How does delayed childbearing promote child gender diversity? - Causal evidence and mechanism analysis from China.

Cancer-related cognitive impairment (CRCI) is a frequent and clinically meaningful consequence of cancer, yet current evidence is largely derived from older adult populations. Adolescents and young adults (AYAs) may be particularly vulnerable due to ongoing neurodevelopment, high cognitive demands, and cancer-related biological and psychosocial stressors. This review is timely given the growing interest in biological mechanisms and preventive models of CRCI, alongside the persistent lack of AYA-specific syntheses addressing cognitive trajectories, mechanisms, and optimal intervention timing. Approximately 25-30% of AYAs experience CRCI, most commonly affecting attention, processing speed, executive functioning, and working memory. Cognitive alterations may be detectable prior to treatment initiation and can persist across the cancer trajectory. Emerging AYA-specific evidence implicates biological mechanisms such as systemic inflammation and altered neuroplasticity, including changes in brain-derived neurotrophic factor (BDNF). A consistent dissociation between subjective cognitive complaints and objective performance is observed, underscoring the functional impact of subtle inefficiencies in academic and early professional contexts. While non-pharmacological interventions show promise in the general CRCI literature, early and AYA-specific preventive interventions remain scarce. CRCI in AYAs should be conceptualized as a dynamic, biologically grounded process embedded within ongoing neurodevelopment. Early, developmentally sensitive, and multimodal interventions may represent a key opportunity to preserve long-term cognitive, functional, and psychosocial outcomes in this vulnerable population.

Sleep, lipids, and metabolic health in the Indian obesity epidemic: an integrative review of mechanisms, burden, and breakthroughs.

Obesity is a chronic, biologically defended disease, yet its clinical management continues to be shaped by behavioural paradigms that no longer reflect contemporary science, especially outside specialist services. While lifestyle factors such as dietary patterns, physical inactivity, sleep disruption and other environmental influences contribute to obesity development, they do not fully explain or reverse the neuroendocrine mechanisms that defend elevated adiposity. Although calorie restriction can produce short-term metabolic improvements, including improved insulin resistance, it does not modify the underlying neuroendocrine drivers of adipocyte mass regulation; consequently, exclusive reliance on calorie-restriction-centred models may delay the introduction of mechanism-based treatments and allow obesity-related complications to recur or progress over time. In contrast, modern pharmacotherapies act directly on the regulatory systems governing adipocyte mass and thus affect appetite, energy homeostasis and metabolic adaptation, producing durable improvements across cardiometabolic, hepatic, respiratory and musculoskeletal domains. Safety profiles for obesity medications are well characterised, and for appropriately selected patients the benefit-risk balance is favourable. Prevention efforts remain essential, but no population-level strategy has yet demonstrated sustained impact on obesity prevalence. Conceptual analogies help clarify these distinctions: carrying additional weight, like a heavy backpack, does not in itself constitute a disease and treating established pathology cannot depend on upstream environmental reform, just as anaphylaxis cannot be managed by regulating peanut exposure alone. A therapeutic framework grounded in biological mechanisms rather than behavioural assumptions is now both possible and necessary to close long-standing gaps in obesity care.

Understanding intestinal healing following resection and anastomosis is a challenging topic due to the complexity of underlying mechanisms. Anastomotic healing follows the fundamental phases of normal wound repair; however, the intestinal anastomosis represents a unique biological environment in which factors such as the structure of the intestines, as well as the microbiome, may modify the healing process. Disruptions in any of the healing phases, such as the inflammatory, proliferative, and remodeling phase, may result in severe complications, characterized by the intraluminal contents leaking out into the extraluminal space, termed an anastomotic leak (AL). Despite decades of surgical advancements, we are still no closer to understanding the underlying AL etiology. It is clear that ALs are multifactorial in nature and contribute to by patient-, technical-, and biological-related factors; however, emerging evidence suggests that biological mechanisms may play a more significant role in AL pathology than originally believed. Evidence points to an interplay between epithelial healing, tissue oxygenation, and the resident microbiome in influencing mucosal healing at the anastomotic site. However, the precise contribution of these factors to failed anastomotic healing and AL etiology remains unclear. In this review, we examine the phases of healing, discuss the existing literature on biological factors affecting anastomotic healing, and describe the advancements made to improve AL rates by targeting the healing response.

