Aim. To evaluate the association of insulin resistance and secretion of neuropeptide Y with dynapenia in patients with ulcerative colitis (UC).
Materials and methods. A single-center observational cross-sectional study included 80 patients with UC. Participants were divided into two groups: patients with dynapenia and patients with normal hand grip strength. The body mass index (BMI), dietary habits and stress levels were studied, patients underwent dynamometry. C-reactive protein (CRP), TNF-α, interleukin-6, leptin, adiponectin, soluble leptin receptors (sOb-R), neuropeptide Y and peptide YY, insulin and glucose were measured in blood serum. We determined the index of insulin resistance HOMA-IR. Median (Me) of the upper and lower quartiles (P₂₅; P₇₅), proportion and standard error of the proportion were calculated. We also determined the Mann-Whitney and Kruskal-Wallis tests, Yates chi-squared test, and twotailed Fischer’s test. The Spearman’s correlation coefficient was calculated.
Results. 54 ± 5.6% of patients with dynapenia were overweight or obese. It should be noted that patients with dynapenia were relatively young (35 (32; 51) years). Dynapenia is associated with increased CRP levels, insulin resistance, and higher values of neuropeptide Y. We found a positive correlation between neuropeptide Y and the consumption of simple carbohydrates and alcoholic beverages. The study did not reveal relationship between the concentration of neuropetide Y and the activity of UC, the localization of the pathological process, and the course of the disease. A positive association between neuropeptide Y and the level of sOb-R, peptide YY, was established.
Conclusion. Long-lasting chronic inflammation leads to the premature development of dynapenia and insulin resistance in patients with UC at a young age. In patients with dynapenia, the level of neuropeptide Y is significantly higher than in patients without dynapenia, which is probably due to the regulation of energy balance, glucose and insulin homeostasis.

Aim. To conduct a direct comparative analysis of single-photon emission computed tomography (SPECT-CT) with [^99mTc]Tc-ADAPT6 and [^99mTc]Tc-(HE)₃-G3 in patients with HER2-positive breast cancer (BC) with axillary lymph node metastases.
Materials and methods. The analysis included 8 patients with HER2-positive BC with axillary lymph node metastases before the systemic treatment. All patients were injected with [^99mTc]Tc-ADAPT6 (500 µg) and [^99mTc] Tc-(HE)₃-G3 (3,000 µg) with an interval of 3–4 days. The SPECT-CT scans of the chest and upper abdomen were performed after 2 hours for [^99mTc]Tc-ADAPT6 and after 4 hours for [^99mTc]Tc-(HE)₃-G3. The accumulation of radiopharmaceuticals was assessed by measuring the maximum standardized uptake values (SUV_max) in metastatic axillary lymph nodes, projections of the contralateral axillary lymph nodes, liver, latissimus dorsi muscle, and spleen. Additionally, mALN-to-background and mALN-to-reference organs ratios were calculated for each patient.
Results. Comparison of the mALN-to-background ratio revealed the advantage of [^99mTc]Tc-ADAPT6 (38.93 (16.56–56.02)) over [^99mTc]Tc-(HE)₃-G3 (19.39 (8.43–34.52)), p = 0.0391. The comparative analysis of the accumulation of the studied radiopharmaceuticals in the reference organs demonstrated higher SUV_max for [^99mTc] Tc-(HE)₃ -G3 in the liver and spleen (4.44 (2.85–9.08) and 2.47 (1.28–4.41), respectively) than for [^99mTc]Tc-ADAPT6 (2.98 (1.96–3.65) and 0.43 (0.14–0.62), respectively), p = 0.01 and p = 0.04. Comparison of the SUV_max ratios in mALN and reference organs showed higher values of mALN / spleen for [^99mTc]Tc-ADAPT6 (5.93 (1.04–11.85)) compared to [^99mTc]Tc-(HE)₃-G3 (1.83 (0.46–4.54)), p = 0.02. Conclusion. According to the results of the performed analysis, the diagnostic advantage of [^99mTc]Tc-ADEPT6 for the detection of) HER2/neu expression in metastatic lymph nodes in breast cancer patients was revealed.

