047) in group 1 had smaller values than with traditional inferior infarction. The ST elevation at J point and at J+0.06 s point for lead III with the Aslanger pattern was significantly lower than values of such shift in lead III>II and lead II≥III with traditional inferior infarction (p<0.001). An elevation value ≤1.5 mm at J point +0.06 s was a predictor of infarction with the Aslanger pattern. Constructing the ROC curve made it possible to determine that with the Aslanger pattern, the best cutoff value for this index is 2 mm. CONCLUSION: Myocardial infarction with the Aslanger pattern as compared with traditional lower infarction in metabolic syndrome is characterized by specific individual angiographic signs, lower ST segment elevation, cTnI level, and thrombotic disorders.

Meta-Analysis of Non-Alcoholic Fatty Liver Disease and Electromechanical Reconstruction of Myocardium.

In developed countries, non-alcoholic fatty liver disease (NAFLD), which results from obesity, has become endemic and kills many adults annually. Health research centers in most countries are looking to examine the relationship between metabolic syndrome (MetS) and metabolic biomarkers. A bleeding-prone standard liver biopsy or costly magnetic resonance imaging scan is used to diagnose NAFLD. The present study aimed to analyze medical databases using various scientific articles; moreover, this experiment analyzed medical databases using published scientific articles related to NAFLD, endovascular treatment, cardiac arrhythmias and conduction disorders, changes in the geometry of atria and ventricles, changes in myocardial mass volume as well as diastolic flow left and right ventricular systolic functions, coronary blood flow, analysis of the dependence of epicardial fat tissue (EFT) thickness, and the presence of chronic heart failure (CHF). It is demonstrated that the index of EFT in NAFLD positively correlated with the criteria of cardiovascular health, values of the carotid intima-media thickness, and calcification of the coronary arteries on the coronary artery calcium scale (P<0.0001). The index of per EFT significantly correlated with the factor of the age of the NAFLD patients (P=0.04), hemoglobin A1C level (P<0.001), systemic inflammatory index (P=0.02), the index of impaired glucose tolerance (P=0.03), and especially, the patient's diabetes factor (P<0.001). In addition, adiponectin levels were significantly lower in individuals with NAFLD (P=0.001) and patients with MetS (P=0.02). NAFLD in association with an increase in epicardial adipose tissue (EAT) is an independent risk factor for atherosclerosis, coronary heart disease, CHF, as well as structural and electrophysiological myocardial remodeling. The study of pathogenetic mechanisms in the context of the role of EAT and clinical monitoring of its condition are urgent problems of modern medicine.

[Features of a new corOnavirUs infection course and optioNs therapy DEpending on the andRogenic status (FOUNDER): androgenic status in men with COVID-19 and its relationship with the disease severity].

OBJECTIVE: Analysis of androgen status in men hospitalized with a moderate COVID-19 and its relationship with the severity of the disease. MATERIALS AND METHODS: The study included 152 males with a confirmed diagnosis of COVID-19 based on the results of a positive PCR for the SARS-CoV-2 virus and/or computed tomography of the lungs hospitalized at the MSU University Clinic due to the moderate and severe COVID-19. Examination of the level of biochemical blood parameters (CRP, creatinine, urea, glucose, total testosterone (T)); CT of the lungs. To objectify the severity of the clinical symptoms, the NEWS2 distress syndrome severity scales and the original scale for assessing the clinical condition of patients with COVID 19 (SHOCS-COVID) were used. RESULTS: The median T level in 152 examined patients was 2.14 [1.21; 3.40] ng/ml. In patients with a T level below the median, the CRP level was more than two times higher, and the D-dimer value was almost two times higher than in patients with T level above median. The duration of treatment in the hospital was longer in men with COVID 19 and an initial T level below the median than in patients with T about the median (13 days vs 10.5 days, p=0.003). Low T level was correlated with lung damage by lung CT. After improving the clinical condition, there was a linear increase in the level of T independent of its initial level. CONCLUSION: Among men with moderate and severe COVID-19, a decreased testosterone level is detected in 46.7% of cases. Patients with low testosterone levels on admission have more severe COVID-19. A significant increase in testosterone level was observed after successful COVID-19 treatment without any special action regarding testosterone level.

