Abstract The congenital dysferlinopathy phenotype is the rarest and earliest manifestation variant, described in two closely related Spanish and Turkish families, with a homozygous pathogenic frameshift variant in exon 26 of the DYSF gene. This article presents a 1.6-year-old patient from a consanguineous Uzbek family with a clinical diagnosis of congenital dysferlinopathy phenotype and Marinesco–Sjögren syndrome with transient postnatal hypotonia, motor development delay, muscle weakness in the flexors of the neck and proximal limbs, convergent strabismus, cerebellar truncal ataxia, minimal intention tremor of the upper limbs, a slight increase in the levels of creatinine phosphokinase (CK) to 353 U/L (2.4×N) and that of myoglobin to 40 µg/mL (2×N). Magnetic resonance imaging (MRI) revealed pronounced edematous changes in the gastrocnemius muscle on short tau inversion recovery (STIR). MRI signs of minimal fat replacement and hypotrophy were noted in the medial and posterior thigh and gastrocnemius muscles. MRI of the head revealed hypoplasia of the vermis and cerebellar hemispheres. Whole-exome sequencing revealed compound heterozygous DYSF variants: NM_001130987.2:c.1000 C > T (p.(Arg334Trp)) and NM_001130987.2:c.518 C > T (p.(Thr173Met)), and a previously described homozygous SIL1 variant NM_022464.5:c.178G > T (p.(Glu60Ter)). Histopathological examination revealed minimal signs of myopathy and dysferlin in only 1% of the muscle fibers. At the ultrastructural level, signs of dysferlinopathy and Marinesco–Sjögren syndrome were detected. This clinical case is an example of the cosegregation of two diseases that mutually potentiate damage to skeletal muscles.

Dysferlinopathy is a rare muscular dystrophy characterized by chronic muscle damage and ineffective regeneration. While late-stage morphological changes, such as fibroadipose replacement, are well described, the early molecular mechanisms driving muscle fiber loss and regenerative failure at the onset of the disease remain largely uncharacterized. To address this gap, we investigated the skeletal muscles of dysferlin-deficient Bla/J mice during the early manifestation stage (3 months of age). This exploratory study aimed to identify primary pathomorphogenetic events by correlating the transcriptomic profile of the tissue with its specific histopathological and ultrastructural alterations. We performed a comparative analysis of the m. gastrocnemius in 3-month-old Bla/J mice versus wild-type controls using RNA sequencing, RT-qPCR, histomorphometry and transmission electron microscopy. The results revealed atrophy and muscle fiber necrosis without the expected induction of Fbxo32 and Trim63 ubiquitin ligases, suggesting ubiquitin-proteasome system-independent muscle mass loss. Furthermore, the absence of Casp3, Bak1, and Bad induction, confirmed by the lack of active caspase-3, excluded apoptosis as the primary death mechanism. A differentiation block in satellite cells was confirmed by the lack of Myf5, Myod1, and Myog induction and a trend toward Tead4 suppression, pointing to an early failure of the reparative program. Exploratory RNA sequencing also identified a suppression of Prkn expression accompanied by LC3B-II-positive autophagosome accumulation. Immunohistochemical and immunofluorescent evaluation of the mitochondrial network (TOMM20) revealed abnormal accumulations and dense clumping, indicating impaired organelle clearance. Furthermore, ultrastructural analysis demonstrated internal organelle damage and the presence of myelin-like structures, consistent with a state of stalled mitophagy. Collectively, this exploratory study demonstrates that early muscle atrophy and myofiber necrosis in dysferlinopathy occur independently of canonical ubiquitin-proteasome and apoptotic pathways. Instead, the disease manifestation stage is structurally characterized by stalled mitochondrial clearance and a delayed regenerative response.

