Aim. To investigate the proinflammatory activity markers of adipose tissue in a rat model of metabolic syndrome (MetS).Materials and methods. The experiments were performed on male Wistar rats maintained on either a standard diet or a high-fat, high-carbohydrate diet (HFHCD). Physiological and biochemical parameters were assessed in the respective animal groups. The concentrations of adipokines (leptin and adiponectin) and cytokines: tumor necrosis factor alpha (TNF-α), interleukins (IL-6 and IL-10) and monocyte chemoattractant protein-1 (MCP-1) secreted by adipose tissue cells were determined using enzyme-linked immunosorbent assay. The phenotypic profile of adipose tissue cells expressing the CD68 marker was examined by immunohistochemistry, and the level of CD68 gene expression was additionally assessed using real-time polymerase chain reaction. A histological examination of visceral adipose tissue fragments was performed.Results. It was found that in rats fed a HFHCD, there was a significant correlation (p < 0.05) between an increase in adipose tissue mass and elevated serum levels of leptin (r = 0.57), glucose (r = 0.62), and insulin (r = 0.61). In the experimental group, the concentrations of proinflammatory cytokines (IL-6, TNF-α, and MCP-1) and leptin produced by adipose tissue cells were higher than in the control group (p < 0.05). Additionally, we demonstrated that rats fed a HFHCD exhibited a significant (p < 0.05) decrease in the secretion of the anti-inflammatory cytokine IL-10 and adiponectin. Histological examination of the experimental group revealed adipocyte hypertrophy and anisocytosis, venous vessel congestion, and thickening of the interlobular connective tissue layer. Furthermore, rats fed an HFHCD exhibited an increased number of CD68-positive cells in visceral fat samples and elevated CD68 gene expression.Conclusion. Thus, in experimental diet-induced metabolic syndrome, adipose tissue acquires a proinflammatory phenotype due to adipocyte hypertrophy, infiltration by immune-competent cells (CD68+ macrophages), and increased secretion of proinflammatory chemo- and adipokines (TNF-α, IL-6, MCP-1, and leptin).
Aim. To identify risk factors leading to a cognitive decline 5–7 years after CABG, and to develop a model for predicting the development of POCD in patients in the long-term period of CABG.Materials and methods. The observational prospective study included 146 patients; average follow-up period was 6.4 years. The patients underwent general clinical, neurological, and instrumental examinations 3–5 days before and 5–7 years after surgery. Neuropsychological testing included assessment of psychomotor and executive functions, attention, and short-term memory. The method of binary logistic regression was used to build a predictive model.Results. Cognitive decline was detected in 67 patients (45.9%) at 5–7 years after CABG. The presence of carotid artery (CA) stenosis (p = 0.01), smoking (p = 0.005), reduced left ventricular ejection fraction (p = 0.039), and high triglyceride levels (p = 0.011) was associated with a cognitive decline. The model`s sensitivity was 0.61 and specificity was 0.82, indicating a good quality. Results indicate that the model can accurately predict the presence or absence of cognitive decline with a high level of accuracy.Conclusion. Five to seven years following CABG, 46% of patients experienced a decrease in cognitive functions, manifested in the form of neurodynamic dysfunction, as well as deterioration of short-term memory. The factors included in the prognostic model were CA stenosis, reduced left ventricular ejection fraction, and high triglyceride levels, as well as smoking. The findings indicate the need to improve approaches to postoperative follow-up of patients who have undergone cardiac surgery in order to minimize adverse neurological consequences.
The aim of the lecture was to consider the role of gene ontology (GO) and the GO Consortium in shaping the knowledge base for genomics, proteomics, and biology. GO organizes and continually updates data on the molecular functions and biological processes in which genes and their products are involved.The structure of GO, the features of GO term hierarchy and the connections between them, as well as the elements of each term are considered. The features of services for working with basic knowledge and various ways to access civil defense data are given. In addition to term characteristics, GO pays great attention to annotations – statements that link a gene product to a certain ontology term. The annotation process captures the action and location of a gene product using terms, providing a reference and a type of evidence.The areas of application of GO related to the analysis of genomics and proteomics data are considered. The main approaches used by researchers are functional annotation of genes and pathway enrichment analysis. Analysis of large volumes of data (for example, when assessing gene expression) allows to gain knowledge about the involvement of genes and their products in various processes, extract biological meaning, and evaluate the features of molecular mechanisms in various diseases. The increasing role of GO in the formation of new knowledge in the relevant field is shown.