[Anatomometric characteristics and pleural cavity changes after pneumonectomy]. / Anatomo-metricheskaya kharakteristika i dinamika izmenenii plevral'noi polosti posle pnevmonektomii.

OBJECTIVE: To analyze the anatomometric characteristics of post-pneumonectomy cavity and their changes at various times after surgery. MATERIAL AND METHODS: The study included 47 patients aged 39-75 years after pneumonectomy (right-sided - 23 cases, left-sided - 24 cases). Computed tomography was performed prior to surgery, in 10-12 days, 6 and 12 months after intervention. Transverse, anteroposterior dimensions, height and volume of pleural cavity were evaluated using CT scans and 3D models. RESULTS: Post-pneumonectomy cavity decreases and changes own shape in postoperative period. Reduction is mainly caused by decrease in its height. The volume of post-pneumonectomy cavity was decreased in early postoperative period by 1.8 times compared to preoperative values (from 3351.5±150.0 cm3 to 2112.1±152.6 cm3 on the right side and from 2674.3±125.2 cm3 to 1460.1±84.1 cm3 on the left side). After 12 months, this value was reduced by 3.68 times compared to early postoperative period (714.3±100.7 cm3 on the right and 401.5±42.5 cm3 on the left). The shape changes consist of flattening and sinus depth reduction. Exudate density was similar throughout a year. The capsule was formed in 74.1% of patients after 12 months. There was no correlation between the cavity reduction and patient constitution. CONCLUSION: Post-pneumonectomy cavity is a dynamically changing anatomical formation participating in the mechanisms of compensation for changes after pneumonectomy. The most significant collapse of post-pneumonectomy cavity occurs in early postoperative period. Cavity reduction degree does not depend on individual characteristics of patients.

PRIMARY HYPERTROPHIC PYLORIC STENOSIS IN ADULTS.

THE AIM: to present some information-about the rare primary hypertrophy of the pylorus in adults and a clinical case of a patient with this disease. MATERIALS AND METHODS: the patient A., 52 years of age, after which clinical-instrumental and laboratory research was diagnosed with infiltrative form of cancer of the pylorus with decompensated stenosis. The used: videothoracoscopy, fluoroscopy, peripheral computer electrogastrogram, local fluorescence spectroscopy. The General blood and urine tests, biochemical blood tests, PCR for the determination of tumor markers. RESULTS: The resection of 2/3 of the stomach Billroth I. histological examination of the pylorus diagnosed with hypertrophy of circular muscle fibers, to a lesser extent, hypertro- phy of the longitudinal fibers with inflammatory changes. CONCLUSION: in cases of suspected infiltrative form of cancer of the pylorus in adults differential diagnosis it is advisable to include the primary hypertrophy of his.

MIOBLASTOMA GRAINYCLY CELL OF ESOPHAGEAL.

PURPOSE OF THE STUDY: Pay attention endoscopists doctors, oncologists surgeons, gastroenterologists on the ability to detect mioblastoma in the esophagus, as well as to present its endoscopic semiotics. MATERIAL AND METHODS: 32583 A primary esophagogastroduodenoscopy and only one patient S., 39 years old (0.0031%) showed polypoid masses in the lower third of the esophagus. Esophagogastroscopy underwent endoscopy XP iSON system Exera II. Patients underwent clinical evaluation and morphological study of endoscopically resected of education. RESULTS: Patient 39 years old 20.01.2012, in the lower third of the esophagus revealed polypoid formation with a flat, smooth surface covered with a mucous membrane, not different from the surrounding mucosa. Morphologic study after endoscopic resection of the tumor - grainycly cell mioblastoma. When viewed within four years of changes in the mucosa and not detected change in the esophageal wall. CONCLUSION: Abrikosov tumor in the esophagus is extremely rare localization has exophytic growth after endoscopic rernoval requires regular endoscopic surveillance.

EXPERIMENTAL SUBSTANTIATION AND CLINICAL APPLICATION OF MICROSURGICAL ANTIREFLUX GASTROINTESTINAL ANASTOMOSES IN GASTRIC RESECTION.