BACKGROUND: High-performance sport represents a unique model of morphological adaptation, but systematic studies of the anthropometric profiles of national team athletes using large samples and modern sport classifications are lacking. It remains unclear how far athletes' body parameters can deviate from general population norms while maintaining high levels of performance. AIM: To characterize the anthropometric profiles of professional athletes of the Russian national teams and assess the degree of their deviation from the general population parameters to reflect the phenomenon of sports-related morphological adaptation. METHODS: A retrospective comparative study was conducted, including data from 15,157 athletes from Russian national teams who underwent in-depth medical examinations at Federal Medical and Biological Agency (FMBA) facilities between 2021 and 2025. Sports were divided into six Olympic clusters: cyclic, speed-strength, complex-coordination, combat sports, sports games, and combined events. Anthropometric parameters, body composition (bioimpedance), dynamometry, and integral body composition indices were analyzed. Statistical processing was performed in the R environment, calculating mean values, 95% confidence intervals, medians, and interquartile ranges. RESULTS: The study included 15,157 athletes (mean age 19.91 years). Significant differences were revealed between sport disciplines: maximum body weight (92.71 kg), BMI (30.38 kg/m²), skeletal muscle mass (45.72 kg) and strength indicators were recorded in speed-strength events in men; minimum ones — in complex coordination disciplines in women (body weight 56.88 kg, BMI 19.94 kg/m², body fat percentage 9.54%, skeletal muscle mass 24.99 kg). The Pigneur index ranged from -37.69 (speed-strength, men) to 24.05 (complex coordination, women). All athletes' parameters systematically differed from the NCHS/NHANES reference values: lower — for BMI, waist circumference, percentage of body fat; higher in skeletal muscle mass and strength indicators. CONCLUSION: The anthropometric profile of athletes on the Russian national teams is influenced by selection at the recruitment stage and subsequent adaptation to training loads, resulting in parameters outside the general population range. The data obtained substantiate the need to use sport-specific reference values ​​to assess athletes' physical development.

Introduction: Gene therapy for Myoshi myopathy is extremely relevant, as it may become the first pathogenetic treatment for dysferlinopathy. The aim of this study was to study the efficacy and safety of the use of a genetic construct, the AAV9-DYSF-DV3’ virus, for the treatment of limb girdle muscular dystrophy LGMD) type R2. Materials and Methods: Mouse models of limb girdle muscular dystrophy type R2 В6.А-Dysfprmd/GeneJ were used to study the effectiveness of AAV9.DYSF drug and the corresponding C57BL/6J controls were used. During the study, muscle activity was determined on the basis of the following tests: “Grip test”, “Holding an animal on a slippery surface of a vertical rod”, “Forced swimming with a load”, and ”Wire hanging”. In the course of acute and subchronic toxicity, hematological and biochemical blood tests of the rats, histological analysis and ”Open field” behavioral testing were performed. Results and Discussion: In this study, for the first time, a comprehensive investigation of the effectiveness of gene therapy using the two-vector system of adeno-associated AAV9-DYSF-DV3’ virus with overlapping DYSF cDNA sequences was conducted in a mouse model of limb girdle muscular dystrophy type 2 R. Conclusion: During the testing of the drug’s effectiveness, it was discovered that drug AAV9.DYSF showed the best effectiveness in mice with the absence of the protein dysferlin in behavioral testing at the maximum dose (5*1012) with a double intramuscular injection. In the “Grip test”, the index in В6.А-Dysfprmd/GeneJ mice increased by 29% (p=0.0026) relative to that in the K-group. In the tests “Forced swimming with a load”, ”Wire hanging”, and ”Holding an animal on a slippery surface of a vertical rod”, the indicators also improved by 80% (p=0.0019), 104.8% (p=0.001) and 20% (p=0.025), respectively, relative to those of the negative control. During acute and subchronic toxicity, the administration of the drug to animals does not cause death or intoxication.

INTRODUCTION: Cellular senescence is a complex process occurring at all stages of the development and functioning of an organism. On the one hand, it is important as a mechanism protecting against cell damage, but on the other hand, it contributes to the development of age-related diseases and aging of an organism as a whole. AIM: To determine key markers of senescent cells to study pathogenetic mechanisms of aging and to search for new strategies of healthy longevity. A literature search was conducted in PubMed and eLibrary.ru databases until July 1, 2024 and included analysis of the original and review articles using the keywords: ‘senescent cells’, ‘cellular senescence’, ‘senescent cell markers’, ‘SA-β-Gal’, ‘SASP’. The best studied and widely used markers of senescent cells are cell cycle arrest factors: DNA damage response markers p53 and γH2AX, and cyclin-dependent kinase inhibitors p16 and p21. Furthermore, SA-β-Gal is a universal marker of cellular senescence, identified in both tissues and cell models of aging. SASP factors are not direct markers of aging, but an important indicator of complex interactions between senescent cells and their microenvironment. CONCLUSION: Currently, a large number of senescent cells pathogenetic markers have been identified. Their expression can vary depending on the cell type and aging context, which is important to understand for the development of senolytic therapeutic approaches and the maintenance of healthy longevity.