Aim. To evaluate serum vascular endothelial growth factor (VEGF) levels in the dynamics of the acute period of ischemic stroke in patients during clinical and functional recovery.Material and methods. The study included 114 patients with ischemic stroke. Patient groups were the following: Group 1 – mild stroke (n = 57 patients), Group 2 – moderate stroke (n = 25 patients), Group 3 – severe stroke (n = 32 patients). Observation period was 14 days. Observation points included: I – the first 48–72 hours from the onset of the disease; II – the 14th day. We used the following assessment scales National Institute of Health Stroke Scale (NIHSS) and the modified Rankin Scale (mRS). VEGF was determined in blood serum on a multiplex analyzer. Statistical processing of the results was carried out using the Statistica 13.0 software package.Results. Patients of groups 1 and 2 showed a statistically significant decrease in points on the NIHSS and mRs scales (p < 0.001) in the dynamics of observation, in patients of group 3 no significant changes were found (p = 0.157 and p = 0.315, respectively). VEGF in the comparison group did not show reliable differences relative to patients at points I (pz–1 = 0.73, pz–2 = 0.738, pz–3 = 0.129) and II of observation (pz–1 = 0.66, pz–2 = 0.817, pz–3 = 0.276). Analysis of the dynamics of the marker revealed an increase in VEGF between points I and II of observation in group 3 (p = 0.021), ΔVEGF positively correlated with a higher score on the NIHSS scale at point I (r = 0.691; p = 0.027). No correlation relationships were found in group 1 (рI–II = 0.078, r∆VEGF-NIHSS_I = –0.294; р∆VEGF-NIHSS_I = 0.237) and group 2 patients (рI–II = 0.285, r∆VEGF-NIHSS_I = –0.305; р∆VEGF-NIHSS_I = 0.392).Conclusion. Heterogeneity of ischemic stroke pathogenesis reduces the prognostic value of VEGF as an isolated biomarker. A comprehensive analysis of the temporal patterns of VEGF regulation and other angiogenic factors is needed to understand the dynamics of vascular remodeling and predict the outcomes of ischemic stroke.
Aim. The research aims to systematize current data on the prevalence, diagnosis, and clinical significance of iron deficiency (ID) in patients with acute decompensated heart failure (ADHF).Materials and methods. A systematic analysis of studies from 2019 to 2024 in PubMed and eLibrary databases was conducted, including data from 6,500 patients with ADHF. Selection criteria were as follows: confirmed ADHF diagnosis, assessment of iron status using standard parameters (ferritin and transferrin saturation (TSAT)), and availability of clinical outcome data.Results: To differentiate the type of iron deficiency, optimal diagnostics of simultaneous assessment of ferritin and TSAT levels requires: ferritin < 100 μg/L – absolute ID; ferritin 100–299 μg/L in combination with TSAT < 20% – functional ID. ID was found in 45–89% of ADHF patients and was associated with: more severe disease progression (functional class III-IV according to the New York Heart Association system in 68% of cases), elevated of N-terminal propeptide of type B natriuretic peptide levels (35% higher compared to non-ID patients), reduced exercise tolerance (six-minute walk test: 278±45 m vs 342±38 m in non-ID group).Conclusion: Iron deficiency is an independent prognostic factor in ADHF. Early diagnosis and correction, particularly through intravenous ferric carboxymaltose administration, may improve clinical outcomes and reduce hospital readmission rates.
