The specifics of individual immune reactions after COVID-19 have not been studied sufficiently. This study aimed to describe the changes in indicators of cellular and humoral levels of immunity after COVID-19, and gage general trends and individual characteristics. We sampled blood of 125 unvaccinated COVID-19 patients (29 men and 96 women, median age 53 years) 1 to 4 months after recovery, and determined the relative content of T-lymphocytes (CD3+), B-lymphocytes (CD19+), and cells with late activation markers (CD3+HLA–DR+) in them using flow cytometry. With the help of ELISA, we have registered the level of circulating immune complexes, which can be medium molecular weight (CICmed) and low molecular weight (CIClow), and the content of antibodies to SARS-CoV-2. In the mild course group, significant differences from the normal values (p < 0.001) were found for T cells (growth, 74.4 ± 1.2% vs. 68.6 ± 1.1%) and B cells (decline, 10.2 ± 0.7% vs. 13.9 ± 0.9%). In the moderately severe course and severe course groups, the level of CD3+HLA–DR+ lymphocytes was increased (7.7 ± 0.4% and 15.7 ± 2.5%, respectively, versus 3.9 ± 0.8% in the control group; p < 0.01). All the examined patients had high levels of CIClow (2.6-2.9-fold increase) and CICmed (1.6–1.8-fold increase). The protective level of antibodies to SARS-CoV-2 above 150 BAU/ml was registered in about 50% of the mild group participants, 75% of the moderately severe group members, and 100% of patients who had the disease in a severe form. We detected no connections between immune disorders and clinical features of the course of the disease and the period thereafter, with the exception of abdominal syndrome peculiar to the acute stage of the disease. The article also describes a clinical case of detection in the early post-COVID-19 period of a pathological clone characteristic of B cell chronic lymphocytic leukemia, and its subsequent disappearance and normalization of the immunophenotype as registered during a follow-up 1.5 years after recovery. The persistent immunological shifts should be taken into account when assessing the risks of reinfection and possible complications.
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Vitamin D deficiency that remains non-compensated for a long time is associated with high risk of rickets in children and osteomalacia in adults, myopathies and low-energy fractures, as well as secondary hyperparathyroidism (SHPT). SHPT represents one of the main mechanisms, through which vitamin D deficiency can contribute to pathogenesis of low-energy fractures. The study was aimed to assess the calcium and phosphorus metabolism state and the bone tissue metabolism markers in highly trained athletes with SHPT, as well as the prevalence of SHPT in elite sports. The study involved 527 young athletes aged 12–18 years (average age 15.2 years) doing 32 sports. The group with SHPT included 16 children (11 girls and 5 boys) with the average age of 15.0 years. The control group with normal levels of parathyroid hormone consisted of 511 children (254 boys and 273 girls) with the average age of 15.2 years. The studied subgroups were matched by age (p = 0.678). Girls predominated in the group with SHPT (р = 0.02). SHPT associated with vitamin D deficiency was revealed in 3% of young highly trained athletes, it was more prevalent among girls. The SHPT development does not result in alteration of the calcium and phosphorus metabolism indicators, however, it is accompanied by the increase in bone resorption markers, β-CrossLaps and total alkaline phosphatase. Many aspects related to vitamin D deficiency in SHPT are currently poorly understood, and there are no clinical guidelines on the cholecalciferol replacement therapy. Large-scale clinical trials are required to determine the optimal threshold values of 25(ОН)D3 and the powerful and effective treatment regimens for young athletes having SHPT associated with vitamin D deficiency.
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Toxic effects of the myeloablative cyclophosphamide (CP) doses include damage to the gastrointestinal tract. This is manifested by gastrointestinal stasis, cytostatic drug-induced damage to the small intestinal mucosa, and acute gut-derived endotoxemia. The study was aimed to identify causal relationships between gastrointestinal stasis, enterocytopenia, and acute gut-derived endotoxemia in the rat model of the CP myeloablative conditioning. We assessed the effects of the intragastrically administered 0.48 М sodium bicarbonate (NaHCO3) solution or the 0.1 М hydrochloric acid (HCl) solution on the indicators of gastrointestinal stasis, enterocytopenia, portal blood levels of endotoxin, ammonia, urea, and urinary indican excretion. The stomach overfilled with chyme, decreased alkaline phosphatase and cholinesterase activity in the small intestinal tissues, 4.4-fold increased endotoxin levels, 4.6-fold increased urea levels, twofold increased portal blood plasma creatinine levels, and twofold increased urinary indican excretion were observed three days after intravenous administration of CP in a dose of 390 mg/kg. Intragastric administration of NaHCO3 or HCl partially prevented gastric stasis, but not acute gut-derived endotoxemia. Administration of NaHCO3, not HCl, prevented enterocytopenia in the duodenum. Acute gut-derived endotoxemia resulted mainly from the more intense release of the cecal microflora waste products into blood. Testing the use of sodium bicarbonate intragastric administration combined with the enteral detoxification and/or options for suppression of colonic microflora vegetation for prevention of the myeloablative cytostatic therapy complications is promising.