AIM: An improvement of the stomach through the development of reconstructive operations results of anatomical - the experimentally study and clinical testing of a series of new microsurgical areflux gastrointestinal anastomosis with sphincter properties. MATERIALS AND METHODS: The study was performed on 60 animals (dogs) and 52 organocomplexes people dead. 4 A series of experiments, developed new ways to 4 gastro-intestinal anastomosis with sphincter properties gastroduodenostomii way to "end to end" (patent number 2,197,903); pilorosohranyayuschey gastrectomy method (patent number 2,201,714); gastronesteostomy way to "end to side" (patent number 2,201,716); gastroduodenostomii way to the formation of artificial pyloric sphincter (patent number 2,212,195). RESULTS: Anatomical studies on cadaveric organocomplexes installed, but that the use of the formation of the gastro-intestinal anastomosis of microsurgical techniques and a separate cross-linking methods of internal and external casings of hollow organs without entrainment into the joint mucosa anastomosis gives high.impermeability and durability, retains histotopography linkable tissues. Gastric resection methods developed to form microsurgical gastrojejunal anastomosis and gastro used in clinical practice in 20 patients. Operated patients were examined after 1-6 years after surgery. When gastroscopia they celebrated, good function Form-balanced, the sphincter, the absence of duodenal reflux. CONCLUSION: The use of microsurgical techniques with gastric resection with the formation of functionally active gastroduodenal and gastrojejunal anastomosis can create gastrointes.inal anastomosis with anti-reflux properties and save the porter, without violating its contractile function, ensures minimum trauma to the tissues, the exact adaptation of the histologic homogeneous layers of the walls of bound bodies.

[DAILY INTRAESOPHAGEAL pH-MONITORING IN THE DIAGNOSIS OF THE SEVERITY OF ESOPHAGITIS WITH GASTROESOPHAGEAL REFLUX DISEASE].

OBJECTIVE: To identify criteria of pH-grams to diagnose the severity of esophagitis and preneoplastic complications of GERD. MATERIALS AND METHODS: 63 patients aged from 18 to 70 with A, B, C degree of GERD, according to the Los Angeles classification and 15 patients with intestinal metaplasia of columnar epithelium and leukoplakia of the stratified squamous epithelium of the esophagogastric transition were examined. For daily intraesophageal pH-monitoring "Gastroscan-24", pH probes manufactured by ZAO NPP "Istok- system", Fryazino (Russia) were used. pH-grams were estimated according for indicators DeMeester. Endoscopy was performed by videoesofagogastroscopes of Evis Exera- system--160 and by the tools company "Olympus" (Japan). RESULTS: 5 options of pH-grams were selected, each of them may correspond to some degree of esophagitis, preneoplastic changes of the esophageal mucosa, esophageal and extraesophageal manifestations of GERD. CONCLUSION: Daily pH-monitoring of the esophagus can serve as a screening for the severity of esophagitis, preneoplastic changes of esophagogastric transition, for addressing the need of morphological studies and differential diagnosis of extraesophageal manifestations of GERD.

Critical behavior of a random diode network.

We study the percolation properties of a random diode network (RDN) which contains two kinds of directed bonds on a square lattice. This network is a special case of the random insulation-resistor-diode network. Both Monte Carlo simulations and series expansion for the percolation probability show that an estimated critical exponent, beta=0.1794+/-0.008, is different from known values for a conventional insulation-resistor-diode network. RDN belongs to neither the isotropic percolation universality class nor to the directed percolation universality, which we attribute to a difference of symmetry breakdown around the critical point.

Pharmacokinetics, antifolate activity and tissue distribution of PT523 in SCC VII tumor-bearing mice.

