The article presents the results of an analysis conducted among age-based comparative groups of girls and women under the age of 18 infected with HIV. It is also noted that the distribution rates of transmission routes vary across administrative regions. The study emphasizes the need to consider age-specific indicators when strengthening epidemiological control over the spread of HIV infection among women in the Republic of Uzbekistan. Epidemiological analysis confirmed that 65.3% of women contracted HIV primarily through unprotected sexual intercourse. The findings highlight the necessity of conducting regular awareness-raising activities among vulnerable groups and mobile populations, as well as the importance of continuously monitoring their level of awareness through modern digital systems.

India aims to eliminate dog-mediated human rabies by 2030 — an ambitious but achievable goal that requires coordinated, multisectoral action. This critical review synthesizes evidence from epidemiology, veterinary and public-health practice, policy analyses, and implementation studies to evaluate the effectiveness of integrated One Health strategies and recent policy innovations across India. We examine core interventions (mass dog vaccination, improved post-exposure prophylaxis access and affordability, community education, and humane dog population management), enabling systems (surveillance and reporting, diagnostic capacity, vaccine supply chains, workforce training), and governance mechanisms (intersectoral coordination bodies, public–private partnerships, and financing instruments). The review identifies notable progress — localized successful mass-vaccination campaigns, advances in cold-chain and rabies biologics procurement, and nascent digital surveillance pilots — alongside persistent barriers: fragmented responsibilities between health and animal sectors, inequitable PEP access in rural and peri-urban areas, data gaps and underreporting, cultural and operational challenges in dog management, and unstable financing. We propose a prioritized, evidence-based roadmap emphasizing (1) national scale-up of sustained dog vaccination to ≥70% coverage, (2) universal, decentralized access to WHO-recommended PEP, (3) integrated real-time surveillance with One Health data sharing, (4) community-led behaviour change and risk communication, and (5) predictable multi-year financing with performance-linked metrics. Closing research and implementation gaps through operational research and routine program evaluation is essential. With sustained political commitment and coordinated implementation, India can plausibly meet the 2030 elimination target — but only if current momentum is translated into scalable, accountable action now.

Over the past decade, scientific research on stress physiology has provided a deeper understanding of the mechanisms of response and adaptation of homeostatic systems in the human body to stress factors [1]. In a state of stress, the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS) are closely interconnected, causing the body to undergo a complex adaptive response aimed at maintaining homeostasis [2]. As a result of the activation of these systems, stress hormones such as cortisol, adrenaline, and noradrenaline are released, which leads to accelerated cardiovascular activity, increased glucose metabolism, and a temporary weakening of the immune system [3]. The main physiological role of cortisol is to protect the body from energy deficiency during stress, regulate protein and fat metabolism, and control immune inflammatory responses [4]. At the same time, the sympathetic nervous system activates the “fight or flight” mechanism, increasing heart rate and directing blood flow to the muscles [5]. However, chronic exposure to stressors leads to HPA axis imbalance, which leads to increased cortisol secretion, metabolic syndrome, depression, and cardiovascular disease [6].

Recent studies (Kloet, 2024; Chrousos, 2020) have shown that individual stress reactivity is modulated by genetic and epigenetic control of cortisol. This suggests that the level of stress tolerance of each individual is formed by the interaction of genetic and environmental factors [7]. In addition, dysfunction of stress response systems directly affects the functioning of the central nervous system, affecting memory, emotional balance, and decision-making processes [8].

This article provides an in-depth analysis of the homeostatic changes that occur in response to stress, the interplay between cortisol and the sympathetic nervous system. Also, based on modern scientific sources, the short- and long-term physiological consequences of stress, as well as the role of cortisol in the disruption of adaptation mechanisms, are highlighted [9].

