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.
