The structure of modern habitat: an ontological and a factor model

The article proposed the analysis of evolutionary variations for the formation of human environment. The preconditions and consequences of technosphere historical emergence are analyzed. The transformation the technical system role is demonstrated from the perspective of social and cultural sphere element to the position of a primate sphere, the determinant of the human environment development vecto

Health as a space-time continuum

The purpose of work is to quantify the changes of the organism functional reserves during the successive phases of the human health Space-Time Continuum (STC) on the basis of postulates of reliability complex systems theory. The study is devoted to the problem of age-related human involution, which is evaluated not from the causal, but from the kinetic point of view The analysis of 10 most important basic life support systems of human body – cardiovascular (CVS), respiratory (RS), nervous (NS), digestive (DS), endocrine (ES), immune (IS), excretory (EXS), brain (BS), musculo-skeletal (MSS), hematopoietic (HS) was carried out. Based on this analysis two levels of ensuring the reliability of organism’s work were revealed: sequential and parallel. The system of logical equations for reduced sequential system is: Ys1 = CVS RS BS, where is the notation for the conjunctions of set elements. The system of logical equations for the reduced parallel system is: Ys2 = NS DS ES IS HS EXS MSS, where is the disjunction of the scheme elements. Visualization of human STC changes the concept of the kinetics of age-related changes in the organism and the role of determinants of health as a stable factor accompanying a uniform, smooth transition from the most pronounced functions of the body to their gradual extinction. For human STC is formulated the following regularity kinetics of involutionary processes: after 30 years of age in the human body morphological changes regress in arithmetic progression, and the functions of organs in a geometric one. Assumption of health as a state redundancy of functions is suggested

Pathophysiological Role of Thermoregulatory Reactions in the Development of Common Cold Diseases: Paradigmatic Shift from Pathogen-Centric to Host-Response Model: A Critical Review

This review synthesizes research on the pathophysiological role of thermoregulatory responses in the development of cold-related diseases, focusing on the physiological mechanisms underlying thermoregulation and their interaction with the immune system. Special attention is given to the effects of cold stress on mucosal barriers and systemic effects, the role of gut microbiota in thermoregulation considering age and gender differences, as well as the application of host-responsive models in clinical settings with potential therapeutic approaches.   The aim of the review was to evaluate thermoregulatory-immune interactions, analyze the impact of cold stress on mucosal integrity and systemic inflammation, compare age and gender variations in gut microbiota, and identify therapeutic strategies targeting microbiota and immune modulation.   A critical analysis of multidisciplinary studies using animal and human models with molecular, immunological, and microbiome profiling was conducted. Results indicate that cold exposure modulates immune cell populations and cytokine profiles, disrupts gut barrier function through changes in tight junctions and inflammatory pathways, and consistently alters gut microbiota diversity with limited research on sex and age effects.   Integration of these findings highlights the complex interaction between thermoregulation, immunity, and microbiota in cold-related diseases. These concepts inform the development of targeted clinical interventions and emphasize the need for standardized integrative models

Somato-Regulatory Imbalance as a Pathophysiological Basis of Civilization Diseases: A Systematic Review and Meta-Analysis

Objective: To conduct a systematic literature review on the role of somato-regulatory imbalance in the pathogenesis of civilization diseases and evaluate the effectiveness of therapeutic interventions. Methods: We searched PubMed, Embase, Cochrane Library, and Web of Science databases for the period 2000-2025. PRISMA 2020 criteria and Cochrane Handbook methodology were applied. A meta-analysis of homogeneous studies was performed using a random-effects model. Results: We identified 2,847 potentially relevant publications, of which 127 met inclusion criteria (34 RCTs, 58 cohort studies, 23 cross-sectional studies, and 12 systematic reviews). The meta-analysis showed that the combination of chronic psycho-emotional stress and reduced physical activity increases cardiovascular disease risk by 2.8-fold (RR = 2.80; 95% CI: 2.34-3.35), type 2 diabetes by 2.1-fold (RR = 2.12; 95% CI: 1.78-2.52), and metabolic syndrome by 3.2-fold (RR = 3.21; 95% CI: 2.67-3.86). Conclusions: Somato-regulatory imbalance represents a key pathophysiological mechanism of civilization diseases, requiring a comprehensive approach to prevention and treatment that considers both somatic and regulatory components

Somato-Regulatory Imbalance as a Pathophysiological Basis of Civilization Diseases

Background The global burden of non-communicable diseases (NCDs), particularly cardiovascular diseases (CVD) and type 2 diabetes mellitus (T2DM), continues to rise, posing a serious challenge to public health. Understanding the complex pathophysiological mechanisms underlying these conditions is critical for developing effective prevention and treatment strategies. Aim This study aims to investigate the interconnected pathways linking metabolic dysfunction, endothelial dysfunction, and cardiovascular complications, with a particular emphasis on the role of advanced glycation end-products (AGEs), reactive oxygen species (ROS), and dysregulation of the autonomic nervous system (ANS). Methods A comprehensive analysis of the renin-angiotensin-aldosterone system (RAAS), activation of the sympathetic nervous system (SNS), and dysfunction of endothelial nitric oxide synthase (eNOS) was conducted. Biomarkers were evaluated, including free fatty acids (FFAs), lipoproteins (HDL, LDL, VLDL), and inflammatory mediators such as interleukin (IL) and tumor necrosis factor alpha (TNF-α). Results The results demonstrate significant correlations between metabolic syndrome (MetS), endothelial dysfunction (ED), and ischemic heart disease (IHD). Elevated body mass index (BMI) and blood pressure (BP) were associated with increased somatoregulatory imbalance (SRI) and activation of the hypothalamic-pituitary-adrenal axis (HPA). Angiotensin-converting enzyme (ACE) activity showed strong associations with nitric oxide (NO) bioavailability and vascular function. Conclusions The study reveals complex interactions between metabolic and cardiovascular pathways, highlighting the importance of integrated therapeutic approaches targeting multiple systems simultaneously. These findings contribute to the understanding of the disability-adjusted life years (DALYs) burden and inform World Health Organization (WHO) guidelines on NCD prevention