Percutaneous coronary intervention (PCI) with stenting is the cornerstone of revascularization in ischemic heart disease. However, in-stent restenosis (ISR), a pathobiological response to vascular injury, remains a significant limitation, affecting a substantial subset of patients and necessitating repeat interventions. This review aims to critically analyze the multifactorial pathogenesis of ISR, focusing on the pivotal roles of inflammation, smooth muscle cell (SMC) phenotype switching, and extracellular matrix (ECM) dysregulation. Moving beyond conventional anti-proliferative strategies, we explore a novel pathogenetic approach centered on the pleiotropic properties of specific sulfated glycosaminoglycans (GAGs)—chondroitin sulfate (CS) and glucosamine sulfate (GS). Traditionally used in osteoarthritis management, these molecules exhibit potent anti-inflammatory, anti-thrombotic, and ECM-modulating effects relevant to vascular pathophysiology. We synthesize evidence from molecular, experimental, and early clinical studies suggesting that CS/GS can inhibit key drivers of ISR, such as versican-CD44-mediated signaling and NF-κB activation. The review also discusses the importance of pharmaceutical-grade purity for clinical translation and positions this approach within the evolving landscape of adjunctive pharmacotherapy for PCI, highlighting its potential to improve long-term vascular patency and patient outcomes.

Objective: To compare the clinical results of anterior cruciate ligament (ACL) reconstruction using autologous versus allogeneic grafts, by means of a systematic review with meta-analysis. Methodology: The review was conducted according to the PRISMA guidelines, with searches in PubMed/MEDLINE, Embase, Cochrane Library and Scopus. Randomized clinical trials published between 2011 and 2025 involving adult patients undergoing primary ACL reconstruction were included. The outcomes assessed were function (subjective and objective IKDC, Lysholm, Tegner, Cincinnati), joint stability (clinical tests and arthrometer) and complications, including graft failure. Methodological quality was assessed using the Cochrane Risk of Bias tool. Results: After initial screening of 14 articles, 5 studies met the inclusion criteria, totaling 471 patients (238 autogenous and 233 allogenous). Both groups showed significant improvement in joint function and stability at follow-up ≥ 24 months, with no statistically significant differences in functional scores. However, the failure rate was higher in allografts (up to 26% in some studies). Conclusion: ACL reconstruction with autografts and allografts results in significant clinical improvement, but autografts have a lower risk of failure and greater stability, making them the preferred option in high-demand individuals.

Gestational diabetes mellitus (GDM) is a glucose intolerance of any degree that is first detected during pregnancy and is one of the most common perinatal diseases, affecting 1–25% of pregnant women worldwide. [1] GDM increases the risk not only of short-term complications for the mother and fetus but also of long-term metabolic consequences and is a significant risk factor for the development of type 2 diabetes (T2D). [2] Studies show that women with GDM have a 35–60% risk of developing T2D within 7 years postpartum, which is almost 10 times higher compared to the general population. [3] This review article provides a comprehensive analysis of GDM and its metabolic consequences in the postpartum period, as well as strategies for identifying and preventing the risk of T2D, based on scientific research conducted over the past decade (2015–2025). The article discusses the pathophysiological mechanisms of T2D development in women with GDM, genetic and environmental factors, and various screening methods and their effectiveness. [4] In addition, various preventive strategies, including lifestyle modification, pharmacological interventions, and new approaches, are thoroughly examined. [5] Systematic reviews indicate that lifestyle modification programs, including diet therapy and physical activity, can reduce the risk of developing T2D by 35–40%. [6] Pharmacological interventions, such as metformin, may reduce the risk by up to 50%. [7] The article emphasizes that a personalized approach to postpartum screening and treatment of women with GDM plays an important role in delaying or preventing the development of T2D. [8] In conclusion, it should be noted that GDM is not only a problem of the pregnancy period, but also a condition that poses a serious threat to long-term metabolic health. The implementation of effective screening, monitoring, and preventive programs offers an opportunity to reduce the prevalence of T2D. [9].

Background

Food safety significantly influences the global burden of disease, particularly in rapidly urbanising regions. In low- and middle-income countries such as Nigeria, there is limited understanding of how consumer concerns about food safety shape eating habits and dietary choices. This review aimed to synthesise evidence on food safety perceptions and how it influences consumer behaviour in Nigeria. The study examined existing research on Nigerian consumers’ perceptions, attitudes, and behaviours regarding food safety, providing insights into knowledge gaps and areas requiring future investigation.

