Cerebral palsy is a leading cause of chronic motor disability in childhood and is characterized by persistent neurological impairments resulting from early brain injury. Despite the stability of the primary lesion, the neurological manifestations of cerebral palsy are highly heterogeneous and vary according to clinical form and dominant neurological syndrome [1, 2]. This study examines neurological characteristics in children with different forms of cerebral palsy, focusing on pyramidal, extrapyramidal, and cerebellar dysfunctions and their association with functional limitations [3]. A cohort of 150 children aged 6–16 years was analyzed, allowing identification of form-specific neurological patterns and their impact on motor performance and adaptive abilities [4]. The findings provide a neurological basis for differentiated neurorehabilitation and support the use of targeted therapeutic strategies to improve functional outcomes in children with cerebral palsy.

Homocysteine has emerged over several decades as a biologically potent sulfur-containing amino acid whose accumulation in plasma reflects a convergence of nutritional status, genetic susceptibility, and pharmacological exposure, particularly in individuals receiving long-term antiepileptic drug therapy. Early clinical observations linking anticonvulsant use with alterations in folate and vitamin B12 metabolism gradually evolved into a more complex understanding of hyperhomocysteinemia as a multifactorial metabolic disturbance with implications extending far beyond epilepsy control alone. Drawing exclusively upon the existing body of literature referenced in this article, the present study develops an integrative, theory-driven analysis of homocysteine dysregulation in epileptic populations, situating antiepileptic drugs within broader biochemical, genetic, and vascular frameworks.

The abstract synthesis foregrounds three interlocking dimensions: first, the biochemical pathways governing homocysteine metabolism and the essential roles of vitamins B6, B12, and folate; second, the pharmacodynamic and pharmacokinetic mechanisms through which classic and newer antiepileptic drugs disrupt these pathways; and third, the clinical consequences of sustained hyperhomocysteinemia, particularly its association with vascular disease, thrombosis, and neurocognitive outcomes. By integrating early nutritional studies, molecular genetic investigations of methylenetetrahydrofolate reductase polymorphisms, and epidemiological analyses of vascular risk, the article positions epilepsy not merely as a neurological disorder but as a chronic systemic condition shaped by long-term metabolic perturbations.

Methodologically, the study employs an interpretive synthesis approach, systematically contextualizing findings from observational studies, mechanistic investigations, and clinical cohorts without recourse to new empirical data. This approach allows for a nuanced interpretation of convergent and divergent findings, highlighting both consensus and unresolved debates within the field. Particular emphasis is placed on pediatric and adult populations treated with enzyme-inducing antiepileptic drugs, whose vulnerability to B-vitamin depletion and homocysteine elevation underscores important clinical and ethical considerations.

The findings suggest that hyperhomocysteinemia in epilepsy represents a predictable yet frequently under-recognized consequence of chronic antiepileptic therapy, modulated by nutritional intake, genetic variation, and drug-specific metabolic effects. The discussion extends these findings into theoretical and clinical domains, arguing for a reconceptualization of epilepsy management that incorporates metabolic monitoring and preventative strategies against long-term vascular complications. In doing so, the article contributes a comprehensive, interdisciplinary perspective to ongoing scholarly discourse and delineates clear avenues for future research and clinical practice grounded firmly in the existing literature.

Background: Chemotherapy-related cardiotoxicity is a serious complication in acute leukemia patients, with significant interindividual variability suggesting a genetic component. Polymorphisms in genes regulating oxidative stress and vascular tone, such as SOD2 and EDN1, may influence individual susceptibility.

Objective: To evaluate the impact of SOD2 C14510A and EDN1 Lys197Asn polymorphisms, both individually and in combination, on the risk of cardiotoxic complications in acute leukemia patients undergoing chemotherapy.

Methods: A clinical-genetic study included 102 acute leukemia patients (64 with cardiotoxicity, 38 without) and 97 healthy controls. Cardiotoxicity was defined by clinical, biomarker, and echocardiographic criteria. Genotyping was performed using PCR. Statistical analysis included allele/genotype frequency comparison and odds ratio calculation.

Results: The SOD2 A allele (34.3% in patients vs. 22.0% in controls; *p*<0.05) and A/A genotype (15.6% in cardiotoxicity subgroup vs. 5.2% without) were more frequent in patients with complications. The EDN1 Asn allele was also more common in patients with cardiotoxicity (28.1% vs. 22.4%). While individual polymorphisms showed non-significant trends toward increased risk (e.g., SOD2 A/A OR=3.46, *p*>0.05), combined carriage of SOD2 A and EDN1 Asn alleles was associated with a significantly higher frequency of cardiotoxicity (OR=3.26, 95% CI: 0.87–12.19, *p*=0.04).