Aim. To study the features of the expression of the integrin subunit β4 in primary tumor tissue depending on the clinical and morphological parameters of breast cancer.
Materials and methods. We examined biopsy samples from 49 patients with T1–4N0–3M0 breast cancer; the median age was 51.0 [44.0; 60.0] years. Patients did not receive neoadjuvant therapy. Surgical intervention involved resection of the mammary gland with axillary lymph node dissection or radical mastectomy. The expression of markers of estrogen receptor, progesterone receptor, c-erB-2 (Her2/neu), Ki67, CD104 (integrin subunit β4) was assessed using immunohistochemistry. Statistical processing of the results was carried out using the Statisctica 10.0 software package.
Results. In the group of patients with N3 degree, cases with positive cytoplasmic/membrane colocalization of integrin subunit β4 expression were more frequently detected (45%), compared with observations where no such expression was found (8%; p = 0.002).
Conclusion. Positive cytoplasmic/membrane colocalization of integrin subunit β4 expression is associated with the prevalence of lymphatic metastasis, which corresponds to N3 degree.

The aim of the study is to investigate the association of rs2306283 and rs4149056 variants of the SLCO1B1 gene with benign unconjugated hyperbilirubinemia.
Materials and methods. A case-control study design was employed. The group with the Gilbert syndrome (GS) phenotype comprised 414 individuals (mean age 36.7 ± 15.9 years, 49.8% men). The control group consisted of 429 individuals (mean age 38.5 ± 14.3 years, 52.2% men) randomly selected from DNA banks of MONICA project participants, young adults aged 25–44 years, and participants in a cross-sectional study of schoolchildren in Novosibirsk. Genotyping of the groups for nucleotide sequence variants rs2306283 and rs4149056 of the SLCO1B1 gene was performed using real-time polymerase chain reaction.
Results. No statistically significant differences were found between the GS and control groups regarding the frequencies of genotypes and alleles of rs2306283 (p > 0.05). Carriers of the TT rs4149056 genotype were less common (OR = 0.67, 95% CI 0.51–0.89, p = 0.005), while carriers of the TC genotype were more prevalent (OR = 1.46, 95% CI 1.1–1,94, p = 0.009) in the GS group compared to the control group. The frequency of the C allele rs4149056 was higher in the GS group compared to the control group (OR = 1.35, 95% CI 1.07–1.7, p = 0.012). These differences persisted for carriers of the 6TA/7TA genotype but not for the 6TA/6TA and 7TA/7TA genotypes rs3064744 of the UGT1A gene.
Conclusion. The single nucleotide variant rs2306283 of the SLCO1B1 gene is not associated with benign unconjugated hyperbilirubinemia. The TC genotype and C allele of the single nucleotide variant rs4149056 of the SLCO1B1 gene are the genotype and risk allele of Gilbert syndrome, while the TT variant genotype exhibits a protective effect against the development of the syndrome, particularly for carriers of the 6TA/7TA genotype rs3064744 of the UGT1A gene.

Aim. Using statistical modeling techniques, we aim to develop a model that optimizes the prediction of severity of sarcoidosis that affects the respiratory system (SRS) based on the identification and determination of signs (anamnestic, clinical, laboratory, instrumental examination data, etc.) associated with disease severity and subsequent stratification of the long-term risk for pulmonary hypertension (PH) development.
Materials and methods. The 12-year observational cohort comparative study included 298 participants, both male and female, who had SRS. More than 200 different patient examination parameters were analyzed. The models were built using logistic regression and linear discriminant analysis. The quality of the models was assessed by constructing a classification matrix, calculating sensitivity and specificity as well as calculating the area under ROC curve.
Results. As a result of the study, optimal classification models were developed for predicting SRS severity, constructed using various methods of statistical modelling. The models demonstrated that several characteristics, including parameters of echocardiography examination of patients (including indicators that allow for indirect diagnosis of PH), are associated with disease severity. A set of characteristics associated with particular sarcoidosis severity will allow prediction of it upon confirmation of diagnosis (individual prognosis), as well as patient management (observation or requiring the prescription of pathogenetic immunosuppressive therapy).
Conclusion. Such a complex model for predicting disease severity in patients with a non-cardiac profile (SRS) is of great importance for risk stratification in terms of PH development in patients with severe sarcoidosis. Further analysis of the features identified during model construction can help clinicians to contribute to more accurate predictions of SRS severity in real-world clinical practice.