Methods

A systematic review was conducted following PRISMA guidelines. The PECO model guided the development of a comprehensive search strategy, initially applied to PubMed and adapted for other databases. Keywords relevant to food safety, consumer behaviour, and Nigeria were used. Reference lists of relevant studies were also screened. Inclusion criteria focused on peer-reviewed research that addressed consumer perceptions or behaviours related to food safety.

Results

Twenty-four studies met the inclusion criteria. Research was concentrated in urban areas, particularly the southwestern region, with prepared and ready-to-eat foods being the most studied. Most studies relied on single-method data collection, primarily structured surveys. Findings indicated that although participants generally had good knowledge of food safety, self-reported practices were often inadequate and in most cases absent or underreported. Methodological limitations, including lack of validated instruments and overreliance on self-reporting, were identified across several studies.

Conclusion

Future research should prioritise fresh produce and traditional markets, incorporate observational and qualitative approaches, and explore the cultural, social, and contextual factors influencing food safety behaviours. Understanding consumers’ motivations, perceptions, and values in specific cultural contexts will be critical to developing effective interventions to improve food safety practices in Nigeria.

Carbon monoxide (CO) intoxication is one of the most common severe poisonings worldwide, affecting millions of people annually and leading to significant morbidity and mortality. [1] In addition to hypoxia, the main pathophysiological effect of CO poisoning is associated with direct cellular-level toxic effects, particularly liver damage. [2] Due to its metabolic activity and central role, the liver is highly sensitive to the toxic effects of CO, which is often not sufficiently considered in clinical practice. [3]

This article deeply examines the pathogenetic mechanisms of liver damage in CO intoxication and methods to correct them. Key pathogenetic aspects such as the direct cytotoxic effect of CO on liver cells, increased oxidative stress, mitochondrial dysfunction, activation of inflammatory reactions, and apoptotic pathways are studied. [4] The central role of mitochondria in CO-related liver damage is particularly emphasized, as it is considered the main cause of energy metabolism disruption and cell death. [5]

Oxidative stress arises from excessive production of reactive oxygen species (ROS) and deficiency in the antioxidant defense system, leading to lipid peroxidation, protein oxidation, and DNA damage, which cause structural and functional disruptions in liver cells. [6] Inflammatory processes develop in association with nuclear factor kappa B (NF-κB) and various cytokines (TNF-α, IL-1β, IL-6), leading to the expansion of liver damage and disruption of regeneration processes. [7]

Among the methods to correct pathogenesis, in addition to the traditional method of hyperbaric oxygen therapy (HBOT), new pharmacological approaches are discussed, including antioxidants (N-acetylcysteine, melatonin), anti-inflammatory agents, inhibitors of apoptotic pathways, and substances that restore mitochondrial function. [8] Data show that N-acetylcysteine not only exerts an antioxidant effect but also protects liver cells by restoring the glutathione system. [9] Melatonin, due to its strong antioxidant and anti-inflammatory properties, is considered effective in reducing liver damage in CO intoxication. [10]

This review article provides valuable information not only on the in-depth study of pathogenetic mechanisms but also on modern treatment strategies, which will help effectively manage the consequences of CO intoxication in clinical practice. [11] Early diagnosis of liver damage and the introduction of pathogenetically based therapy can significantly reduce complications and mortality rates after CO intoxication. [12].

Eosinophils belong to the immunological granulocytic group, the main function of which is protection against infectious diseases and allergic diseases. Finally, eosinophils also have the ability to phagocytosis, which makes them important as natural effector and immunomodulatory cells. The article analyzes the mechanisms of phagocytosis of eosinophils, molecular signaling processes and clinical significance.

This study aims to analyze the changes that occur in the human psyche during migration or a change in place of residence, their causes and consequences. Against the background of the acceleration of the global migration process, psychological health issues have become a relevant topic.