Aim. To investigate the relationship between the differentiation status of breast cancer (BC) tumor cells (TC) of various molecular subtypes, the ability to metastasize, and the modulation of various cytokines in BC samples in vitro.Materials and methods. Biopsies from invasive breast carcinoma of a non-specific type in 50 women, classified by the presence (Met+) and absence (Met–) of metastases in regional lymph nodes, were examined and categorized into 4 groups based on their molecular subtypes: luminal A (Lum A), luminal B (Lum B), HER2/neu positive (HER2+), and triple negative (TN). Using enzyme-linked immunosorbent assay, spontaneous and mitogen complex-stimulated (MC) production of 14 cytokines was determined in the supernatant of cultured BC samples (IL-2, IL-6, IL-8, IL-10, IL-17, IL-18, IL-1β, IL-1Ra, TNF-α, IFN-γ, G-CSF, GM-CSF, VEGF, and MCP-1), on the basis of which the index of the MC effect (IMCE) on cytokine production was calculated. The effect of stimulating the differentiation of TC was evaluated on the basis of cytomorphological criteria for reducing the relative content of low-grade cells (LGC) in BC samples.Results. A statistically significant decrease in the relative content of LGC under the influence of MC was detected in the Met+ and Met– groups. MC had a differentiating effect in luminal and HER2-positive subtypes, while in TN breast cancer samples there was only a downward trend in the proportion of LGC. To assess the role of cytokines in the mechanism of the differentiating effect of MC on LGC, a neural network analysis of IMCE in the relationship of various cytokines was carried out. According to the results obtained, in Lum A, the leading role in the manifestation of the differentiation effect was associated with IL-1Ra and IL-6; in Lum B, with MCP-1 and GM-CSF; in HER2+, with IFN-γ and MCP-1, and in TN – with IL-1β and IL-6.Conclusion. The data obtained indicate that the immune mechanisms mediating the differentiating MC effect on BC may vary in different molecular subtypes of BC.
Aim. To study the proliferative activity of non-small cell lung cancer with tumor spread through air spaces.Materials and methods. The study included 88 patients with stage IA-IIIA non-small cell lung cancer. The operative material was evaluated. Histologic and immunohistochemical examination was performed according to the standard technique. Antibodies to Ki67 (clone SP6, Cell Marque) were used. On digitized preparations using automated system Pannoramic MIDI with software Slide Viver V2.8. and multi-module platform Quant Center (3D HISTECH, Hungary) we counted the percentage of cells with positive nuclear expression of Ki67 in the tumor as a whole and in the area of spreading. Statistical processing was performed using the STATISTICA 10.0 software package. Differences at p < 0.05 were considered statistically significant.Results. The percentage of Ki67 expression in the tissue of the primary tumor node was higher in cases with the presence of tumor spread through air spaces, including stage IA lung adenocarcinoma. The percentage of Ki67 expression in the area of air space spread of the tumor was higher compared to the percentage of expression in the tumor as a whole. Higher proliferative activity in the zone of tumor air space spread was observed in cases with extensive spread compared to cases with a limited variant of air space spread.Conclusion. The results obtained complement the existing data on the mechanisms of tumor spread through air spaces as a form of invasive growth and one of the variants of tumor progression characteristic of lung cancer.
Stroke can lead to motor, cognitive, and speech disorders that require long-term correction. Rehabilitation potential (RP) indicates the level of maximum possible recovery of a patient in the given time period. Maintaining RP at the second stage of medical rehabilitation (MR) is one of the important tasks of a medical psychologist. However, current Russian scientific literature has not sufficiently disclosed the scope and theoretical foundation of such work. The authors of this lecture analyzed the concept of RP from the theoretical and methodological perspectives of Russian medical (clinical) psychology. In addition, they investigated current studies on the relationship between psychological factors and neuroplasticity mechanisms. Scientific data allow to consider RP as a complex and dynamically changing system formed due to various effects, including psychological ones. The theoretical and methodological tradition of Russian medical (clinical) psychology gives grounds to regard illness perception (IP) as a psychological component of the RP, which is 1) social in origin, 2) mediated in structure, 3) subject to voluntary control. Within the second stage of MR of patients after stroke, formation and improvement of IP to maintain the RP require joint efforts of a neuropsychologist and a pathopsychologist. Modern studies on the relationship between psychological factors and neuroplasticity mechanisms provide scientific grounds for the methods of work of a medical psychologist in medical rehabilitation.