Aim. To assess the impact of thyroid stimulating hormone (TSH), free triiodothyronine (FT3) and free thyroxine (FT4) concentrations in the blood serum of patients with schizophrenia with suicide risk.
Materials and methods. A total of 120 patients with schizophrenia (75 women and 45 men) were examined. Suicide risk was assessed using the Beck Hopelessness Scale (BHS). Serum levels of FT3, FT4 and TSH in patients with schizophrenia were determined using enzyme immunoassay kits. Multiple linear regression analysis and single-factor analysis of variance (ANOVA) were used to identify the relationships between the studied indicators.
Results. Among 120 patients with schizophrenia, 11 patients (9.2%) had elevated serum TSH values (> 4.0 mME/L), 108 (90%) had decreased FT3 levels, (< 4.0 pmol/L), 42 (35%) had decreased FT4 levels (< 10.3 pmol/L). The study revealed statistically significant differences in the level of hopelessness between the groups of patients with normal and elevated TSH (F (1.118) = 5.160, p = 0.025), as well as with normal and decreased FT3 (F (1.118) = 4.568, p = 0.035).
Conclusion. It was found that TSH and FT3 concentrations in blood serum significantly affect the level of hopelessness assessed using the Beck scale in patients with schizophrenia. The results of this study confirm the need for regular dynamic monitoring of hormone levels of the hypothalamic-pituitary-thyroid axis in patients with schizophrenia in order to maintain its normal functioning, as well as prevent adverse effects in the form of suicide attempts and suicide.

Background. A study of the mechanisms of infarct size-limiting effects of lithium chloride (LiCl) on a model of myocardial infarction in vivo. Myocardial infarction is one of the main causes of death among the adult working population in economically developed countries. Currently, there are no drugs in clinical practice that would effectively protect the myocardium against ischemia – reperfusion injury, so there is a need to develop new drugs that can limit infarct size and reduce mortality.
Aim. To study the mechanisms of infarct size-limiting effects of lithium chloride.
Materials and methods. A study was performed in anesthetized Wistar rats with coronary artery occlusion (45 min) and reperfusion (120 min). The molecular mechanism of the protective effects of LiCl was examined in this model using appropriate blockers, including non-selective and selective blockers of ATP-sensitive potassium channel and NO synthase.
Results. Administration of LiCl before ischemia significantly reduced infarct size as well as the as the incidence of ventricular arrhythmias. Administration of LiCl after ischemia also promoted a decrease in infarct size. NO synthase, cycloxigenase-2, protein kinase C, and endogenous opioids were not involved in the cardioprotective effect of lithium. The cardioprotective effect of LiCl is mediated via sarcolemmal ATP-sensitive potassium channel (sarcK_ATP channel) opening.
Conclusion. LiCl reduced infarct size and prevented reperfusion cardiac injury. The main cellular ways of the infarct size-limiting effects of LiCl are mediated through the sarcK_ATP channel opening.

Interleukin-4 (IL-4) and interferon gamma (IFNγ) are key participants in the polarization of the immune response toward Th1 or Th2 types in bronchial asthma. However, their role in bronchial remodeling in patients with asthma and cold airway hyperresponsiveness (CAHR) remains unclear.
Aim. To study the involvement of IL-4 and IFNγ in the disorganization of bronchial epithelium and the regulation of airway remodeling in asthma with CAHR.
Materials and methods. A total of 47 patients with mild persistent asthma were examined. Induced sputum collection, blood sampling for biochemical studies, spirometry, and the isocapnic hyperventilation test with cold (-20 °C) air (IHCA) were performed. The sputum was analyzed for cellular composition (in %), and the cytokine profile (IL-4 and IFNγ in pg / ml) was evaluated in peripheral blood.
Results. The patients were divided into groups with CAHR (group 1, 17 patients) and without cold-induced bronchoconstriction (group 2, 30 patients). Forced expiratory volume in 1 sec. (FEV₁ ) and maximal mid-expiratory flow (MMEF) in group 1 were lower compared to group 2: 84.0[83.0; 93.0]% and 99.0 [85.0; 105.0]% (p = 0.012); 55.0[51.0;67.0]% and 76.0[59.0;88.0]% (p = 0.021), respectively. The blood content of IL-4 and IFNγ in group 1 was 11.48[10.82;22.48] pg / ml and 26.98[17.24; 73.5] pg / ml, while in group 2, it was 1.88 [0.66; 5.96] (p = 0.003) and 7.24[1.5; 26.98] pg / ml (p = 0.047), respectively. In group 1, an association was found between blood IL-4 and IFNγ levels (Rs = 0.65; p = 0.016), between FEV₁  and the number of epithelial cells in sputum (Rs = –0.74; p = 0.0003), and between IL-4 and airway response (ΔFEV₁ /Vital Capacity) after the IHCA (Rs = –0.70; p = 0.007).
Conclusion. The escalation of the proinflammatory and pro-oxidant function of IFNγ indicates a shift from Th2 immune response activation, regulated by IL-4, toward a Th1 response, which stimulates bronchial remodeling in patients with asthma and CAHR.

