Anemia, hemostasis disorders, and blood group incompatibilities remain major challenges in hematology and transfusion medicine. Recent advances have clarified the molecular regulation of iron metabolism—particularly the roles of hepcidin and erythroferrone—improving the diagnosis and classification of anemias. Understanding of hemostasis has also evolved, emphasizing the interaction between coagulation factors, platelets, and the endothelium in thrombus formation. Meanwhile, molecular immunohematology has expanded knowledge of ABO and Rh systems, revealing clinically significant antigen variants that influence transfusion safety. These developments support a shift from traditional serologic typing to genotype-based matching, reducing immunologic risks. Integrating findings from anemia research, hemostasis, and blood group genetics enables more precise diagnostics and enhances the safety and effectiveness of modern transfusion practices. [1]

Background: Vascular diseases, primarily chronic ischemic heart disease (CIHD) and cerebrovascular pathology, remain leading causes of mortality in Uzbekistan and Central Asia. Atherothrombosis, resulting from plaque destabilization and subsequent thrombosis, is the key mechanism underlying disease progression and cardiovascular complications. Biomarkers of coagulation, fibrinolysis, and extracellular matrix remodeling, as well as genetic determinants, may improve risk prediction; however, their prognostic value in regional populations has not been sufficiently studied.

Objective: To identify clinical, biochemical, and genetic predictors of cardiovascular complications in patients with CIHD, to develop a long-term risk stratification scale, and to evaluate factors influencing the efficacy of antiplatelet therapy.

Methods: A prospective observational study was conducted in 2023–2024 at the Republican Specialized Scientific-Practical Medical Center of Cardiology (Tashkent) and included 503 patients with stable CIHD. Clinical characteristics, biochemical markers of coagulation and fibrinolysis (D-dimer, plasmin–α2-antiplasmin complexes [PAP], matrix metalloproteinases MMP-2 and MMP-9), platelet reactivity, and genetic polymorphisms related to hemostasis, homocysteine metabolism, and antiplatelet drug response were assessed. Patients received aspirin, clopidogrel, or dual antiplatelet therapy according to clinical indications. Follow-up duration was at least 12 months. Primary endpoints included vascular death, acute coronary syndrome (ACS), ischemic stroke/transient ischemic attack (IS/TIA), peripheral arterial thrombosis, and revascularization. Statistical analysis was performed using Cox proportional hazards models and Kaplan–Meier survival analysis.

Results: During follow-up (mean 1.5 years), cardiovascular events occurred in 31% of patients. Independent clinical predictors included angina pectoris class II–III, previous myocardial infarction, multivessel coronary disease, history of IS/TIA, abnormal ankle–brachial index, body

mass index ≥31.6 kg/m², creatinine clearance <67 mL/min, and erosive gastritis. Based on these variables, a risk scale stratified patients into low-, intermediate-, and high-risk categories with event rates of 13%, 20%, and 39%, respectively. Percutaneous coronary intervention did not demonstrate superiority over optimal medical therapy and was associated with worse outcomes in the low-risk subgroup. Elevated D-dimer (OR 3.1), MMP-2 (OR 2.1), and PAP levels showed prognostic significance, with the highest risk observed when MMP-2 and PAP were elevated simultaneously (OR 3.6). Polymorphisms in homocysteine metabolism genes (MTHFR C677T, A1298C; TCN2 C776G) were associated with increased risk in a folate-dependent manner. Reduced clopidogrel efficacy was observed in carriers of CYP2C19*2 alleles, while dose escalation to 150 mg improved outcomes in poor metabolizers after PCI. Proton pump inhibitor co-administration was associated with increased thrombotic risk. Prolonged dual antiplatelet therapy beyond 12 months did not provide additional benefit.

Conclusion: An integrated approach combining clinical parameters, biomarkers, and pharmacogenetic testing improves long-term risk stratification and enables personalized antiplatelet therapy in patients with CIHD in Uzbekistan. Routine incorporation of genetic and biochemical markers may enhance secondary prevention strategies in stable coronary disease.

Рrеvеntiоn аnd trеаtmеnt оf аdhеsivе disеаsе is а рrеssing issuе in mоdеrn surgеrу, аs еvidеnсеd bу а lаrgе numbеr оf ехреrimеntаl аnd сliniсаl studiеs in this аrеа. This is duе tо thе fасt thаt thе frеquеnсу оf аdhеsivе intеstinаl оbstruсtiоn (2.1-3.8% аmоng аll disеаsеs оf thе аbdоminаl саvitу оrgаns), thе numbеr оf rеlарsеs (12-15%), аnd mоrtаlitу (7.2-11.0%) соntinuе tо rеmаin high.

Electrical injuries are most commonly associated with cutaneous burns, arrhythmias, and neuromuscular damage; however, thromboembolic complications are rarely described. Low-voltage electrical exposure may trigger endothelial disruption, inflammation, and a hypercoagulable state that predisposes to in-situ pulmonary artery thrombosis. We present the case of a 34-year-old male who developed progressive dyspnoea, chest pain, and hypoxaemia several days after an occupational electrical injury. Diagnostic evaluation revealed elevated D-dimer levels, right ventricular dilatation with signs of pulmonary hypertension on echocardiography, and no evidence of deep venous thrombosis. CT pulmonary angiography identified acute segmental pulmonary embolism with pulmonary infarction. The patient was successfully treated with anticoagulation and supportive therapy, resulting in clinical improvement. This case highlights the potential for low-voltage electrical trauma to precipitate pulmonary vascular injury and emphasizes the importance of early imaging and prompt anticoagulant therapy. Further studies are necessary to better understand the pathophysiological mechanisms and incidence of thromboembolic events following electrical injury.