Aim. To experimentally test the hypothesis of the participation of MEK1/2 and ERK1/2 kinases in the mechanism of the probiotic cardioprotection in the implementation of the signaling stage of the cardioprotective response to the administration of probiotic strains in the systemic inflammatory response in rats.Materials and methods. The experiments were performed on male Wistar rats using a model of systemic inflammatory response syndrome, which includes obesity and chemically induced colitis. To provide probiotic cardioprotective effects, the animals were administered probiotic strains LA-5 and BB-12 orally. An inhibitor of MEK1/2 kinase and its associated ERK1/2 kinase PD98059 at a dose of 0.3 mg/kg were administered intravenously 20 minutes before the start of Langendorff perfusion of an isolated heart., The size of the necrosis zone (SNZ) was histochemically determined after 30 minutes of global ischemia and 90 minutes of reperfusion were simulated. Markers of the systemic inflammatory response (SIR) were detected in the blood.Results. In the group of rats on the model of SIR in comparison with the control, a significant increase in the number of leukocytes and an increase in the level of proinflammatory cytokines in the blood, as well as a significant increase in SNZ (by 39% in relation to CTR, p < 0.05). In the group with probiotic correction, a significantly lower SNZ was noted in relation to SIR, whereas in rats with the introduction of probiotics and the substance PD98059, SNZ was significantly higher, i.e. the cancellation of the cardioprotective effect of probiotic therapy occurred.Conclusion. Based on the conclusion that the cardioprotective effect has been abolished by PD98059 administration, it can be assumed that the probiotic effect is provided by the MEK1/2 and ERK1/2 kinase pathways.
Proteomic studies have made a significant contribution to the study of the pathogenesis of cardiovascular diseases, creating the basis for the development of new potential biomarkers for assessing the risk of developing diseases and their complications. We analyzed the main foreign and domestic publications over the past 15 years using the PubMed/Medline and RSCI/elibrary.ru databases and summarized the available data on proteomic studies in the field of atherosclerotic cardiovascular diseases and coronary atherosclerosis. In this literature review, priority was given to studies on the search for new proteomic biomarkers of coronary atherosclerosis, including proteomic markers of unstable atherosclerotic plaques. The data from our own proteomic studies on potential biomarkers of coronary atherosclerosis are presented.
Aim. To assess the ovarian reserve and ovarian response to controlled ovarian hyperstimulation (COS) in patients in assisted reproductive technology (ART) programs with compensated chronic autoimmune thyroiditis (CAIT) and with predicted premature ovarian insufficiency (POI).Materials and methods. A retrospective study of 166 patients with infertility and compensated CAIT (group I, n = 44), predicted signs of POI (group II, n = 62), tubal infertility factor (group III, n = 60), including a comparative analysis of clinical and patient history data, indicators of ovarian reserve, and the effectiveness of COS (number of oocytes retrieved). The groups are divided by age into subgroups: patients younger than 35 years of age and 35 years and older (Ia, Ib, IIb, IIb, IIIa, and IIIb, respectively).Results. Significant differences in the values of follicle-stimulating (FSH) and (AMH) were revealed in the study groups under 35 years of age: FSH (7.24 (6.0-9.63) mIU/l and 10.35 (10.13–11.01) mIU/L, respectively; p < 0.001) and AMH (3,2 (1.48–6.80) ng/ml and 0.68 (0.44–2.91 ng/ml), respectively; p = 0.015). The poor ovarian response in COS programs is most often obtained in patients under 35 years of age with infertility with occult POI. In the age groups 35 years and older, the poor ovarian response of COS was equally common in groups I and II. Estradiol levels in the groups of 35 years of age and older were lower in patients with occult POI.Conclusion. In groups of patients under 35 years of age with compensated CAIT and with tubal infertility factor, higher rates of ovarian reserve and the effectiveness of COS were recorded than in the groups with occult POI. A decrease in estradiol in patients 35 years of age with occult POI and older indirectly indicates a lesion of the ovarian somatic cells, probably as a result of autoimmune aggression.
