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The paper covers the production, analysis of the microstructure, crystallographic texture and deformation mechanisms of the ultrafine-grained (UFG) Zn–1%Mg–1%Fe zinc alloy demonstrating unique physical and mechanical properties compared to its coarse-grained analogues. The zinc alloy with improved mechanical properties was developed in two stages. At the first stage, based on the analysis of literature data, an alloy with the following chemical composition was cast: Zn–1%Mg–1%Fe. Then, the alloy was subjected to high-pressure torsion (HPT) to improve mechanical properties, due to grain structure refinement, and implementation of dynamic strain aging. The conducted mechanical tensile tests of the samples and assessment of the alloy hardness, showed that HPT treatment leads to an increase in its tensile strength to 415 MPa, an increase in hardness to 144 HV, and an increase in ductility to 82 %. The obtained mechanical characteristics demonstrate the suitability of using the developed alloy in medicine, as some implants (stents) requiring high applied loads. To explain the reasons for the improvement of the mechanical properties of this alloy, the authors carried out comprehensive tests using microscopy and X-ray diffraction analysis. The microstructure analysis showed that during the formation of the ultrafine-grained structure, a phase transition is implemented according to the following scheme: Zneutectic + Mg2Zn11eutectic + FeZn13 → Znphase + Mg2Zn11phase + MgZn2particles + Znparticles. It was found that as a result of high pressure torsion in the main phases (Zn, Mg2Zn11), the grain structure is refined, the density of introduced defects increases, and a developed crystallographic texture consisting of basic, pyramidal, prismatic, and twin texture components is formed. The study showed that the stability of pyramidal, prismatic and twin texture components at the initial stages of high-pressure torsion, determines the level and anisotropy of the strength properties of this alloy. The relationship between the discovered structural features of the produced alloy and its unique mechanical properties is discussed.

Currently, scientists search for new materials for temporary implants that can dissolve in the body, which leads to the fact that there is no need for repeated surgery. In the last decade, scientific interest has focused on zinc-based materials because, unlike other metals, it has suitable corrosion rates and good biocompatibility. The paper describes an experiment for the study of the influence of deformation on the microstructure, strength and corrosion properties of an alloy of the Zn–Fe–Mg system. The authors carried out energy dispersive analysis and calculation of the volume fraction of the second phase of the Zn–Fe–Mg zinc alloy. The corrosion properties of the Zn–Fe–Mg zinc alloy with different microstructures (before and after high-pressure torsion) were studied using the gravimetric method under conditions simulating conditions inside a living organism (temperature, corrosive environment composition). During the tests, the corrosion mechanism was determined, its rate and mass loss of the samples were calculated. The relief of the corrosion surface was studied using scanning electron microscopy. It has been found that the destruction of the material in a corrosive environment occurs through a matrix containing the active Mg metal. The results of calculations of the corrosion rate for the original sample and samples subjected to high-pressure torsion differed due to a more even distribution of second phase particles during severe plastic deformation. In this work, by alloying zinc with iron and magnesium, as well as using high-pressure torsion, it was possible to increase the microhardness of the samples to 239.6±8 HV, which is a high indicator for zinc alloys.

