Background The COVID‐19 pandemic has led the international community to conduct extensive research into potential negative effects of the disease on multiple organs and systems in the human body. One of the most discussed areas is potential of the virus to compromise the testicular function. However, the lack of prospective studies on this topic makes it impossible to draw reliable conclusions on whether the disease affects the male reproductive system and, if so, to what extent. Objectives The current trial is aimed at investigating the effect of SARS‐CoV‐2 on the testicular function, hormone levels and determining the extent of impact on spermatogenesis and damage to testicular tissue. Materials and methods This prospective study included healthy controls and cases of patients suffering from viral pneumonia based on chest computed tomography (CT) and a positive SARS‐CoV‐2 throat swab exhibited moderate symptoms (World Health Organization (WHO) classification). Epidemiological, clinical, laboratory and ultrasound data were collected. A semen analysis was performed in cases during their hospital stay and 3 months after the discharge home. We also assessed the testicles obtained during autopsies of patients who died of COVID‐19 ( n = 20). Results A total of 88 participants were included (44 controls and 44 cases). Blood testosterone levels were significantly decreased in 27.3% of the cases (12/44). The mean level (7.3±2.7 nmol/L) was lower than that in the healthy controls (13.5±5.2 nmol/L, p < 0.001). An increase in luteinizing hormone (LH) and follicle‐stimulating hormone (FSH) was also detected compared to the healthy controls ( p = 0.04 and p = 0.002). The semen analysis revealed decreased motility in COVID‐19 patients ( p = 0.001), and a higher number of immobile sperm (during COVID‐19: 58.8% and at 3 months 47.4%, p = 0.005). All parameters returned to normal at 3 months after discharge. Direct mixed agglutination reaction (MAR) test at 3 months showed an increase of Ig A ( p = 0.03). In the majority of autopsies (18/20), structural disorders of the testicular tissue, with signs of damage to germ cells were observed. Discussion and conclusion COVID‐19 and its management strategies significantly affect male hormone levels and sperm quality at the onset of the disease. Postmortem examination of testicular tissue confirmed inflammation and viral infiltration of the testicles. However, in patients with moderate to severe disease, the studied parameters of the testicular function returned to normal values within 3 months.

The study was aimed at the applicability of a bioink based on 4% collagen and chondrocytes for de novo cartilage formation. Extrusion-based bioprinting was used for the biofabrication. The printing parameters were tuned to obtain stable material flow. In vivo data proved the ability of the tested bioink to form a cartilage within five to six weeks after the subcutaneous scaffold implantation. Certain areas of cartilage formation were detected as early as in one week. The resulting cartilage tissue had a distinctive structure with groups of isogenic cells as well as a high content of glycosaminoglycans and type II collagen.

Autopsy data from 80 patients who died of the COVID-19 infection were analysed. Using macro- and microscopic studies, specific features of pathological processes in various organs were identified. The obtained experimental data, along with information from literature sources, allowed conclusions to be drawn about the mechanisms of damaging internal organs and body systems, as well as assumptions to be made about individual links in the pathogenesis of COVID-19. The thanatogenesis of the disease and the main causes of death are discussed, including acute cardiopulmonary failure, acute renal failure, pulmonary thromboembolism, shock involving multiple organ failure and sepsis. The critical importance of autopsy is emphasized, which provides valuable information on the morphological substrate for this infection closely associated with possible clinical manifestations.

β-TGF: β-transforming growth factor family; GCA: germ cell abnormalities/atypia; JS: Johnsen score; FSH: follicle stimulating hormone; TESE: testicular sperm extraction; LH: luteinizing hormone; F-Testo: free testosterone; ELISA: the enzyme-linked immunosorbent assay; CV: coefficient of variance; DR: range of definitions; AZF: azoospermia factorI; HC: immunohistochemical; HIER: heat induction of epitope retrieval; H&E: hematoxylin and eosin.

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The aim of this study was to verify the applicability of high-concentration collagen-based bioink with MSC (ADSC) and decellularized ECM granules for the formation of cartilage tissue de novo after subcutaneous implantation of the scaffolds in rats. The printability of the bioink (4% collagen, 2.5% decellularized ECM granules, derived via 280 μm sieve) was shown. Three collagen-based compositions were studied: (1) with ECM; (2) with MSC; (3) with ECM and MSC. It has been established that decellularized ECM granules are able to stimulate chondrogenesis both in cell-free and MSC-laden scaffolds. Undesirable effects have been identified: bone formation as well as cartilage formation outside of the scaffold area. The key perspectives and limitations of ECM granules (powder) application have been discussed.