Aim. To predict impaired lung diffusion capacity after SARS-CoV-2 infection depending on the criteria of pathological deviation of DLco value (carbon monoxide transfer factor).
Methods. The retrospective study included 341 patients (median age was 48 years, 76.8% of the participants were men) after SARS-CoV-2-associated lung injury. The median volume of lung injury during the acute phase of COVID-19 was 50%. All patients underwent a diffusion test. Descriptive statistics, logistic regression analysis were applied, taking into account the previously obtained model for prognosis of abnormal DLco (<80% of the predicted value (%pred.)) [11]. In the present study on the same sample of patients, the prognosis of abnormal DLco was studied depending on the criterion 1: DLco < 80%pred. or criterion 2: DLco < predicted – 1.645SD (SD — standard deviation. ROC analysis was used to assess the quality of the binary classifier models.
Results. The coefficients of the logistic regression equations were obtained on the training sample with regard to the chosen criterion of pathological deviation of DLco. The ROC analysis procedure showed that, when applying criterion 1, area under curve (AUC) was 0.776, p < 0.001 (0.707–0.824 95% confidence interval (CI)), sensitivity and specificity of the training model were 81% and 66%, respectively. When applying criterion 2, AUC was 0.759, p < 0.001 (0.701–0.817 95% CI), sensitivity and specificity of the training model were 83.4% and 59%, respectively.
Conclusions. The criterion for determining the lower limit of normal DLco (LLN_DLco) does not significantly affect the quality of the model for impaired lung diffusion capacity prognosis after SARS-CoV-2-associated lung injury. It is advisable to give preference to a method that is easier to apply in practice.

Aim. Determine the influence of genetic factors of innate immunity on the risk of development and severity of COPD.
Materials and methods. The study included 103 patients diagnosed with chronic obstructive pulmonary disease and 47 conditionally healthy people without any chronic bronchopulmonary pathologies. The expression level of TLR genes and alleles of rs5743551 (TLR1), rs5743708 (TLR2), rs3804100 (TLR2), rs3806790 (TLR4), rs5743810 (TLR6), rs3804880 (TLR8) single nucleotide polymorphisms were analyzed via real-time polymerase chain reaction (PCR).
Results. Several tendencies were observed: an increase in the proportion of GG homozygotes in the rs5743810 (TLR6) locus in patients with severe COPD and a negative correlation between TLR2 and TLR6 genes expression level and oxygen saturation in blood, dyspnea and COPD severity.
Conclusion. No statistically significant association with rs5743551 (TLR1), rs5743708 (TLR2), rs3804100 (TLR2), rs4986790 (TLR4), rs5743810 (TLR6), rs3764880 (TLR8) single nucleotide polymorphisms was found. The observed tendency of the TLR gene expression level increase may be associated with the remodeling of lung tissues and activation of the immune response that occur during COPD.

Aim. To assess the osteogenic potential of mesenchymal stem cells (MSCs) of epicardial adipose tissue (EAT) in patients with stable coronary heart disease based on obtaining gene profiles (osteogenesis markers).
Materials and methods. In EAT MSCs, the expression levels of the RUNX2 (RUNX transcription factor encoding gene), BGLAP (osteocalcin encoding gene), SPP1 (osteopontin encoding gene), SP7 (Osterix encoding gene) genes were determined using real-time polymerase chain reaction (PCR). Using immunofluorescence staining, the amount of RUNX2, osteocalcin, osteopontin, and Osterix proteins was determined in the supernatant of cultured MSCs.
Results. It was found that the expression of RUNX2 in cells cultured in a medium with osteoinducers was 1.88 times higher than in undifferentiated MSCs (p = 0.012). The level of RUNX2 protein was also higher in a differentiated cell culture (p < 0.05). Similar results were obtained regarding the level of SPP1 mRNA expression (p = 0.012). BGLAP expression did not differ between differentiated and undifferentiated MSC cultures. The level of SP7 gene expression did not differ in cells either with or without an osteoblastic medium. It is worth noting that using immunofluorescence staining, there were no differences detected in the expression of Osterix and OCN between cultures of differentiated and undifferentiated cells.
Conclusion. It was found that EAT MSCs have osteogenic potential, which was manifested by the expression of osteogenesis genes in both differentiated and undifferentiated MSCs. The increase in the expression level of SSP1 and RUNX2 mRNA on the 15th day of cultivation with osteoblastic medium indicates that the studied cells are preosteoblasts and are at the stage of extracellular matrix synthesis.