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BACKGROUND: With the sharp increase in mine-explosive injuries, one of the key tasks of modern histology is to assess the morphogenesis of high-energy limb tissue damage. AIM: This study aimed to characterize striated skeletal muscle tissue in the zone of mine-explosive limb segment avulsion during the early post-traumatic period (days 1–4). METHODS: Histological methods (hematoxylin and eosin staining and Martius Scarlet Blue [MSB] staining for fibrin age determination), immunohistochemical and immunofluorescence techniques (antibodies to CD3, CD20, CD31 [Platelet Endothelial Cell Adhesion Molecule-1], CD68, and NETs [Neutrophil Extracellular Traps]), transmission electron microscopy, and morphometric analyses were applied. RESULTS: Post-traumatic pathological changes affected both muscle tissue (necrosis, fiber fragmentation, traumatic edema) and endomysial and perimysial connective tissue (traumatic edema, fibrin infiltration). Disruption of the cytoskeletal structure (sarcomeres), loss of myosatellite cells, and endothelial cell death in capillaries were observed. Local hemodynamic disturbances manifested as mosaic thrombosis, embolism, and hemorrhage. Within the first 24 hours, arterial and arteriolar spasms led to reduced tissue perfusion. Partial resolution of the spasms by day 4 likely corresponded to the second stage of traumatic shock (the torpid phase). Among leukocytes, CD68+ macrophages were the first to respond, with extravasation beginning on day 2 after injury. A similar trend was observed for CD3+ T cells. CD20+ B cells showed no morphological signs of reactivity during this period. NET formation was observed both intravascularly and in the extravascular compartment. CONCLUSION: Structural and ultrastructural changes in skeletal muscle tissue within the first 4 days after mine-explosive injury have been characterized.

Objective. To develop artificial intelligence-based software algorithm for quantitative assessment of reparative bone tissue regeneration, as well as to compare the results of histomorphometric analysis carried out by neural network and human. Material and methods. Morphometric parameters were determined and standardized. The authors developed artificial intelligence-based software algorithm with subsequent neural network training based on high-resolution images. Efficacy of human and software algorithm was compared. Results. Original software allows for automatic analysis of bone regenerate tissue composition within the shortest possible time. Conclusion. Original software may be equivalent for quick and effective analysis of bone regenerate tissue components. These data may be comparable with manual marking regarding reproducibility and accuracy.

BACKGROUND: Disruption of the stages of reparative regeneration leads to insufficient formation of the extracellular matrix and the development of chronic wounds, which require a personalized therapeutic approach. Modern regenerative medicine utilizes biopolymers, such as silk proteins, as the basis for wound dressings and drug delivery systems, which possess a number of unique properties. The biocompatibility, influence on intracellular signaling pathways, and antibacterial activity of spidroin (spider silk protein), fibroin, and sericin (the basis of insect silk) make them potentially applicable as wound healing agents. AIM: The aim of the study is to characterize the effect of a cream based on a solution of silk spidroin, fibroin, and sericin proteins on skin regeneration in a comparative experiment. MATERIALS AND METHODS: The study was conducted on 30 male rats with surgically created full-thickness excisional skin defects measuring 20 mm in diameter on their backs. The rats were then divided into three groups: group 1 received daily topical application of the investigated cream, group 2 received a commercial panthenol product, group 3 served as the control group, with wounds left to heal spontaneously. The process of reparative regeneration and reactive changes were assessed through clinical blood analysis, planimetric measurements of wound closure, and histomorphometric analysis of tissue samples. RESULTS: The treatment group exhibited a positive trend in wound healing (p=0.010) with faster complete skin closure (by day 14) compared to the control group. Evaluation of the inflammatory response revealed no significant changes in blood parameters (moderate granulocytosis and signs of acute posthemorrhagic anemia) and reduced immune cell infiltration compared to the control group. CONCLUSION: The combination of spider silk proteins (spidroin) and insect silk proteins (fibroin and sericin) has the potential to enhance cell migration, proliferation, and differentiation, as well as extracellular matrix production. They also exhibit anti-inflammatory activity without possessing immunogenic properties. These characteristics provide a basis for the potential use of these proteins as standalone therapeutic agents, including in the clinical management of wounds with impaired healing.