Pathophysiological mechanisms of integrated regulation of water-sodium homeostasis: from cellular dysfunction of Na-K-ATPase to dysregulation of systemic volume control: a systematic review

Background: Water-sodium homeostasis regulation is a fundamental physiological process that ensures cellular function maintenance, extracellular fluid volume, and arterial pressure. Despite decades of research, the integrated understanding of the dual sodium regulatory system remains incomplete, limiting the development of effective therapeutic approaches for cardiovascular and renal diseases. Objective: To conduct a systematic review and meta-analysis of evidence regarding integrated dual regulation of water-sodium homeostasis, including cellular mechanisms (digitalis-like compounds and Na-K-ATPase) and systemic mechanisms (natriuretic peptides and neurohormonal volume regulation), with assessment of their pathophysiological interactions and clinical implications. Methods: A systematic search was conducted in PubMed/MEDLINE, Embase, Cochrane Library, Web of Science, and Scopus databases (1957-2025) according to PRISMA 2020 guidelines. Experimental studies, clinical trials, and observational studies investigating sodium regulation mechanisms at cellular and systemic levels were included. Study quality was assessed using RoB 2.0, ROBINS-I, and Newcastle-Ottawa Scale. Meta-analysis was performed using random-effects model (DerSimonian-Laird). Results: We identified 1,847 records, of which 89 studies met inclusion criteria (n=34,156 participants). Meta-analysis of 24 studies showed significant natriuretic increase under digitalis-like compounds influence (SMD = 1.67, 95% CI: 1.52-1.82, p<0.001, I²=68%). Endogenous digitalis-like compound levels were progressively elevated in hypertension (1.87±0.64 vs 0.52±0.18 nmol/L in healthy individuals, p<0.001), heart failure (2.34±0.89 nmol/L), and chronic kidney disease (2.78±1.12 nmol/L). Natriuretic peptides demonstrated coordinated responses with cellular mechanisms: correlation between ANP and Na-K-ATPase activity (r=0.58, p<0.01), BNP and endogenous ouabain levels (r=0.42, p<0.05). Conclusions: The dual regulatory system of water-sodium homeostasis represents an integrated network of mechanisms that coordinate cellular activity and systemic fluid balance through complex pathophysiological interactions. The cellular subsystem (digitalis-like compounds/Na-K-ATPase) is functionally integrated with the systemic subsystem (natriuretic peptides/neurohormonal regulation) to maintain homeostasis. Disruption of this integration underlies the pathogenesis of arterial hypertension, heart failure, and chronic kidney disease. These findings have critical significance for understanding pathophysiology and developing new personalized therapeutic strategies

Pathophysiological aspects of the interaction between endogenous natriuretic factors and digoxin-like substances as different functional systems of central nervous system regulation: a systematic review

Background: Endogenous natriuretic factors (ENFs) and digitalis-like substances (DLS) are key endogenous regulators influencing the central nervous system (CNS) through distinct molecular mechanisms. ENFs, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP), primarily regulate water-salt balance and vascular tone through guanylate cyclase receptor activation, while DLS, including endogenous ouabain and marinobufagenin, modulate Na-K-ATPase activity, affecting neuronal excitability and intracellular signaling cascades.   Objective: To conduct a comprehensive systematic analysis of ENFs and DLS as functionally distinct CNS regulatory systems, evaluating their molecular mechanisms, clinical significance, and therapeutic potential.   Methods: A systematic search was conducted in PubMed/MEDLINE, Embase, Scopus, Web of Science, and Cochrane Library databases from 1957 to 2025. Search terms included: "endogenous natriuretic factors", "digitalis-like substances", "central nervous system regulation", "Na-K-ATPase inhibition", "ouabain-like compounds", "marinobufagenin". Study selection followed PRISMA 2020 guidelines with independent screening by two reviewers. Quality assessment used Cochrane RoB 2.0 for RCTs and Newcastle-Ottawa Scale for observational studies.   Results: From 1,247 identified publications, 89 studies met inclusion criteria (n=15,847 participants). ENFs affect the CNS via cGMP-dependent mechanisms, reducing sympathetic activity by 20-35% and modulating neurotransmission through NPR-A, NPR-B, and NPR-C receptors. DLS activate Src-kinase cascades through selective inhibition of Na-K-ATPase α-subunits, influencing circadian rhythms and cognitive functions. In pathological conditions, characteristic imbalances were observed: DLS levels increased 1.5-2.8-fold in essential hypertension and depression, while ENF activity decreased 25-40% in neurodegenerative diseases.   Conclusions: ENFs and DLS function as independent but interconnected regulatory systems with significant therapeutic potential. Understanding their distinct mechanisms opens new avenues for developing personalized treatment strategies for neurological disorders