Relevance . Despite the large list of biological markers of cardiovascular diseases, not all have evidence-b ased effectiveness and independent prognostic value. Laboratory diagnostics of serum cardiospecific auto-antibodies for the diagnosis of myocyte cell damage has several potential advantages compared to the evaluation of traditional methods. These include the analysis of natural globulins to troponin I (cTnI), to alpha-a ctin 1 (ACTC1), to the heavy chain of beta-myosin 7B (MUN7B), which are based on a self-sustaining immune response to the myocardium’s own auto-antigens, which leads to damage to the cells expressing them. Purpose: To determine the diagnostic and practical value of quantitative indicators for the autoantibody complex to cardiomyocyte proteins to troponin I, to alpha-a ctin 1 and to the heavy chain of beta-myosin 7B in patients with cardiac pathology. Materials and Methods. The study of auto-antibodies to cTnI, ACTC1 and MUN7B in blood serum using laboratory enzyme immunoassay was carried out in patients with cardiac pathology undergoing inpatient treatment at the Regional Clinical Cardiology Dispensary in Stavropol. Additionally, an instrumental and laboratory examination was carried out in accordance with the clinical recommendations developed by the Association of Cardiovascular Surgeons, the Cardiological Society of Russia and approved by the Scientific and Practical Council of the Ministry of Health of the Russian Federation. The work was examined and approved by the Ethics Committee of the North Caucasus Federal University. Results and Discussion . Changes in the level of autoantibodies to cTnI, ACTC1 and MUN7B proteins in blood serum were statistically significant (p 0.01 v. s. p 0.01). A persistent increase in the level of auto-antibodies to cTnI by 2.36 ng/ml (694.11 %), to ACTC1 by 3.6 ng/ml (141.73 %) and to MUN7B by 1.74 ng/ml (119.17 %) was found in individuals with confirmed cardiac pathology, when other criteria for laboratory analysis were within acceptable values, which determine their diagnostic and evidentiary effectiveness. Conclusion . The results of the study showed the relationship of changes in the activity of cardiospecific auto-A T to cardiomyocyte proteins (Anti-cTnI, Anti ACTC1, Anti-M YH7B) in patients with cardiac pathologies, indicating not only systemic membrane disorders (membranopathies), but also serve as convincing evidence of direct chemical changes in cardiomyocytes. A correlation has also been established between cardiomarkers of necrosis and ischemia and autoimmune globulins Anti-cTnI, Anti ACTC1, Anti-MYH7B, that confirms diagnostic and practical value of this laboratory analysis.

Relevance. In conditions of ever-increasing volume of training loads, the frequency of cases of chronic physical overstrain (CPO) among athletes is increasing. It determines the importance of early diagnosis of the formed pathology of the cardiovascular system in order to prevent its further development. The aim of the study was to study the dynamics of autoantibodies to cardiomyocyte proteins using an experimental model of CPO and to determine the prospects of a laboratory method for the determination of autoantibodies for early diagnosis of pathomorphological changes in the heart. Materials and Methods. The study was conducted on male white rats. A treadmill was used to model CPO. In animals, the heart rate was measured, electrical phenomena in the heart were recorded. The content of hemoglobin and erythrocytes was determined in the blood. The level of cardiospecific autoantibodies (auto-AB) to troponin I, to alpha-actin 1, and to the heavy chain of beta-myosin 7B was measured. Heart mass was measured and histomorphological assessment of the state of cardiomyocytes was carried out. Results and Discussion. While modeling CPO, a decrease in body weight of the animals, the development of anemia, and cardiac hypertrophy were recorded. A decrease in body weight by more than 30 % was recorded from days 25 to 35 of the modeled CPO. A decrease in the number of erythrocytes in the blood was noted on day 25 with a peak fall on days 30-35. The mass of heart of animals in the dynamics of 0-15-35 days was 0.39±0.003; 0.41±0.001; 0.44±0.005 g/100 g, respectively. On day 25, sinus tachycardia was recorded in 2 % of the animals. On days 30 and 35, in 10 % of the studied rats, a violation of the processes of repolarization of the left ventricle by the type of subepicardial ischemia was recorded. On the 25th day, fibrosis of the perivascular region was visualized, passing into the interstitial field between the myofibrils. Reticulate structures of connective tissue fibers between cardiomyocytes were found. The period of 30-35 days was characterized by even greater severity of pathomorphological changes: myocardial hypertrophy, moderate myocardial dystrophy, interstitial and perivascular fibrosis. An increase in the number of detectable auto-ABs to cardiomyocyte proteins was noted on the 10th day of the experiment. A multiple increase in autoantibodies to cardiomyocyte proteins was recorded earlier than functional disorders in the heart and morphological changes in cardiomyocytes were detected. Conclusion. The laboratory method for determining auto-ABs to myocardial proteins can be the earliest of the complex methods for diagnosing disorders that are formed in the body in conditions of adaptation to intense and prolonged physical exertion.