As a result of clinical and epidemiological observations by many authors over the past decade, changes in the clinical course of sarcasm have been noted. In particular, a significant increase in the number of purulent-necrotic forms has been revealed, the number of disease relapses has not decreased, their frequent development and high mortality remain. Analysis of available scientific data shows that currently, there is no clearly developed program for the use of magnetic laser therapy in the complex treatment of complicated forms of sarcasm. Information on the morphological features of ulcerative processes and changes in local microcirculation under the influence of this therapy is also insufficient. The significance of the aforementioned problem in practical medicine and the presence of many unexplored issues served as the basis for conducting this scientific research.

Allergic reactions in children during pharmacotherapy represent one of the most complex and pressing issues in modern pediatrics. The high sensitivity of children's bodies, immature enzymatic systems, genetic predisposition, and the rise of polypharmacy lead to an increasing incidence of drug allergies. In recent decades, there has been a steady increase in hypersensitivity to antibiotics, antipyretic drugs, vaccine components, and local anesthetics, necessitating comprehensive clinical monitoring, early diagnosis, and the development of individualized treatment approaches. This article analyzes the key mechanisms of allergic reactions, their clinical forms, risk factors, and diagnostic features in children of different ages. Special attention is given to the problems of differential diagnosis, difficulties in verifying true allergies, errors in clinical practice, and modern prevention strategies. The possibilities of using pharmacogenetics and immunological testing, as well as modern algorithms for managing patients with increased allergic risk, are discussed. Based on an analysis of scientific sources and clinical data, the importance of an interdisciplinary approach, including pediatricians, allergists, pharmacologists, and immunologists, is emphasized. This approach minimizes the risk of complications, increases the safety of therapy, and improves children's quality of life.

This article examines the theoretical and applied aspects of phenotypic variability as a fundamental phenomenon in medical biology. Phenotypic variability is defined as the totality of morphological, physiological, biochemical, and behavioral differences between organisms, arising under the influence of genotype, environmental conditions, and their interactions. It is emphasized that the phenotype is the final manifestation of the organism's hereditary program, modified by a wide range of factors—epigenetic mechanisms, mutations, nutritional conditions, physical activity level, stress, diseases, and environmental conditions.

This scientific paper presents current data on the anatomical structures of the liver as a unique organ performing over 500 vital functions. It examines the morphological features of liver lobes and segments, the vascular and biliary structure, the microarchitectural features of the liver lobules and sinusoidal system, and the functional and structural zones that play a key role in metabolism and detoxification. The paper emphasizes the clinical significance of liver anatomy in surgical interventions, transplantation, and disease diagnosis. It also discusses modern imaging techniques and their contribution to the accurate determination of pathological processes and anatomical variations in the liver.

Hemolytic anemia is a pathological condition characterized by the direct or indirect destruction of erythrocytes before their normal lifespan, manifested by a combination of anemia and laboratory signs of hemolysis in the peripheral blood. The purpose of this article is to provide an in-depth study of various compensatory and adaptive mechanisms activated by the human body in conditions of hemolytic anemia. In patients with hemolytic anemia, the body tries to compensate for oxygen deficiency and minimize the negative consequences of hemolysis through a number of complex physiological processes. Among these compensatory mechanisms are such important processes as adaptation of the cardiovascular system, increased hematopoietic activity, a shift of the oxygen-hemoglobin dissociation curve to the right, increased erythropoiesis, and an increase in the efficiency of tissue oxygen utilization. The article also studies the differences in compensatory mechanisms in the types of hemolytic anemia, the pathophysiological basis of compensation, and the limits of compensatory capacity in various hemolytic anemias (e.g., hereditary spherocytosis, OAVK deficiency, paroxysmal nocturnal hemoglobinuria, etc.). The body's ability to compensate determines the severity of hemolytic anemia and often causes a relatively mild manifestation of clinical signs of anemia. However, compensatory mechanisms are limited, and after a certain point, a state of decompensation may develop. This article also highlights the clinical importance of taking into account compensatory mechanisms in the treatment of patients with hemolytic anemia.

Eosinophils are an important component of the immune system, and their activity plays a central role in allergic reactions, asthma, parasitic infections, and autoimmune processes [1]. Chemotaxis is the main mechanism by which eosinophils are attracted to inflammatory foci. This article reviews the chemotaxis factors of eosinophils, their associated signaling pathways, and molecular mediators.