Modern scientific advancements promote the development of effective wearable biomedical technologies that will improve the quality of life and personalize approaches to prevention, therapy, and rehabilitation. E-textiles or smart clothing technology are attracting significant attention due to the opening of new horizons for monitoring medical and biological health indicators.The review provides a critical analysis of possible modern applications of smart textiles for monitoring physiological health indicators. The article discusses the advantages, current limitations, and future prospects, as well as related research and development needed to implement practical solutions in the field of e-textiles. Smart clothing can be used to collect and process data on human body movement and bioelectric potentials or chemical signals in real time for various medical and everyday purposes. Wearable devices are a promising biomedical technology due to their innovative potential for modernizing healthcare, professional sports, and social sphere, providing continuous and non-invasive recording of physiological parameters.Continuous scientific and technological progress in the development of materials with improved biocompatibility and durability, optimization of analytics based on artificial intelligence, and more accurate assessment of big biomedical data will accelerate the implementation of smart textiles and their integration with other digital applications for intelligent health monitoring. Further development of wearable e-textiles will contribute to improving both their diagnostic efficiency and the quality of life of users.
Aim. To evaluate the association between the expression levels of sirtuin 1 (SIRT1) splicing isoforms and the genes associated with mitochondrial homeostasis (PGC-1α, PPAR-γ, PPAR-α, TFAM, MFN2, OPA1, and DRP1) in the liver of patients with type 2 diabetes mellitus (T2DM).Materials and methods. The study included 59 patients who were divided into two groups: 1) control group, body mass index (BMI) < 30 kg/m2, without cardio-metabolic disorders; 2) patients with T2DM, BMI > 30 kg/m2. A biochemical analysis of the patients’ blood parameters was performed, and the expression level of the genes of interest in the liver tissue was studied using quantitative RT-PCR.Results. It was found that the SIRT1 splicing isoforms V1, V2, and V3 were stably expressed in the liver of patients with T2DM. SIRT1 isoforms occur not only individually, but also in various combinations. The expression of the SIRT1 V3 isoform was significantly increased in the group of patients, while the remaining analytes did not significantly differ between the groups. The SIRT1 V3 isoform positively correlated with glucose levels. It is worth noting that the total SIRT1 did not show significant correlations with the genes of interest and biochemical parameters, which only confirms the need to study the expression of isoforms separately.Conclusion. SIRT1 isoforms were stably expressed in the liver, and the expression level of SIRT1 V3 isoform was significantly higher in patients with T2DM. The results of this work can serve as a basis for further studies of interactions between SIRT1 splicing isoforms and mitochondrial homeostasis proteins at the post-translational level.
Aim. To study the content of interleukin 1β (IL-1β) in exhaled breath condensate (EBC) and interleukin 6 (IL-6) and 17А (IL-17A) in the blood serum of patients with bronchial asthma who experienced COVID-19 of varying severity.Materials and methods. We examined 124 adult asthma patients of both sexes 6–12 months after COVID-19. The design included a general examination to determine the objective status of patients, asthma severity and control, assessment of the lung function, and measurement of IL-1β in EBC and IL-6, IL-17A in the serum of peripheral blood.Results. The patients were divided into 2 groups. Group 1 consisted of 90 patients with mild persistent asthma. Group 2 included 34 patients with moderate asthma. The content of IL-6 and IL-17A in the blood serum of patients in group 1 was significantly lower than in group 2 (p = 0.047 and p = 0.049, respectively). The concentration of IL-1β in the EBC of patients in group 1 was significantly higher than in group 2 (p = 0.019). COVID-19-associated pneumonia was experienced by 40% of patients in group 1 and by 79% of patients in group 2. Post-COVID pulmonary fibrosis was registered in 19 and 62% of cases, respectively. In group 1, a relationship was revealed between the content of IL-17A and IL-6 in the blood (Rs = 0.69; p < 0.001). In group 2, a correlation was found between the content of IL-17A and IL-6 in the blood (Rs = 0.32; p = 0.025), as well as between the forced expiratory flow at 75% of forced vital capacity (FEF75), reflecting the patency of small bronchi, and the levels of IL-6 (Rs =–0.32; p = 0.023) and IL-1β (Rs = 0.49; p = 0.021).Conclusion. In patients who experienced COVID-19, a rise in the content of Th1/Th17 cytokines was observed as the severity of asthma increased. High concentrations of IL-17A and Th17-associated IL-1β and IL-6, which activate neutrophilic inflammation, may increase the risk of systemic inflammation and the development of pulmonary fibrosis.