Cellular senescence is a key mechanism of aging. Senescent cells negatively affect the function of tissues and organs, significantly contributimg to the aging of the organism. Functional and structural characteristics of senescent cells, such as genomic changes and cell cycle arrest, lysosome and mitochondrial dysfunction, and production of SASP factors, are promising therapeutic targets in the context of healthy longevity. The present review was designed to characterize the features of senescent cells in order to discuss current methods and problems of geroprotective therapy and perspective factors for the development of new strategies of anti-aging treatment. Publications were searched based on the analysis of articles containing the keywords “senescent cells, aging, senolytic therapy, SASP, mitochondrial dysfunction” in the PubMed and Scopus databases up to March 2025.

Fibrodysplasia ossificans progressiva (FOP) is an extremely rare genetic disorder with a prevalence of approximately 1 case per 1.5–2.0 million individuals. The primary cause of the disease lies in mutations of the ACVR1 gene, which encodes the homonymous receptor involved in the regulation of bone histogenesis. The most common genetic variant is the 617GA single nucleotide substitution (R206H, rs121912678), resulting in the replacement of arginine with histidine. This variant is observed in over 95% of all registered patients with fibrodysplasia ossificans progressiva. The mutation disrupts intracellular signaling, leading to the formation of abnormal heterotopic bone tissue in muscles, tendons, and ligaments. The clinical presentation may vary: some patients experience additional symptoms presumably associated with rare mutations in other domains of the ACVR1 receptor. Despite active research, the exact precursor cells responsible for pathological osteogenesis remain unidentified. Scientists hypothesize the involvement of multiple cell types, including mesenchymal stem cells and endothelial cells. Currently, no effective treatment exists for fibrodysplasia ossificans progressiva, underscoring the urgent need for novel therapeutic targets. Gene therapy, successfully employed in other monogenic disorders, represents a promising direction. Several experimental approaches, including targeted inhibitors of the ACVR1 signaling pathway, are undergoing preclinical and clinical trials.

Calpainopathy, or limb-girdle muscular dystrophy type R1/2A (LGMDR1/2A), is the most prevalent form of LGMD, comprising about 32% of all cases. The disease is caused by mutations in the CAPN3 gene, leading to dysfunction of the corresponding protein-an enzyme critical for muscle fiber cytoskeleton remodeling and protein signaling regulation through selective proteolysis. Clinical manifestations demonstrate significant phenotypic polymorphisms, ranging from oligosymptomatic forms to severe early-onset cases, with the loss of ambulation occurring 10-25 years after disease onset. A characteristic feature is predominantly symmetrical involvement of limb and trunk muscles, leading to early mobility loss, disability, and reduced work capacity. Noninvasive imaging can suggest dystrophic muscle disease but requires differentiation from other myopathies. Confirming the diagnosis involves histological, immunological, and molecular genetic studies to identify calpain-3 activity or CAPN3 gene expression alterations. Currently, no targeted or etiological therapies are available for calpainopathy. Treatment focuses on symptom management, complication prevention, and slowing disease progression. Preclinical research demands the development of an appropriate animal model that displays disease phenotypes mirroring those observed in humans. Preclinical and clinical research are also investigating therapeutic options, including the use of drugs that have proven effective in other myopathies and genome editing via transgenic CAPN3 delivery to restore protein activity. Gene therapy has shown promise in murine models, but safety concerns, particularly systemic toxicity affecting the heart and other organs, remain significant. This review comprehensively analyzes the clinical features, diagnostic approaches, and advancements in modeling and therapeutic development for calpainopathy.