Conclusion: The SOD2 A allele and EDN1 Asn allele are associated with an increased risk of chemotherapy-induced cardiotoxicity in acute leukemia patients. Their combined presence suggests an additive effect, highlighting the role of genetic predisposition in cardiotoxicity and supporting the integration of genetic markers into personalized risk assessment strategies.

Background: The COVID-19 pandemic has been associated with increased incidence and severity of type 1 diabetes mellitus (T1DM) in children, but pathogenic mechanisms remain unclear.

Objective: To investigate CD95 (Fas receptor) as a biomarker of β-cell apoptosis in children with T1DM following COVID-19 and assess its prognostic value.

Methods: Prospective cohort study of 100 children (6-17 years) with newly diagnosed T1DM: 50 with confirmed prior SARS-CoV-2 infection and 50 controls. Serum CD95, autoantibodies (anti-GAD, anti-IAA, anti-ICA), inflammatory markers (IL-6), and endothelial dysfunction markers (ICAM-1, VCAM-1) were measured at diagnosis, 6, and 24 months.

Results: Post-COVID-19 patients showed markedly elevated CD95 (249.5±72.3 vs. 4.87 pg/mL in controls, p<0.001), representing >50-fold increase. CD95 correlated significantly with autoantibody titers (r=0.58, p<0.001), IL-6 (r=0.67, p<0.001), and disease severity. The post-COVID-19 group had higher diabetic ketoacidosis frequency (38% vs. 16%, p<0.05), greater metabolic decompensation (HbA1c 10.6±2.5% vs. 9.12±0.46%, p<0.05), and no remission phase. A combined risk score incorporating CD95 >100 pg/mL, IL-6 >5 pg/mL, VCAM-1 >150 ng/mL, and ≥2 autoantibodies predicted severe disease (sensitivity 92.1%, specificity 90.0%, AUC 0.94).

Conclusions: CD95 is a valuable biomarker of accelerated β-cell apoptosis in post-COVID-19 T1DM, enabling risk stratification and personalized management.

This article examines the role of the scalp microbiome in the pathogenesis of dermatological conditions (seborrhea, dandruff, and various forms of alopecia) and assesses the impact of modern hairdressing procedures on the scalp ecosystem. The study aims to identify stable correlations between disruptions to the scalp microbiota and the use of invasive cosmetic procedures, as well as to systematize approaches to their diagnosis in trichological and dermatological practice. To achieve this goal, we utilize theoretical, legal, and natural-scientific analyses of recent publications, as well as methods for systematizing and critically interpreting empirical data presented in clinical and experimental studies. The concluding section substantiates the need to integrate new-generation tests aimed at assessing the state of the microbiome, the barrier function of the epidermis, and the acid-base balance of the scalp into professional hairdressing and trichological diagnostic protocols, as well as the development of personalized programs for restoring the microbiota after chemical procedures. The findings and proposed approaches have practical implications for trichologists, hairdressing technologists working with highly aggressive formulations, and dermatologists dealing with secondary dermatoses induced by cosmetic procedures.

Ischemic heart disease (IHD) remains the leading cause of morbidity and mortality worldwide, accounting for millions of victims annually. Since the mid-1950s, coronary artery bypass grafting (CABG) performed via a traditional full median sternotomy has served as the gold standard for myocardial revascularization because it provides unsurpassed exposure of the heart and great vessels. However, this conventional approach is frequently characterized by "surgical aggressiveness," which can lead to significant physiological stress, postoperative bleeding, wound infections, and thoracic wall instability. To address these challenges, minimally invasive cardiac surgery (MICS) has emerged as a patient-centered clinical philosophy. These techniques are designed to reduce tissue trauma and mitigate the systemic inflammatory response without compromising the long-term durability of the surgical repair.

This review evaluates the clinical, functional, and postoperative outcomes of CABG performed via mini-sternotomy in patients with IHD, drawing on a synthesis of 14 primary research articles. A primary focus is placed on assessing myocardial recovery through intraoperative graft patency measurements and the analysis of cardiac markers. The review further investigates complication rates, with a specific examination of postoperative atrial fibrillation (POAF), bleeding volumes, and the incidence of wound infections compared with traditional surgery. Additionally, this analysis evaluates the efficacy of postoperative rehabilitation by examining mechanical ventilation duration, length of hospital stay, and health-related quality of life, including the management of sharp neuropathic pain associated with minimal-access incisions. By aggregating these results, the review aims to define the feasibility and safety of the mini-sternotomy approach in modern revascularization.