Aim. To establish the role of interleukin 1β (IL-1β) and receptor activator of nuclear factor κB ligand (RANK-L) in combination with microbial invasion in chronic periodontitis.Materials and methods. The clinical material was the gingival fluid of patients with chronic periodontitis (60 people) and with an intact periodontium (28 people). The content of IL-1β and RANK-L was determined using enzyme-linked immunosorbent assay (ELISA). Markers of periodontopathogenic bacteria were isolated during real-time polymerase chain reaction (PCR). Statistical data processing was carried out using the STATA v.14 software package.Results. In the group of patients with chronic periodontitis, the levels of IL-1β and RANK-L were significantly higher than in individuals with intact periodontium (median 37.1 [32.9; 41.3] pg/ml versus 2.5 [1.9; 3.4], p < 0.001) and median 6.3 [4.2; 10.4] pg/ml versus 0.0 [0.0; 0.7], p < 0.001), respectively). In patients with chronic periodontitis, periodontopathogens was detected in 100.0% of the cases (A. actinomycetemcomitans – 81.7%, P. gingivalis – 76.7%, T. forsythia – 70.0%, associations – 60.0%), while in the group with intact periodontium, periodontopathogenic bacteria were isolated in only 32.1%. In the group of patients with periodontitis, the quantitative content of IL-1β and RANK ligand positively correlated with all periodontopathogens of the first order, while the strongest correlations were found with an average degree of destruction of periodontal tissues.Conclusion. The presence of relationships between A. actinomycetemcomitans, P. gingivalis, and T. forsythia with an increased content of the proinflammatory cytokine IL-1β and the immune mediator RANK-L and the severity of bone tissue destruction may indicate a key synergistic effect of these cytokines in the inflammatory and bone-plastic events of the pathogenesis of chronic periodontitis.
Aim. To assess the risk of germline transmission of an adeno-associated virul vector of the chimeric serotype PHP. eB into the germ cells of female mice based on the development of an original method for obtaining mouse oocytes devoid of somatic cells and free vector particles.Materials and methods. The vector under study was administered intravenously to female outbred CD-1 mice at a dose of 5 × 10¹⁰ vector genomes/mouse using an original technique which included hormonal superovulation of exposed animals, oocyte isolation, their purification from contaminating somatic cells, and direct quantitative PCR on lysed oocytes. The vector DNA content in the brain tissue, ovaries, and oocytes was assessed on days 1, 3, 7, 14, 30, and 90 after vector administration.Results. Using the developed technique, we examined the ability of the adeno-associated virus vector of the chimeric serotype PHP.eB to undergo germline transmission into mouse oocytes. It was established that, despite persistence in brain and ovarian tissue for up to 3 months, vector DNA was not detected in oocytes at any time after vector administration.Conclusion. The obtained data demonstrate the absence of germline transmission of the studied genetic construct into mouse oocytes. The detection of the adeno-associated vector in the ovaries, despite its absence in oocytes, confirms the effectiveness of the developed technique for obtaining mouse oocytes uncontaminated with somatic cells.