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Bone-seeking radionuclides, in particular 89,90Sr, could get into the environment in the course of various anthropogenic radiation incidents. From there they enter a human body with food and water. This leads to red bone marrow (RBM) internal exposure. These elements were present in the composition of radioactive releases into the Techa River in 1950s, and are the major source of RBM exposure for the residents of the riverside settlements. RBM dose estimation relies on dosimetric modeling which comprises the development of 3D computational phantoms of the skeleton parts. By imitating the energy transfer in these phantoms, the conversion coefficients from the radionuclide activity in a bone to the dose rate in RBM are evaluated. The given study is yet another step in the research aimed at the elaboration of a set of computational phantoms of the skeleton for people of various age. The objective is to develop a computational phantom of a skeleton of a 10-year-old child to estimate dose to RBM due to incorporated beta-emitters. Original SPSD (stochastic parametric skeletal dosimetry) approach was used to create the phantoms. According to this method the skeleton sites containing RBM were divided into smaller segment of simple geometric shape, for which voxel phantoms were generated. The parameters for phantom generation were based on published research data. They included^ linear dimensions of bones, thickness of the cortical layer, characteristics/properties of the bone micro-architecture, density and chemical composition of the modelled media and the percentage of RBM content in bones. Generated computational phantom of the skeleton sites with active hematopoiesis of a 10-year-old child consists of 38 phantom-segments. Linear dimensions of the segments were from 3 to 88 mm, cortical layer thickness: 0.2–2.2 mm.
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Plantar fasciitis (PF) is one of the leading causes of heel pain in athletes. Since the disease etiology and pathogenesis are poorly understood, determination of impaired biomechanical patterns will make it possible to develop effective and safe therapeutic strategies. The study was aimed to reveal biomechanical changes typical for athletes with PF. Analysis of the results of baropodometric examination of 60 athletes, who were assessed and treated at the Federal Research and Clinical Center of Sports Medicine and Rehabilitation of FMBA of Russia due to foot disorders (1–2 degree combined platypodia and PF), was conducted. Athletes were divided into two groups based on the fact of having/not having a verified diagnosis of PF. The study involved 24 males (40%) and 36 females (60%), the athletes’ median age was 24 (19; 28) years. During the study we noted a trend towards higher incidence of PF in female athletes (р = 0.066). Hammertoe deformity was often found in athletes with PF (р < 0.05). Athletes with combined platypodia and PF showed overload or insufficient load in the posterior part of the affected foot, depending on pain severity, in static tests (r = 0.592, р  = 0.001). The dynamic tests revealed deformation of the general pressure vector and changes in the general center of pressure velocity (р < 0.01). Baropodometric examination showed that athletes with PF had deficit or excess increase of plantar pressure in the heel of the affected foot, along with deformation of the general pressure vector.
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The paper provides the results of the comprehensive electron microscopic examination of the venous blood and internal organ tissue samples obtained when studying the imported case of tropical malaria. The study was aimed to assess the fine structure of the erythrocytic stages of Plasmodium falciparum and alterations of the affected tissues in severe tropical malaria. The venous blood, cerebral cortical tissue and myocardial samples were examined by light microscopy and electron (scanning and transmission) microscopy. Numerous Plasmodium falciparum trophozoites were found in blood. Multiple Maurer's clefts were found in the cytoplasm of the infected erythrocytes. Abnormal intercellular contacts between the infected and unaffected erythrocytes were revealed, which resulted in their adhesion and rosette formation (erythrocyte rosetting/e-rosetting). When studying cortical tissue and myocardial samples, fixation of the affected erythrocytes on the endothelium (erythrocyte adhesion) was noted in the capillary lumen. Rosetting and erythrocyte adhesion lead to capillary thrombosis, disruption of microcirculation and sequestration of tissues in vital organs (parasite sequestration). The identified morphological features of the pathogens causing tropical malaria and the affected tissues determine the parasites’ capability of changing properties of the infected erythrocytes’ cell membranes, which leads to formation of abnormal intercellular contacts and constitutes one of the main mechanisms underlying the Plasmodium falciparum virulence.
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Poisoning with acylating pulmonary toxicants results in toxic pulmonary edema (TPE), the approaches to treatment of which are limited. The lung injury similar to poisoning with acylating pulmonary toxicants can be simulation through body’s exposure to the fluoroplastic thermal degradation products containing perfluoroisobutylene. The study was aimed to compare toxic pulmonary edema manifestations in the laboratory animals poisoned with an acylating pulmonary toxicant (carbonyl chloride) and fluoroplastic thermal degradation products. Animals (male rats, n = 78) were divided into three groups: controls; Poisoning 1, where the animals were exposed to carbonyl chloride; Poisoning 2, where the animals were exposed to the fluoroplastic thermal degradation products. The animals’ lung/body ratio was determined and the partial pressure of arterial oxygen (PaO2) and carbon dioxide (PaCO2) was assesed 10 min, 1, 3, 6, 24, and 48 h after the exposure. Histological examination of lung tissue was performed 3 and 6 h after the exposure. The increase in the lung/body ratio, decrease in PaO2, and increase in PaCO2 relative to controls were revealed 3, 6, 24, and 48 h after the exposure to carbonyl chloride and fluoroplastic thermal degradation products. The signs of the interstitial toxic pulmonary edema phase were detected 3 h after the exposure to the studied toxicants, and the signs of alveolar phase were revealed after 6 h. Similar changes were identified in animals of the experimental groups. The findings have shown that the exposure to carbonyl chloride and the fluoroplastic thermal degradation products containing perfluoroisobutylene lead to similar changes in the early post-intoxication period.
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