An urgent issue is the preservation or reconstruction of the volume of bone tissue in planning and surgical treatment in the fields of medicine, such as traumatology, orthopedics, maxillofacial surgery and dentistry. After tooth extraction, resorption of the bone tissue of the alveolar crest of the jaws occurs, which must either be further eliminated by performing additional operations or using osteoplastic material for socket preservation at the extraction stage. Background and Objectives: The aim of the study was a comparative analysis of various osteoplastic materials used to preserve the volume of bone tissue in the preimplantation period. Materials and Methods: As part of the study, 80 patients were treated, who underwent socket preservation using xenografts, plasma enriched with growth factors, an autologous dentin matrix (ADM) and hydroxyapatite. Results: The results of the treatment 16 weeks after removal were comprehensively analyzed using a morphometric analysis of the bone’s volume, cone beam tomography and morphological examination of burr biopsy specimens, as well as by determining the stability of the installed implant at different stages of treatment. Conclusions: The lowest level of bone tissue resorption according to the CBCT data was noted in the ADM and xenograft groups. It should be noted that the use of osteoplastic material in jaw surgery when reconstructing alveolar defects is an essential procedure for preventing the atrophy of bone tissue.

BACKGROUND:Dysferlinopathy is heritable progressive muscular dystrophy caused byDYSFmutation. Currently, although skeletal muscle pathology has been defined, only fragmentary and limited myocardium histopathology data are available. AIM:The study aimed to analyze the pathomorphological status of the myocardium in Bla/J mice models of dysferlinopathy at different ages. MATERIALS AND METHODS:Data from two experimental groups were analyzed: Bla/J mice withDYSFknockout on 3, 6, and 12 months old and control wild-type Balb/C mice aged 6 months. The expressions and patterns of dyeing of protein dysferlin in the immunofluorescent search method were analyzed. These were held such parameters of the histological characteristic of the myocardium of three dyeing protocols (hematoxylin and eosin, iron hematoxylin by Rego, and hematoxylin-basic fuchsin-picric acid by Lie), and morphometry of the parameters of the cardiomyocytes (length, width of cardiomyocytes, and nuclear perimeter). RESULTS:The immunofluorescent search method revealed high levels of dysferlin in the myocardium of the control group. Statistical analysis showed significant differences between Bla/J and Balb/C mice: the increasing length and width of cardiomyocytes in dysferlinopathy by 49.9% ((95% confidence interval, 45.9–57.4) and 35.6 (95% confidence interval, 32.9–37.9)), respectively. Nucleus perimeter was significantly reduced in the dysferlinopathy group with disease duration of 6 months (by 23.9 (95% confidence interval, 20.2–27.5) compared with the group with disease duration of 3 months and by 18.8% (95% confidence interval, 8.5–19.7)) and the control group. Consequently, progressive hypertrophy of cardiomyocytes, increasing deformation in cardiomyocytes, intercalated disk destruction, hypoxia features, and necrosis indication were observed, resulting in fibrosis. A pattern of cardiomyocyte size reduction dependent on the aging process was observed. CONCLUSIONS:Dysferlin deficiency leads to significant damage in the myocardium of Bla/J mice.

The results of autopsies performed in the pathological department of the Infectious Diseases Hospital named after. S.P. Botkin during the siege of Leningrad (from September 8, 1941 to January 27, 1944). The structure of diseases of the deceased varied during different periods of the siege of Leningrad. In the first period (September-December 1941), diphtheria, dysentery, measles, typhoid fever, and scarlet fever prevailed among the diseases. The most common causes of death in the second period (April-December 1942) were typhus, dysentery, tuberculosis, lobar pneumonia, and typhoid fever. Nosological structure in the third period of the blockade (January 1943 - January 1944): tuberculosis, dysentery, cachexia, lobar pneumonia, infectious jaundice. The discrepancy between clinical and morphological diagnoses is most often noted for the following nosology: pulmonary tuberculosis, typhoid fever, pneumonia, stomach and hepatopancreatobiliary cancer, measles, influenza. The first period of the blockade was distinguished by a high specific proportion of examination of children's bodies - 51.2% of all autopsies; in subsequent periods, the specific share of autopsies of deceased adults (20-59 years) increased to 76.2%. The difference in the nosological structure and age groups of those who died during different periods of the siege of Leningrad was determined by the epidemiological situation in the city, social and living conditions and medical and organizational factors. Conducted in the pathological-anatomical department of the hospital named after. S.P. Botkin during the siege of Leningrad, pathological studies made it possible to timely establish the causes of deaths and identify the peculiarities of the course of infectious diseases against the background of cachexia. Regularly held clinical and anatomical conferences contributed to the reduction of defects in the diagnosis and treatment of infectious diseases.