Aim. To study serum concentrations of low-grade inflammation markers and the severity of atherosclerotic processes in the coronary artery in patients with coronary heart disease (CHD) in the context of their clinical and instrumental characteristics.
Materials and methods. The study included 264 participants (161 men and 103 women), with 220 of them being diagnosed with CHD. Subgroups were identified among the participants, including those with a history of myocardial infarction (110 patients) and angina pectoris (152 patients). A control group consisted of healthy volunteers (44 persons). The patients underwent coronary angiography, echocardiography, duplex ultrasound scanning of the extracranial segments of the brachiocephalic arteries. The level of C-reactive protein (CRP (mg/L)), tumor necrosis factor alpha (TNF-α (pg/ml)), growth differentiation factor 15 (GDF-15 (pg/ml)), and endothelial cell specific molecule-1 (ESM-1 (ng/ml)) in the blood serum were measured. Statistical significance was considered at p < 0.05.
Results. A significantly higher concentration of all laboratory markers of low-grade inflammation in the CHD group of patients compared to the control group, as well as a significant increase in their values with enhance in the severity of coronary atherosclerosis (p<0.0001) was found. Significant differences in marker levels were also found between patients with angina pectoris and a history of myocardial infarction compared to those without these conditions. A correlation was revealed between the value of markers and various clinical and instrumental characteristics of the patients. Multivariate linear regression analysis revealed a statistically significant association of SYNTAX score with the concentration of GDF-15 and ESM-1, but not with CRP and TNF-α.
Conclusions. The simultaneous measurement of multiple laboratory parameters may be a more effective method for assessing the risk of CHD progression. The study also showed that endocan and GDF-15 have high prognostic significance in evaluating the severity of atherosclerotic processes in the coronary arteries.

Aim. To analyze the taxonomic composition of the intestinal microbiota in patients with cholangiocarcinoma (CCA) and compare it to individuals without oncopathology.
Materials and methods. The study included patients with histologically verified cholangiocarcinoma (n = 30) and a control group (n = 27). An integrated approach was used, including clinical and anamnestic, laboratory, and instrumental methods. The intestinal microbiota was studied through amplicon sequencing of the bacterial 16S rRNA gene.
Results. The assessment of alpha- and beta-diversity of the microbiota in patients with CCA did not show any significant differences compared to the control group. However, a comparative analysis revealed changes in the representation of a number of microorganisms at different taxonomic levels, including a higher content of Bacteroides and Lachnospiraceae_NK4A136_group in patients with CCA. Additionally, bacteria that influence the change in the global balance of microorganisms were identified in both groups, such as [Ruminococcus]_torques_group, Subdoligranulum, Parasutterella, unclassified Firmicutes in samples of patients with CCA and Oscillospiraceae and Erysipelotrichaceae UCG-006 in the control group.
Conclusion. The study found a number of significant differences in bacterial representation between patients with cholangiocarcinoma and control group participants. Further research on the intestinal microbiota has the potential to develop non-invasive tools for early diagnosis of CCA.

Aim. To identify perinatal and social predictors that determine the health of premature infants in early childhood, based on their birth weight.
Materials and methods. This publication is part of a cohort prospective observational study of premature infants that was initiated in Tomsk in 2014 (Deev I.A., Kulikova K.V., Kobyakova O.S. et al., 2016). The main group consisted of 226 premature infants: 78 infants with low birth weight (LBW), 76 — very low birth weight (VLBW), and 72 – extremely low birth weight (ELBW), while a control group included 76 term infants. The follow-up period was 3 years, with examinations conducted every 12 months.
Results. The study found that 57.1% (n = 36) of ELBW infants, 34.9% (n = 23) of VLBW infants, and 32.9% (n = 23) of LBW infants showed an “improvement” in their health during early childhood (transition from health groups IV and V to III, as well as transition from health group III to II at subsequent visits). The presence of siblings (for the main group OR = 2.6 [95% CI 1.3–5.3], p = 0.006, for children with ELBW OR = 8.4 [95% CI 1.0–69.6], p = 0.045) and the mother’s higher education (for children with VLBW OR = 3.9 [95% CI 1.2–12.2], p = 0.018 and with LBW OR = 3.4 [95% CI 1.2–9.9], p = 0.025) were identified as predictors of a favorable clinical prognosis. Perinatal and social predictors associated with the development of pathological abnormalities included intrauterine growth retardation, intraventricular hemorrhage, severe anemia in the neonatal period, maternal obesity, maternal smoking, parental age over 35 years, and lack of higher education for the mother.
Conclusion. To implement a health-preserving strategy for the group of premature infants, especially those with ELBW, health improvement can be achieved by addressing controllable social factors.