Temperature-controlled logistics ensure the pharmaceutical supply chain in the United States maintains the quality and safety of the drugs. Cold-chain operations, however, require high energy usage and have a problem with sustainability because the cooling system is not efficient, and there is poor demand forecasting. This paper discusses predictive analytics, which can be used to achieve energy optimization in cold-chain logistics in pharmaceutical warehouses. It combines machine-based learning habits and real-time sensor reports to make a vision of temperature alterations, equipment loads, and paths. The study analyzes the data of the past energy utilization, volume of shipment, and climate ambient data in connection with conclusions on the factors that lead to waste and energy spikes. Regulations like regression analysis, random forests, and time-series prediction are used as predictive algorithms to interpolate the best cooling and transport planning direction. According to the results, there is a potential to cut energy consumption by 15- 25% without affecting drug stability. The environmental impact is also evaluated in the study with the reduction in carbon emissions and cost of operations being noted. The suggested model contributes to the sustainable logistics management and complies with the federal interests in lowering the energy intensity of the supply chains. Predictive analytics can therefore act as a viable solution to a more energy-conscious, stable, and sustainably friendly pharmaceutical logistics in the United States.

This study assesses the prognostic significance of polymorphisms in the uromodulin (UMOD) and vitamin D receptor (VDR) genes in the pathogenesis of urolithiasis (ICD) in the Uzbek population. Genotyping of UMOD rs429639 and VDR BsmI (c.IVS7 G>A) single nucleotide polymorphisms was performed by polymerase chain reaction (PCR) with allele-specific primers in 82 patients with urolithiasis and a control group. Results showed that the T allele and TT genotype of UMOD rs429639 (OR = 1.85, 95% CI: 1.05–3.29, p = 0.0337) and the G allele and GG genotype of VDR BsmI (OR = 2.18, 95% CI: 1.05–4.55, p = 0.0347) are significantly associated with increased risk of urolithiasis. Conversely, the C allele/CT genotype of UMOD and the A allele/GA genotype of VDR demonstrate protective effects. The UMOD locus deviated significantly from Hardy–Weinberg equilibrium in both groups, while the VDR locus was in equilibrium. These findings confirm the role of uromodulin and vitamin D receptor in sodium reabsorption, calcium-phosphorus homeostasis, and lithogenesis, and may be useful for developing genetic risk panels for urolithiasis in the Uzbek population.

Nonsteroidal anti-inflammatory drugs (NSAIDs) occupy an important place in pediatric practice due to their pronounced analgesic, antipyretic, and anti-inflammatory effects. However, their use in children requires particular caution due to age-related differences in pharmacokinetics and pharmacodynamics, immature detoxification systems, and increased sensitivity to side effects. The aim of this article is to comprehensively analyze key aspects of the safe use of NSAIDs in children, including indications, dosage, potential risks, drug interactions, and current approaches to minimizing adverse reactions. This paper summarizes clinical observation data, the results of modern research, and international guidelines, allowing for the formulation of practical conclusions for clinicians. Particular attention is paid to issues of gastrointestinal, nephrotoxic, and cardiovascular safety, as well as the rational choice of drug based on age and clinical situation.

In a study on male white outbred rats with a body weight of 180-250 g, it was found that animals with OTG showed higher levels of P53 and TNFα, as well as higher levels of cytochrome C release from mitochondria. The administration of benzonal, an inducer of drug metabolism, at a dose of 50 mg/kg to animals with OTG (CCl4) significantly reduced the symptoms of apoptosis. On the other hand, the administration of cimetidine at a dose of 10 mg/kg stimulated the apoptosis of hepatocytes, which dramatically increased the levels of P53, TNFα, and cytochrome C in biological fluids. In animals with OTG, arginine, an NO L-inducer, reduced the pro-apoptotic indicators. Compared to the OTG group, the non-selective NOS inhibitor L-NAME increased the levels of P53 protein, TNFα, and cytochrome C release from hepatocyte mitochondria.

The rapid increase in daily screen exposure has led to a rising prevalence of visual disorders, including dry eye syndrome (DES) and myopia. This review summarizes current evidence regarding the mechanisms by which digital device use affects tear film stability, accommodation, and myopia progression. Recent studies indicate that reduced blink rate, increased accommodative demand, and circadian rhythm disturbances contribute significantly to both DES and myopization. Diagnostic strategies and potential preventive measures are discussed with consideration of age-related differences in clinical presentation.

Modern healthcare faces a serious challenge associated with combined trauma. Since the 1990s, the nature of injuries has changed significantly: injuries to multiple anatomical regions simultaneously are now frequently recorded. Today's world, characterized by the increasing number and speed of vehicles, the technological advancement of industry, agriculture, and everyday life, the popularity of extreme sports, and a fast-paced lifestyle, is creating conditions conducive to an increase in injuries not resulting from military action. Stressful situations associated with urbanization also play a role in this trend. Bone injuries to the maxillofacial region account for approximately 3% of all bone fractures in humans. Moreover, a quarter of patients seeking treatment in maxillofacial surgery departments suffer from injuries to this region. Studies show that 14-20% of victims are diagnosed with combined craniocerebral trauma.