Mutant forms of the gene IDH1 progress significantly slower, have a lower risk of neoplastic transformation, and generally, mutations of this gene have a pronounced anti-oncogenic effect. At the same time, almost all mutations are quite stereotyped (98,9%) and occur in the same region of the gene - R132H mutations. IDH1 gene mutations is a complex multi-layered process, which is a completely new, not previously described anti-oncogene activation mechanism of intracellular protection. The reason that there is a mutation in the tumor cells is associated with de novo blocking differentiation processes and development of brain cells in the development process, as evidenced by severe cerebral hypoplasia in patients with congenital forms of this mutation. A completely new mechanism of antitumor protection has been described - stereotypical IDH1 gene mutation is a gene, in fact, is a key event, causing a cascade of further anti-oncogenic mechanisms in brain gliomas.

Цель исследования: расширить представления о патогенезе тазовой боли (ТБ) при наружном генитальном эндометриозе (НГЭ). Дизайн: когортное проспективное сравнительное морфологическое исследование. Материалы и методы. В исследовании приняли участие 150 женщин. Пациенток с НГЭ (n = 120) разделили на 2 группы с 2 подгруппами (А и B) в каждой. Участницы групп I и II были в возрасте от 20 лет до 41 года (средний возраст-29,1 ± 3,3 года). I группу (n = 60) составили пациентки с НГЭ, осложненным ТБ: IA (n = 30)-c дефицитом 25(ОН)D, IB (n = 30)-без него; II группа (n = 60)-пациентки с НГЭ без ТБ: IIA (n = 30)-c дефицитом 25(ОН)D, IIB (n = 30)-без него. В группу контроля вошли 30 относительно здоровых женщин, направленных на диагностическую лапароскопию по поводу бесплодия неясного генеза, без дефицита 25(ОН)D и диагностированного НГЭ, без ТБ. У всех участниц исходно определяли уровень общего 25(ОН)D в сыворотке крови методом масс-cпектрометрии. Проводили морфологическое, иммуногистохимическое исследования с использованием компьютерной морфометрии. Результаты. Экспрессия VEGF была статистически значимо выше в биоптатах пациенток с ТБ на фоне дефицита 25(ОН)D), чем в подгруппе без него-77,4 ± 3,5% vs 56,3 ± 2,8% (р < 0,05), что свидетельствует об усилении ангиогенеза. Экспрессия NGF как в эутопическом, так и в эктопическом эндометрии также была значимо выше в подгруппе IА по сравнению с IВ: 63,7 ± 2,1% и 47,3 ± 3,2% vs 45,8 ± 1,9% и 36,1 ± 2,8%, что говорит об активации неонейрогенеза. Значимо более низкий апоптоз на фоне дефектной экспрессии VDR (71,1 ± 3,7% vs 31,5 ± 2,1%, p < 0,05) зафиксирован на основании экспрессии CASP3 в биоптатах женщин с ТБ и дефицитом 25(ОН)D: 26,1 ± 1,5% vs 28,4 ± 1,2% в подгруппе без дефицита 25(ОН)D. Заключение. Выявленные изменения показывают смещение пролиферативно-апоптотического индекса в сторону снижения активности апоптоза в клетках эутопического и эктопического эндометрия при диагностированном дефиците 25(ОН)D. Результаты исследования свидетельствуют о дефектном метаболизме 25(ОН)D. Аналогичная зависимость наблюдается в экспрессии VDR, что подтверждает результаты исследования на маркирование VDR в эндометрии и капсулах эндометриоидных кист у пациенток с НГЭ. Она лежит в основе ведущего патогенетического механизма возникновения ТБ при НГЭ в условиях снижения антипролиферативного действия витамина D. Это сопровождается усилением локального неоангиогенеза и роста нервных волокон с изменением пролиферативно-апоптотического паттерна в сторону угнетения апоптоза и усиления пролиферации. Ключевые слова: витамин D, патогенез тазовой боли, наружный генитальный эндометриоз.