PURPOSE: To monitor the pharmacokinetics of PT523 and methotrexate in C3H mice with transplanted SCC VII tumors; to compare the impact of PT523 and methotrexate on tumor and normal host 5,10-methylenetetrahydrofolate levels; and to synthesize [14C]PT523 and determine its time-dependent tissue distribution in tumor and host tissues. METHODS: C3H mice bearing SCC VII tumors were given i.p. PT523 or methotrexate. Plasma drug levels and tumor, gut and marrow 5,10-methylenetetrahydrofolate were assayed. [14C]PT523 was synthesized and administered i.v. to tumor-bearing mice for tissue distribution analysis. RESULTS: Areas under the curve, mean residence times, whole body clearances, apparent distribution volumes, and plasma protein binding of PT523 vs methotrexate were, respectively, 4311 vs 6472 microM x min(-1); 20 vs 16 min; 0.56 vs 0.36 ml min(-1); 532 vs 325 ml x kg(-1); and 70% vs 30%. Both PT523 and methotrexate caused time-dependent declines in 5,10-methylenetetrahydrofolate in tumor and marrow, but not in gut mucosa [corrected]. Gut levels began to recover within 4 h in the PT523-treated group only. [14C]PT523 distributed mainly into the liver, duodenum, kidneys, lungs, tumor, pancreas and muscle; less into the spleen, blood cells, heart, brain and testicles; and very little into gut [corrected. Only 35% of the dose was excreted, and 2.9-fold more in feces than urine. CONCLUSIONS: Despite its more rapid clearance, accumulation of PT523 in extravascular tissues was greater than that of methotrexate. Consequently, less PT523 was recovered in feces and urine and its apparent volume of distribution was greater. PT523 selectively depleted 5,10-methylenetetrahydrofolate pools in tumor and, less persistently, in marrow, but spared the gut mucosa [corrected]. [14C]PT523 tissue distribution correlated with organ mass and blood supply.

Endothelial cell tolerance to hypoxia. Potential role of purine nucleotide phosphates.

The ability of cells to tolerate hypoxia is critical to their survival, but varies greatly among different cell types. Despite alterations in many cellular responses during hypoxic exposure, pulmonary arterial endothelial cells (PAEC) retain their viability and cellular integrity. Under similar experimental conditions, other cell types, exemplified by renal tubular epithelial cells, are extremely hypoxia sensitive and are rapidly and irreversibly damaged. To investigate potential mechanisms by which PAEC maintain cellular and functional integrity under these conditions, we compared the turnover of adenine and guanine nucleotides in hypoxia tolerant PAEC and in hypoxia-sensitive renal tubular endothelial cells under various hypoxic conditions. Under several different hypoxic conditions, hypoxia-tolerant PAEC maintained or actually increased ATP levels and the percentage of these nucleotides found in the high energy phosphates, ATP and GTP. In contrast, in hypoxia-sensitive renal tubular endothelial cells, the same high energy phosphates were rapidly depleted. Yet, in both cell types, there were minor alterations in the uptake of the precusor nucleotide and its incorporation into the appropriate purine nucleotide phosphates and marked decreases in ATPase and GTPase activity. This maintenance of high energy phosphates in hypoxic PAEC suggests that there exists tight regulation of ATP and GTP turnover in these cells and that preservation of these nucleotides may contribute to the tolerance of PAEC to acute and chronic hypoxia.

Endothelial cell phospholipid distribution and phospholipase activity during acute and chronic hypoxia.

We have previously reported alterations in cyclooxygenase metabolism in cultured aortic and pulmonary arterial endothelial cells exposed to acute and chronic hypoxia. These alterations depended on the duration and degree of the hypoxic exposure, on the vascular bed from which the endothelial cells were derived, and possibly on the availability of arachidonic acid secondary to modifications in metabolic substrate, membrane phospholipids, and/or membrane phospholipase activity. To investigate this last point further, we have compared plasma membrane phospholipid distribution and phospholipase activity in cultured aortic and pulmonary arterial endothelial cells exposed to both acute and chronic hypoxia, using two different precursors (acetic acid and arachidonic acid) and three different membrane preparations (cell homogenates, partially purified plasma membranes, and highly purified plasma membranes). We found that exposure to acute and chronic hypoxia has profound and complicated effects on endothelial cell phospholipid composition and phospholipase activity and that these effects depend on the origin of the endothelial cells and the duration of hypoxia. Furthermore, we found that the alterations in endothelial cell phospholipid distribution in response to hypoxia depend on the purity of the plasma membrane preparation and the metabolic precursor used to study phospholipid metabolism. Finally, these studies suggested that alterations in phospholipids during hypoxia occurred to a greater extent in compartments of endothelial cells other than the plasma membranes and that the well-recognized tolerance of endothelial cells to hypoxia may be due, in part, to preservation of the integrity of their plasma membranes during exposure to acute and chronic hypoxia.