BACKGROUND: The steady increase in the number of inflammatory bowel diseases and the absence of reliably significant diagnostic markers require the search for new morphological criteria for differential diagnosis. AIM: This study aimed to determine the cellular-differential composition of the intestinal epithelium in the phases of exacerbation and remission in Crohn’s disease and ulcerative colitis. MATERIALS AND METHODS: Tissue samples of 60 patients with inflammatory bowel diseases (Crohn’s disease, n=30; ulcerative colitis, n=30) and with irritable bowel syndrome (control group, n=15) were studied using histological, immunohistochemical, morphometric and statistical methods. RESULTS: Distinct features of the cellular-differential composition of the epithelium in the mucous membrane of the ileum, ascending colon, sigmoid colon, and rectum were identified across these conditions, with differences observed during exacerbation and remission in inflammatory bowel diseases. The proportion of goblet cells in the epithelial lining varied by intestinal region and disease type and phase. Goblet cell differentiation: 25.0% more goblet cells of the superficial epithelium between the crypts of the ileum in acute Crohn’s disease compared with remission (p=0.0002); 42.9% more goblet cells in the superficial epithelium of the ascending colon compared with irritable bowel syndrome (p=0.0001); 23.0% more goblet cells crypt in the sigmoid colon compared with ulcerative colitis in the acute stage (p=0.0024). There were no significant differences in the differentiation of Paneth cells. There was a threefold increase in endocrinocytes in the sigmoid colon in acute Crohn’s disease compared with irritable bowel syndrome (p=0.0238). Nonepithelial differon cells: fewer interepithelial lymphocytes in Crohn’s disease in remission compared with Crohn’s disease in the acute stage by 2.4 times in the sigmoid colon, 4.0 times in the rectum (p 0,0001); compared with irritable bowel syndrome by 4.8 times in the ileum, 2.7 times in the ascending intestine, 4.0 times in the sigmoid colon (p 0,05); 8.0 times in the rectum compared with ulcerative colitis in remission (p=0,0004). Additionally, the study found proliferative activity of crypt cells (mainly goblet-shaped) increased by 4.2 times in the sigmoid colon in acute Crohn’s disease compared with acute ulcerative colitis (p=0,0016). CONCLUSIONS: Morphometric parameters of the cellular-differential composition of the intestinal epithelium can serve as potential differential diagnostic criteria. Acute Crohn’s disease is characterized by a higher proliferation index in the sigmoid colon compared with acute ulcerative colitis, while Crohn’s disease in remission shows a lower number of interepithelial lymphocytes in the rectum compared with ulcerative colitis in remission.

The DYSF gene encoding dysferlin protein is one of the largest and has many transcripts. Pathogenic variants in the gene can lead to various types of myopathies, which makes it a good object for studying the events occurring in it during genome editing by the CRISPR/Cas method. In this study, we evaluated the possibility of permanent skipping of exons 3-4, and 26-27 which deletion does not violate the reading frame and allows to eliminate truncated variants within exons. Editing was performed with simultaneous transfection of two sgRNA- and sa/ spCas9-containing plasmids on HEK293T cell cultures and healthy donor myoblasts. Skipping of exons 3-4 was performed by destroying the splicing acceptor sites, and exons 26-27 by cuts in the flanking exons with the corresponding deletion in the DNA. Some unexpected results were obtained, when exons 26-27 were skipped, exon 30 was also absent in the transcript, although it is not alternatively spliced and is normally present in all transcripts. This event indicates that DNA changes near splicing sites can affect adjacent exons and the whole gene. However, this fact requires further study.

