[Comparative epidemiology of thermal injury and hypothermia]. / Sravnitel'naya epidemiologiya termicheskoi travmy i gipotermii.

The paper presents the results of a comparative epidemiological study of thermal injury and fatal hypothermia based on the results of consolidated reports of the Bureau of Forensic Medicine of the Moscow Department of Health for 2017-2019. It was analyzed the archival material for three calendar years. It was used a continuous retrospective research method with an assessment of the general aggregate of the death incidence from thermal injury and hypothermia in Moscow in 2017-2019 by means of nonparametric statistical methods. Deaths from thermal injury and hypothermia are the most often accidents. The incidence of this type of death is characterized by ups and downs depending on the season. May, January and December are the most dangerous for burns. A similar pattern, with the exception of May, was noted for hypothermia. It was found that men aged 50-70 and women of 70-90 years old die most often. It was determined that most social characteristics (education, being married, etc.) alter the average age when deaths occur. The results obtained provide statistical justification for further more thorough study of thermal injury and hypothermia.

[Forensic diagnosis of sudden death of young people based on morphological analysis of the cardiac conduction system]. / Sudebno-meditsinskaya diagnostika vnezapnoi smerti lits molodogo vozrasta na osnovanii morfologicheskogo analiza provodyashchei sistemy serdtsa.

The aim of study was to develop a comprehensive assessment of the central and peripheral parts of the nervous system with a determination of degree of severity of alterative changes in comparison with the condition of myocardial contractile apparatus. Own observations on modern methods of morphological study of the cardiac conduction system in the sudden death of young people are presented. Particular attention is paid to the technique of isolating and coloring the nervous structures of sympathetic and parasympathetic parts of the autonomic nervous system, including the medulla oblongata, sinus-atrial and atrial-ventricular nodes, atrioventricular bundle (the His bundle), Purkinje fibers. The features of morphological changes in the nerve structures of the heart, due to various etiological factors are highlighted.

[The forensic medical characteristic of sudden death associated with metabolic syndrome]. / Sudebno-meditsinskaia diagnostika vnezapnoi smerti pri metabolicheskom sindrome.

The detection of grade II-III central obesity on a corpse in conjunction with the identification of two additional criteria (such as arterial hypertension and impaired glucose tolerance) provides, if combined with the autopsy data (including the visual reduction of muscular mass, the increased total amount of the adipose tissue, gynecomastia in men together with hypertrophied abdominal adipose tissue accumulation, decreased face and body pilosis), a basis for diagnostics of metabolic syndrome (MS). The objective parameters for this purpose are waist circumference measurements, corpse weight and height, the degree of visceral obesity, narrowing of the renal arteries as a result of their compression by the surrounding adipose tissue, and accumulation of epicardial fat confirmed by the results of the biochemical analysis. The signs of plasmorrhagia combined with fibrinoid degeneration of the vascular walls in the microcirculatory bed make it possible to suspect, with a high degree of probability, the development of hypertensive crisis that may result in a sudden death of the patients presenting with metabolic syndrome.

A 23bp insertion in the endothelial protein C receptor (EPCR) gene impairs EPCR function.

EPCR is a type I transmembrane protein, highly expressed on the endothelium of large vessels, that binds protein C and augments its activation. In this study, a 23bp insertion in the EPCR gene was found in 4/198 survivors of myocardial infarction and 3/194 patients with deep vein thrombosis. The EPCR gene with the insertion predicts a protein that lacks part of the extracellular domain, the transmembrane domain and the cytoplasmic tail. Expression studies showed that the truncated protein is not localized on the cell surface, cannot be secreted in the culture medium, and does not bind activated protein C. Since protein C activation depends on the concentration of EPCR, patients with the EPCR insertion could have a diminished protein C activation capacity. Further clinical studies of adequate samples size are necessary to establish whether or not the EPCR insertion predisposes to the development of thrombotic events.

Identification of the protein C/activated protein C binding sites on the endothelial cell protein C receptor. Implications for a novel mode of ligand recognition by a major histocompatibility complex class 1-type receptor.

The endothelial cell protein C receptor (EPCR) is an endothelial cell-specific transmembrane protein that binds both protein C and activated protein C (APC). EPCR regulates the protein C anticoagulant pathway by binding protein C and augmenting protein C activation by the thrombin-thrombomodulin complex. EPCR is homologous to the MHC class 1/CD1 family, members of which contain two alpha-helices that sit upon an 8-stranded beta-sheet platform. In this study, we identified 10 residues that, when mutated to alanine, result in the loss of protein C/APC binding (Arg-81, Leu-82, Val-83, Glu-86, Arg-87, Phe-146, Tyr-154, Thr-157, Arg-158, and Glu-160). Glutamine substitutions at the four N-linked carbohydrate attachment sites of EPCR have little affect on APC binding, suggesting that the carbohydrate moieties of EPCR are not critical for ligand recognition. We then mapped the epitopes for four anti-human EPCR monoclonal antibodies (mAbs), two of which block EPCR/Fl-APC (APC labeled at the active site with fluorescein) interactions, whereas two do not. These epitopes were localized by generating human-mouse EPCR chimeric proteins, since the mAbs under investigation do not recognize mouse EPCR. We found that 5 of the 10 candidate residues for protein C/APC binding (Arg-81, Leu-82, Val-83, Glu-86, Arg-87) colocalize with the epitope for one of the blocking mAbs. Three-dimensional molecular modeling of EPCR indicates that the 10 protein C/APC binding candidate residues are clustered at the distal end of the two alpha-helical segments. Protein C activation studies on 293 cells that coexpress EPCR variants and thrombomodulin demonstrate that protein C binding to EPCR is necessary for the EPCR-dependent enhancement in protein activation by the thrombin-thrombomodulin complex. These studies indicate that EPCR has exploited the MHC class 1 fold for an alternative and possibly novel mode of ligand recognition. These studies are also the first to identify the protein C/APC binding region of EPCR and may provide useful information about molecular defects in EPCR that could contribute to cardiovascular disease susceptibility.

Transferable clastogenic activity in plasma from persons exposed as salvage personnel of the Chernobyl reactor.

Clastogenic factors were first described in the plasma of people who had been accidentally or therapeutically irradiated. They were found also in A-bomb survivors, where they persisted for many years after the irradiation. The present study searched for these factors in the plasma of 32 civil workers from Armenia, who had been engaged as "liquidators" around the Chernobyl atomic power station in 1986. It also included 15 liquidators who had emigrated from the ex-Soviet Union to Israel. Reference plasma samples were obtained from 41 blood donors from the Armenian Blood Center in Yerevan. The samples were tested for their clastogenic activity in blood cultures from healthy donors. The majority of results from the liquidators exceeded those from the unexposed reference samples. The samples from the first Armenian group, with the higher average irradiation dose (0.6 +/- 0.6 Gy), were more clastogenic than those from the second group exposed to 0.2 +/- 0.2 Gy. The number of aberrations in the test cultures was 17.9 +/- 2.9% and 10.5 +/- 3.8% respectively, compared to 5.7 +/- 3.2% in the cultures exposed to the reference ultrafiltrates from Armenian blood donors. The samples from the Israeli liquidators also induced significantly increased aberration rates (14.0 +/- 3.9% aberrant cells). The clastogenic activity was regularly inhibited by superoxide dismutase, indicating that the chromosome-damaging effects of radiation-induced clastogenic factors are exerted via the intermediation of superoxide radicals, as is known for clastogenic factors of different origin.