Aim. To study the content of unsaturated fatty acids (FAs) in blood plasma in men from Novosibirsk (ESSERF3 in the Novosibirsk region) with established type 2 diabetes mellitus (DM2), newly diagnosed diabetes, and prediabetes, as well as to evaluate the associations of various types of FAs with the presence or absence of diabetes and fasting glucose levels.
Materials and methods. Within the framework of the multicenter, single-stage epidemiological ESSE-RF3 study in the Novosibirsk region, 1 200 residents of Novosibirsk (600 men, 600 women) aged 35–74 years were examined. The present study included 563 men with an average age of 54.4 ± 11.48 years, comprising: 61 individuals diagnosed with DM2 based on anamnestic data (Group I); 65 men with newly diagnosed diabetes (Group II); 46 men with conditional prediabetes (Group III); and 391 men without diabetes – (Group IV). The levels of unsaturated FAs in blood plasma were determined via high-performance liquid chromatography.
Results. An increase in omega-3, -6, and -9 FA levels was revealed in Group I compared to Group IV. An increase in the level of oleic acid (p = 0.040) was found in Group II compared to Group IV. The relative chance of DM2 is directly associated with an increase in the levels of omega-3 alpha-linolenic acid (odds ratio (OR) = 1.030, 95 confidence interval (CI) 1.002–1.058; p = 0.034) and omega-6 gamma-linolenic acid (OR = 1.026, 95 CI 1.001–1.051; p = 0.044). Newly diagnosed diabetes is inversely associated with the level of linoleic acid in blood plasma (OR = 0.545, 95 CI 0.301–0.996; p = 0.048), as well as directly associated with the level of oleic acid (OR = 1.961, 95 CI 1.054–3.648; p = 0.034). Prediabetes is inversely associated with the level of hexadecenoic acid (OR = 0.969, 95 CI 0.943–0.996; p = 0.025).
Conclusion. Detection of changes in the profile of unsaturated FAs in blood plasma can be used as an additional prognostic biomarker to identify patients at risk of developing DM.

Aim. To conduct a comparative analysis of two available kits that contain all necessary reagents and additives in a single reaction mixture, including 100 mM Tris-НCl, 100 mM KCL, 4 mM MgSO4, 0.2% of Tween 20, for the amplification of the three most common EGFR (epidermal growth factor receptor) gene polymorphisms in patients with non-small cell lung cancer (NSCLC): 181946 G/A (rs2293347), -191 C/A (rs712830) and -216G/T (rs712829).
Materials and methods. The protocol for genotyping 181946C>T, 191C>A and -216G/T was refined according to previously reported data. Polymerase chain reaction (PCR) products measuring 197 bp were detected using electrophoresis in a 2% agarose gel, followed by staining with ethidium bromide.
Results. The Biomaster HS Taq-PCR Color 2× and Biomaster LR HS PCR 2× reagent kits were effective for amplification of 181946 G/A polymorphism located in the intron of the EGFR gene. Additionally, polymorphisms -191 C/A (rs712829) and -216G/T (rs712829), located in the promoter region and containing a high GC content, were successfully amplified using the Biomaster LR HS PCR 2× kit.
Conclusion. The present study shows that the Biomaster HS Taq-PCR Color 2× and Biomaster LR HS PCR 2× reagent kits are effective for amplification of 181946 G/A polymorphism located in the intron of the EGFR gene. Furthermore, the EGFR SNP -191 C/A, located in the promoter region with a high GC content, was successfully amplified using the Biomaster LR HS PCR 2× reagent kit. 