Osteogenesis imperfecta (OI) is a clinically heterogeneous genetic disorder whose primary clinical manifestations include susceptibility to recurrent pathological fractures and progressive skeletal deformities. In clinical practice, cases are observed where the proband’s parents show no overt signs of the disease despite having multiple affected children. This may suggest gonadal mosaicism – a condition in which the causative variant is present only in a subset of parent’s germ cells.Gonadal mosaicism remains an understudied inheritance mechanism in monogenic diseases, complicating genetic counseling and reproductive risk assessment. In OI, this phenomenon may account for sporadic cases or recurrent births of affected children to clinically healthy parents.This article presents a case report of a family in which the proband and his younger sister were diagnosed with COL1A1-associated OI, while the parents and other children showed no disease manifestations. Based on clinical and genetic data, the likelihood of gonadal mosaicism in one parent is discussed, along with considerations for differential diagnosis, patient management strategies, and family genetic counseling.This case highlights the importance of molecular genetic testing not only for the probands but also for their parents to clarify the inheritance mechanism and predict the risks of disease recurrence in the family.
The authors of this lecture performed a comprehensive analysis of possible mechanisms for stimulating reparative processes after thermal skin damage using nanosecond repetitive pulsed microwave (RPM) radiation. The study analyzes both thermal and non-thermal mechanisms of the biological action of electromagnetic radiation, with special emphasis on the molecular aspects of the effects of nanosecond microwave pulses. Special attention is paid to the role of membrane proteins, calcium-dependent signaling pathways, and extracellular matrix components in realizing the regenerative potential of low-intensity microwave exposure. The study reveals the complex relationships between the physical parameters of RPM radiation (intensity, frequency, duration of pulses) and the activation of key cellular processes that ensure accelerated healing without scarring. The work uses experimental data obtained on models of burn injuries in laboratory animals (Wistar rats) using spectrophotometric, hematological, and histological methods. RPM radiation is a promising physical factor for stimulating skin regeneration, acting through non-thermal mechanisms. The combination of RPMs with cell therapy and pharmacological agents can become the basis of new protocols for the treatment of burns and other skin injuries. Further research is aimed at developing personalized treatment regimens, taking into account phases of the injury.
Aim. To evaluate the response of mesenchymal stromal/stem cells (MSCs) in vitro and the status of bone cells (osteoblasts, osteocytes) during regeneration of the femoral bone after local thermoablation at 55–60 °C.Materials and methods. Morphology and viability (MTT assay) of human adipose tissue-derived MSCs were analyzed after incubation at 37 °C or 56 °C for 0–60 minutes. In vivo, a heating cuff was applied to the femur of anesthetized rabbits, and intraoperative thermoablation was performed for 30 minutes (bone marrow canal temperature: 55–60 °C). Bone tissue was histologically examined (hematoxylin – eosin and Einarson staining) immediately and 14 days post-treatment. Quantitative morphometry was implemented in ImageJ, with subsequent statistical analysis performed in R.Results. In vitro, signs of massive MSC death were observed after 15 minutes of heating; at 30 minutes, viable fibroblast-like cells were nearly absent. In vivo, local thermoablation caused direct death of osteoblasts and osteocytes, evidenced by morphological signs of apoptosis and necrosis, as well as impaired DNA/RNA synthesis. Morphological and molecular markers of cellular damage significantly increased by day 14 post-treatment.Conclusion. Moderate thermoablation (55–60 °C) exerts significant direct and delayed damaging effects on osteogenic cells, from stem to mature forms. These findings are relevant for combined treatment of tumor and metastatic bone lesions.
Infantile hemangioma (IH) is a significant and common interdisciplinary issue in the pediatric population. The etiology of this condition is not fully understood. Several hypotheses exist regarding the origin of IH: the placental hypothesis, genetic mutations, and the influence of external factors. Treatment approaches for IH are diverse and include systemic pharmacotherapy, local treatment, and surgical intervention. Each of these methods has both advantages and limitations, making it impossible to use any single approach as a universal solution for all patients. The beta-blocker propranolol is currently recognized as the first-line medication. The authors of the lecture presented a literature review of modern approaches to selecting treatment for IH, as well as predictors of propranolol efficacy and its possible mechanism of action.