Acute coronary syndrome (ACS) remains a major cause of cardiovascular morbidity in Uzbekistan. This prospective study evaluated serum selenium levels and free radical status in 122 patients with ACS variants (new-onset angina, unstable angina, non-Q-wave myocardial infarction) admitted to the Republican Specialized Scientific-Practical Medical Center of Cardiology in Tashkent. Selenium levels were suboptimal (mean 61.6 ± 1.6 µg/L), with evidence of intensified free radical oxidation and reduced antioxidant protection. Negative correlations existed between selenium and chemiluminescence parameters. Results support selenium status monitoring and potential organic selenium supplementation to mitigate oxidative stress and improve prognosis.

Background: Central Asia, including Uzbekistan, faces one of the highest burdens of cardiovascular mortality globally, with rates exceeding those in many other regions. The primary mechanism underlying acute coronary events is the rupture or erosion of vulnerable atherosclerotic plaques. Despite this, there has been a notable absence of studies in Central Asia that incorporate direct histological classification of plaques to differentiate between stable and unstable morphologies. This gap in research limits the understanding of region-specific risk factors and biomarkers. Methods: This prospective study, conducted between 2020 and 2023, enrolled 94 ethnic Uzbek men (mean age 58.5 ± 8.6 years) who were undergoing elective coronary artery bypass grafting (CABG) or endarterectomy procedures at a specialized cardiac center in Tashkent, Uzbekistan. Coronary artery segments obtained intraoperatively were histologically examined and classified according to the established criteria proposed by Virmani et al. [1]. To assess endothelial dysfunction and hemostatic parameters, plasma levels of monocyte chemoattractant protein-1 (MCP-1), endothelin-1, soluble vascular cell adhesion molecule-1 (sVCAM-1), asymmetric dimethylarginine (ADMA), homocysteine, plasminogen activator inhibitor-1 (PAI-1), and coagulation factors II, VII, XII, along with antithrombin III, were quantified using enzyme-linked immunosorbent assays (ELISA) and chromogenic substrates. Additionally, genetic polymorphisms including CCL2 rs1024611, SERPINE1 rs1799889, IL6 rs1800795, F7 rs6046, and F2 rs1799963 were genotyped via TaqMan real-time polymerase chain reaction (PCR). Statistical analyses included univariate comparisons, multivariable logistic regression, and receiver operating characteristic (ROC) curve assessments to identify independent predictors of plaque instability. Results: Histological analysis revealed unstable plaques in 55 patients (58.5% of the cohort). Patients with unstable plaques exhibited significantly elevated levels of MCP-1 (182.4 ± 68.1 pg/mL vs. 125.8 ± 52.3 pg/mL in stable plaques; p=0.019) [2] and increased factor XII activity (128.6 ± 22.4% vs. 98.7 ± 19.8%; p=0.017) [3]. Other markers, such as endothelin-1, sVCAM-1, ADMA, and PAI-1, showed trends toward higher levels in the unstable group but did not reach statistical significance. In multivariable logistic regression models adjusted for age, body mass index (BMI), hypertension, diabetes, smoking status, and lipid profiles, MCP-1 (odds ratio [OR] 1.009, 95% confidence interval [CI] 1.003–1.015, p=0.004) and factor XII activity (OR 1.014, 95% CI 1.006–1.023, p=0.001) emerged as independent predictors of unstable plaque morphology. Genetically, the carriage of the F7 rs6046 GG genotype was associated with a markedly increased risk (OR 5.12, 95% CI 1.89–13.86, p=0.001) [4], while the SERPINE1 rs1799889 4G/4G genotype conferred an OR of 4.91 (95% CI 1.62–14.91, p=0.005) [5]. A combined predictive model incorporating these biochemical and genetic factors yielded an area under the curve (AUC) of 0.879 in ROC analysis, indicating strong discriminatory power. Conclusion: Among ethnic Uzbek men, heightened plasma concentrations of MCP-1 and factor XII activity, coupled with specific risk genotypes in F7 and SERPINE1 genes, are strongly linked to histologically verified unstable atherosclerotic plaques. These findings underscore the potential for targeted biomarker screening and genetic profiling to identify high-risk individuals in Central Asian populations, paving the way for personalized preventive strategies against acute coronary events.

In this study, we investigated a hybrid framework that integrates large language models (LLMs) with conventional machine learning for early-stage skin lesion assessment using the UCI dermatology dataset as a proxy for early skin cancer detection. We first developed a baseline model using only structured clinical and histopathological attributes and trained classical classifiers, with a gradient boosting model achieving an accuracy of 0.89, macro-averaged F1-score of 0.87, and macro-AUC of 0.93. We then generated textual summaries for each patient case and used an LLM to derive high-level semantic features, such as inferred risk level and lesion-type descriptors, which were added to the structured feature space. This structured-plus-LLM-features configuration improved performance to an accuracy of 0.92, macro-averaged F1-score of 0.91, and macro-AUC of 0.96, indicating that LLM-derived features captured clinically meaningful abstractions not fully exploited by the baseline model. Finally, we implemented a hybrid decision-refinement approach in which a primary gradient boosting classifier handled most cases, while low-confidence predictions were escalated to the LLM for refined diagnostic suggestions. This hybrid model achieved the best results, with an accuracy of 0.94, macro-averaged F1-score of 0.93, and macro AUC of 0.97, and demonstrated fewer misclassifications across challenging classes. These findings suggest that LLMs can enhance structured-data models both as semantic feature generators and as second-stage reasoning engines, offering a promising and interpretable pathway for embedding AI-driven decision support into dermatology workflows aimed at earlier and more reliable skin lesion risk stratification.