BACKGROUND: Inflammation of the synovial membrane is a common manifestation in osteoarthritis which plays a role in complex pathophysiology of osteoarthritis. Synovitis leads to complications during knee replacement. AIM: To give clinical and morphological characteristics of the knee joint condition by histological assessment of the synovial membrane. MATERIALS AND METHODS: In the clinic of traumatology and orthopedics of North-Western State Medical University named after I.I. Mechnikov in 2022, 187 total knee arthroplasty operations were performed in patients with osteoarthritis. For morphological study of the synovial membrane of the knee joint biopsy specimens were taken from 30 patients (19 women and 11 men) by randomized sampling method. The age of patients: from 40 to 76 years, the average age was 59,3 ± 6,7 years. Immunohistochemical reactions were performed to characterize the cellular composition of the inflammatory infiltrate; antibodies to CD68, CD3, CD20, CD138, Ki-67 were used. Morphometry was performed at ×400 magnification. RESULTS: Only 48 (25.7%) patients had at least one course of inpatient conservative or minimally invasive surgical treatment for osteoarthritis of the knee joint before total knee arthroplasty. 18 (9.6%) patients had intraoperative and postoperative complications. Among 30 morphological studies conducted, 3 (10%) patients had verified stage I osteoarthritis of the knee joint, 8 (26.7%) were diagnosed with stage II osteoarthritis, and 19 (63.3%) — stage III osteoarthritis. Significant correlation was obtained between cells stained with antibodies to CD3 and CD20 (r = 0.69; p 0.05), CD68 and CD138 (r = 0.66; p 0.05). Cluster analysis identified three groups of patients with severe (10%), moderate (30%) and weak/absent infiltration (60%). CONCLUSIONS: To correct the treatment strategy for patients with osteoarthritis of the knee joint, it is advisable to strengthen the role of arthroscopic methods in the diagnostic and treatment processes.

Background Dysferlinopathy is a phenotypically heterogeneous group of hereditary diseases caused by mutations in the DYSF gene. Early contractures are considered rare, and rigid spine syndrome in dysferlinopathy has been previously reported only once. Case presentation We describe a 23-year-old patient with Miyoshi myopathy with a rigid spine and multiple contractures, a rare phenotypic variant. The disease first manifested when the patient was 13 years old, with fatigue of the gastrocnemius muscles and the development of pronounced contractures of the Achilles tendons, flexors of the fingers, and extensors of the toes, followed by the involvement of large joints and the spine. Magnetic resonance imaging revealed signs of connective tissue and fatty replacement of the posterior muscles of the thighs and lower legs. Edema was noted in the anterior and medial muscle groups of the thighs, lower legs, and the multifidus muscle of the back. Whole genome sequencing revealed previously described mutations in the DYSF gene in exon 39 (c.4282 C > T) and intron 51 (c.5785-824 C > T). An immunohistochemical analysis and Western blot showed the complete absence of dysferlin protein expression in the muscle fibers. Conclusions This case expands the range of clinical and phenotypic correlations of dysferlinopathy and complements the diagnostic search for spine rigidity.

BACKGROUND: An important feature of COVID-19 is the development of pronounced hypercoagulation with an increased risk of thrombotic damage to the pulmonary vascular bed, mainly the pulmonary arteries. Thrombosis of the pulmonary blood vessels causes a local violation of hemodynamics with the development of hyperemia, edema, which leads to a decrease in ventilation of the lung tissue area and serves as one of the causes of respiratory failure. AIM: This study aimed to conduct a morphological and morphometric analysis of the vascular bed of lung tissues in deceased with severe and extremely severe forms of new coronavirus infection who were on inpatient treatment in the period 2020–2022. MATERIALS AND METHODS: A pathomorphologic study of 129 autopsy cases with a confirmed diagnosis of a new coronavirus infection COVID-19 was performed. Morphometric analysis and statistical data processing of the pulmonary vascular system in histologic preparations stained with hematoxylin and eosin stain, orcein stain and Martius Scarlet Blue (MSB) stain was performed. The control group consisted of 14 patients who died of cardiovascular disease with bilateral focal confluent pneumonia. RESULTS: It was found that the proportion of thrombosed vessels in the lung tissues of the deceased was 27.6%. In 87.2% of cases, thrombosis develops in small arteries (lumen diameter 30-500 microns) and small veins (lumen diameter 40–500 microns). The vascular-functional indices of Kernogan and Vogenworth were statistically significantly increased in small arteries and small veins of the 4th order (p=0.001), small arteries (p=0.001) and small veins of the 5th order (p=0.014) compared with the control group. CONCLUSIONS: Diffuse involvement of small caliber blood vessels in the pathological process reflects the severity of specific hemocoagulopathic disorders in the lung tissue. Such disorders lead to the development of ventilation-perfusion disorders and entail an increase in right ventricular failure.