In this paper, the authors consider the mechanisms of formation of high-strength states in the Zn–1%Li–2%Mg alloy as a result of its processing by the high pressure torsion (HPT) method. For the first time, the study showed that using HPT treatment, as a result of varying the degree of deformation at room temperature, it is possible to increase the ultimate strength of a zinc alloy from 155 to 383 MPa (with an increase in the yield stress from 149 to 306 MPa) without losing its ductility. To explain the reasons for the increase in the zinc alloy mechanical properties, its microstructure was analyzed by scanning electron microscopy (SEM), X-ray phase analysis (XPA), X-ray diffraction analysis (XRD), and small-angle X-ray scattering (SAXS). Using XPA, the authors established for the first time that Zn(eutectic)+β-LiZn4(eutectic)→~LiZn3+Zn(phase)+Zn(precipitation) and MgZn2→Mg2Zn11 phase transformations occur in the zinc alloy during HPT treatment. SEM analysis showed that at the initial stages of HPT treatment, cylindrical Zn particles with a diameter of 330 nm and a length of up to 950 nm precipitate in β-LiZn3 phase. At the same time, the SAXS method showed that needle-like LiZn4 particles with a diameter of 9 nm and a length of 28 nm precipitate in the Zn phase. The study established that, only spherical Zn and LiZn4 particles precipitate at high degrees of HPT treatment. Precision analysis of the zinc alloy microstructure showed that HPT treatment leads to grain refinement, an increase in the magnitude of crystal lattice microdistortion, a growth of the density of dislocations, which are predominantly of the edge type. As a result of the analysis of hardening mechanisms, the authors concluded that the increase in the zinc alloy strength characteristics mainly occurs due to grain-boundary, dislocation, and dispersion hardening.

Relevance. Early diagnosis of chronic overstress among athletes remains an important problem for coaches and specialists in the field of sports physiology and medicine. The goal is to study in an animal model the dynamics of autoimmune response to physical activity of different duration and intensity and to establish the prospects of the method of determining autoantibodies to cardiomyocyte proteins as an indicator of the morphofunctional state of the heart in the conditions of adaptation to muscle loads. Materials and Methods. The study was conducted in male white rats. Animals were subjected to 9 weeks of training simulated with treadban. The intensity of the load changed the angle of inclination and the speed of the tape. The amount of cardiospecific autoantibodies (auto-AB) to troponin I, to alpha-actin 1, to the human cardiac beta-myosin heavy chain MYH7 was determined in the blood by enzyme immunoassay. The relative heart mass was measured. Histomorphological assessment of cardiomyocyte condition was carried out. Statistical processing was carried out using the Student and Mann-Whitney criteria. Results and Discussion. Animal training was accompanied by moderate cardiac hypertrophy of pathological changes in cardiomyocytes. Heart weight increased by 6.9 %; 10.6 %; 12.9 % in the dynamics of 6-8-9 weeks of training. Concentrations of auto-AB to troponin I and to alpha-actin 1 were characterized by cyclicity, manifested by an increase in week 2 and a decrease by the 8th and 9th weeks of training. In the dynamics of 0-2-8-9 weeks of the experiment, the amount of auto-AB to troponin I was: 3.10.3; 4.20.9; 2.10.2; 2.00.04 ng/ml. For auto-AB to actin: 26.71.2; 31.31.4; 13.71.8; 12.11.6 ng/ml, respectively. The level of auto-AB to beta-myosin was manifested by a decrease in the dynamics of 0-6-9 weeks of training and amounted to: 16.30.9; 10.91.5; 8.20.8; 9.6 0.9 ng/ml. Conclusion. The results of determining cardiospecific auto-AB demonstrate a clear response of the immune system to the processes taking place in cardiomyocytes, which makes it possible to recommend further study of the method of determining auto-AB to cardiomyocyte proteins as a diagnostic test of the functional state of the heart muscle during the period of adaptation to physical activity.

Abstract Background Fecal microbiota transplantation (FMT) has been recently approved by FDA for the treatment of refractory recurrent clostridial colitis (rCDI). Success of FTM in treatment of rCDI led to a number of studies investigating the effectiveness of its application in the other gastrointestinal diseases. However, in the majority of studies the effects of FMT were evaluated on the patients with initially altered microbiota. The aim of our study was to estimate effects of FMT on the gut microbiota composition in healthy volunteers and to monitor its long-term outcomes. Results We have performed a combined analysis of three healthy volunteers before and after capsule FMT by evaluating their general condition, adverse clinical effects, changes of basic laboratory parameters, and several immune markers. Intestinal microbiota samples were evaluated by 16S rRNA gene and shotgun sequencing. The data analysis demonstrated profound shift towards the donor microbiota taxonomic composition in all volunteers. Following FMT, all the volunteers exhibited gut colonization with donor gut bacteria and persistence of this effect for almost ∼1 year of observation. Transient changes of immune parameters were consistent with suppression of T-cell cytotoxicity. FMT was well tolerated with mild gastrointestinal adverse events, however, one volunteer developed a systemic inflammatory response syndrome. Conclusions The FMT leads to significant long-term changes of the gut microbiota in healthy volunteers with the shift towards donor microbiota composition and represents a relatively safe procedure to the recipients without long-term adverse events.