Atherosclerosis and atherosclerosis-related cardiovascular diseases are a significant public health concern and a rapidly evolving area of research in both fundamental and clinical medicine. Despite the extensive history of studying, many aspects of atherosclerosis etiology and pathogenesis remain unclear.
Traditionally, the pathogenesis of atherosclerosis has been viewed in terms of the localized accumulation of specific lipoprotein fractions in the arterial wall. However, both innate and adaptive immunity play active roles in atherogenesis. Cells and mediators of the immune system engage in intricate interactions with cellular and extracellular components in all layers of the vascular wall. For this reason, scientific community have reached a consensus on the crucial role of inflammation in the onset, progression, and destabilization of an atherosclerotic plaque.
Therefore, atherogenesis can be considered not only as a metabolic disorder, but also as an immunoinflammatory process. The aim of this lecture was to summarize contemporary data regarding the role of inflammation at various stages of the atherosclerotic continuum. 

The lecture synthesizes and analyzes the findings of research concerning the impact of sleep disordered breathing (SDB) on the progression of the most prevalent chronic non-infectious lung diseases (CNLDs). SDB, including conditions, such as snoring, sleep hypoventilation syndrome, and obstructive and central sleep apnea syndrome, constitutes a significant medical concern due to its high prevalence and adverse health consequences. SDB is regarded as an independent risk factor for the development and progression of a range of CNLDs. Timely diagnosis and management of SDB may serve as an effective preventive measure against severe manifestations and complications associated with this group of diseases.

In this lecture, we presented current clinical studies on targeted radionuclide imaging of breast and prostate tumors with overexpression of the gastrin-releasing peptide receptor (GRPR). The gastrin-releasing peptide receptor is a transmembrane receptor, the activation of which promotes the growth and proliferation of tumor cells. The highest level of GRPR expression is observed in malignant pathologies of breast and prostate, which is of particular interest for radionuclide diagnostics.
The conducted clinical studies assessed the safety, pharmacological properties, and effectiveness of imaging of radiopharmaceuticals based on peptide agonists and antagonists of GRPR labeled with technetium-99m and gallium-68 radionuclides. The results clearly demonstrate the advantage of GRPR antagonists over GRPR agonists, since they have optimal pharmacological properties, good tolerability, rapid elimination by organs with a physiological level of receptor expression, and high imaging efficiency of mammary and prostate tumors with overexpression of GRPR.

Chronic opisthorchiasis is recognized as a precancerous condition that can present similarly to other diseases of the hepatopancreatoduodenal zone. Statistically, there is a proven correlation between the duration and intensity of parasitic invasion and the development of carcinogenesis, with the manifestations of opisthorchiasis often obscuring the early symptoms of cancer. Many researchers are working to find methods for the early diagnosis of pancreatic cancer against the background of chronic opisthorchiasis, which may enable timely treatment of the disease in the early stages.
The authors of this lecture present a literary review of the data on the incidence of pancreatic cancer in patients with chronic opisthorchiasis. Additionally, some factors contributing to cholangiocarcinoma carcinogenesis are discussed, since the exact mechanisms leading from the introduction of a trematode to the formation of a malignant process are multifunctional. Certain phenomena regarding the effect of opisthorchis on the human body currently lack explanation and require further study and clarification.

Aortic aneurysm and atherosclerosis are characterized by high clinical heterogeneity. The uncertainty in their comorbidity evaluations may be related to polyetiology of these diseases and the presence of not only common but also specific risk factors, as well as the complex pathogenesis of these conditions.
The aim of this review is to summarize information on the prevalence and risk factors of aortic aneurysm and atherosclerosis, explaining the possible mechanisms underlying the comorbidity of these pathologies. We conducted a search for scientific publications in Russian (eLIBRARY.RU) and international (PubMed) electronic libraries, prioritizing works published in the last 10 years.
Aortic aneurysm and atherosclerosis exhibit an age-dependent pattern of prevalence. The high prevalence of atherosclerosis compared to aortic aneurysm, along with the approximately similar age ranges for the manifestation of these pathologies,is related to their comorbidity. Conversely, these diseases share some common risk factors, albeit with varying contributions to atherosclerosis and aortic aneurysm of different localizations. Type 2 diabetes mellitus and lipid metabolism profiles are examples of risk factors with multidirectional influences. To understand the reasons for the discordant estimates of comorbidity between aortic aneurysm and atherosclerosis from an epidemiological perspective, a comprehensive approach to patient characterization, including a detailed analysis of risk factors recorded in the analyzed groups, is essential.