Abstract This study analyzed the effect of thermal stress on erythrocytes of Notothenia rossii and Notothenia coriiceps, abundant notothenioids in Admiralty Bay, Antarctic Peninsula. In both species, the antioxidant defense system enzymes, superoxide dismutase, catalase, glutathione peroxidase, glutathione-S transferase, glutathione reductase were punctually altered (8°C for 1, 3 and 6 days) in erythrocytes, indicating that these markers are not ideal for termal stress. However, under the influence of thermal stress, morphological changes in Notothenia coriiceps erythrocytes were observed at all exposure times (1, 3 and 6 days at 8°C), and in Notothenia rossii occurred in 6 days. These results suggest that Notothenia corriceps presents a lower tolerance to thermal stress at 8°C for up to 6 days, since the cellular and nuclear alterations recorded are pathological and may be deleterious to the cells. Among the morphological markers analyzed in this work, we believe that the shape change and nuclear bubble formation may be good stress biomarkers in erythrocytes of Notothenia rossii and Notothenia coriiceps.

Summary: An increase in the probability of death has been a defining feature of aging, yet human perinatal mortality starts high and decreases with age. Previous evolutionary models suggested that organismal aging begins after the onset of reproduction. However, we find that mortality and incidence of diseases associated with aging follow a U-shaped curve with the minimum before puberty, whereas quantitative biomarkers of aging, including somatic mutations and DNA methylation, do not, revealing that aging starts early but is masked by early-life mortality. Moreover, our genetic analyses point to the contribution of damaging mutations to early mortality. We propose that mortality patterns are governed, in part, by negative selection against damaging mutations in early life, manifesting after the corresponding genes are first expressed. Deconvolution of mortality patterns suggests that deleterious changes rather than mortality are the defining characteristic of aging and that aging begins in very early life. : Kinzina et al. highlight the importance of adequate definition of aging and address long-standing questions on the onset of aging and causes of early-life mortality. They show that aging is better represented by the accumulation of deleterious changes rather than mortality and thus starts early in life. Keywords: aging, lifespan, mortality, selection, age-related, cancer, incidence, damage, mutations, clock

Geneticamente, a leucemia promielocítica aguda (LPA) caracteriza-se por alterações cromossômicas estruturais recorrentes, na grande maioria das vezes translocações, envolvendo sempre o lócus gênico para o receptor alfa do ácido retinoico (RARα) localizado no braço longo do cromossomo 17 (17q21), levando à formação de genes quiméricos e oncoproteínas de fusão. Em aproximadamente 98% dos casos, o gene RARα se encontra fusionado com o gene PML resultante da translocação cromossômica recíproca t(15;17)(q22;q21) e, em cerca de 2% dos casos, o gene RARα pode estar fusionado com outros genes que não o PML, levando à formação de proteínas de fusão conhecidas genericamente como X-RARα. A leucemia promielocítica aguda é um exemplo de malignidade hematológica onde se tem a combinação de alterações genéticas e epigenéticas (acetilação, desacetilação e metilação) no processo de leucemogênese, alterações cromossômicas estruturais influenciando no equilíbrio dinâmico da cromatina na região promotora de alguns genes. A utilização de técnicas moleculares que auxiliam no diagnóstico genético mais preciso e o desenvolvimento de uma terapia alvo molecular permitiram alcançar alta taxa de cura desta doença.Acute promyelocytic leukemia (APL) is characterized by structural chromosomal abnormalities involving the RARα (retinoic acid receptor a) gene located on the long arm of chromosome 17 (17q21) that lead to the formation of chimeric genes and fusion oncoproteins. In about 98% of cases, the RARα gene is fused to the PML gene, the result of a reciprocal chromosomal translocation t(15;17)(q22;q21) and in the other 2% of cases the RARα gene may be fused to other genes, leading to the formation of fusion proteins known generically as X-RARα. Acute promyelocytic leukemia is an example of a hematologic malignancy where there is a combination of genetic and epigenetic (acetylation, deacetylation and methylation) changes in the leukemogenesis process, chromosome structural changes that affect the dynamic equilibrium of chromatin in the promoter region of some genes. The use of molecular techniques that improve genetic diagnosis and the development of targeted molecular therapy have provided a high cure rate of this disorder.