Results of the American Venous Forum research retreat on C2 disease confirms that the biology of varicose veins including etiology, progression, and novel therapeutics, as well as disparities, are top research priorities.

Social determinants of health (SDoHs) are increasingly recognized as important contributors to the development, course, and outcomes of psychiatric disorders. However, their integration into clinical psychiatry and mechanistic models remains limited. This overview synthesizes emerging evidence on the biopsychosocial mechanisms through which SDoHs influence mental health. There is a need to distinguish between individual-level, clinically actionable health-related social needs and family-, community-, and society-level structural SDoHs, and to consider both adverse and protective social factors. Converging research demonstrates that social experiences are biologically embedded through interacting pathways, including exposomics, epigenetics, allostatic load, accelerated inflammaging, immune dysregulation, and gut-brain-microbiome signaling. These mechanisms influence neural circuitry underlying stress regulation, reward processing, and social cognition. Psychological processes-including individual differences in resilience, wisdom, compassion, and purpose in life-shape responses to SDoHs and are supported by identifiable neurobiological substrates. Social connection has emerged as a central, potentially modifiable SDoH that is strongly associated with whole health and longevity. Loneliness and social isolation have become major global public health challenges. The authors propose a biopsychosocial framework that integrates social exposures, biological mechanisms, neural systems, and psychological processes to better understand the risk, course, and prevention of mental illnesses. Clinical and public health implications include the need for routine assessment of SDoHs, incorporation of protective factors at individual and societal levels, and development of pragmatic, multidomain interventions. Finally, rapidly evolving digital technologies, including artificial intelligence, offer new opportunities but also require careful governance. Advancing toward human-centered "artificial wisdom" may enhance the capacity of technology to promote whole health in individuals with mental illnesses globally.

Choline, a nexus for neurocognitive nutrients: A narrative review.

METTL3-mediated m6A modification of circWDR85 drives breast cancer bone metastasis via the CKB/c-Jun axis.

Depression is a common and severe neuropsychiatric disorder, and its underlying biological regulatory mechanisms remain unclear. Microglia are resident immune cells of the central nervous system (CNS) that critically mediate the occurrence and development of CNS diseases, including depression. As the most abundant RNA modification, N6-methyladenosine (m6A) regulates microglial function. However, its role and molecular mechanisms in depression remain unclear. In this study, we found that m6A levels decreased in the microglia of the chronic restraint stress (CRS)-induced depression mouse model. Among m6A modulation factors, Alkbh5, a demethylase, showed a significant increase in expression level. Therefore, we generated microglial-specific conditional Alkbh5 knockout mice and found that Alkbh5 deficiency alleviated CRS-induced depression-like behaviors. Mechanistically, microglial Alkbh5 deficiency inhibited excessive microglial activation, rescued dendritic spine loss, and regulated the vascular changes during CRS. Together, these results highlight the important role of Alkbh5 in regulating microglial function in the CRS-induced depression mouse model, providing a potential therapeutic target for depression.

Investigation of the impact of catechol on the fluidity of lipid monolayers.

Childhood maltreatment and pregnancy-related reproductive health in middle adulthood: a prospective investigation.

CBL proto-oncogene C-mediated synaptophysin 1 regulates prostate cancer progression in the TGF-beta signalling pathway.

Exosomes in the prevention and treatment of photoaging based on biological molecular mechanisms: From animal-derived to plant-derived innovative approaches

Tumor evolution in an ecological context: How genetic and microenvironmental factors shape the pathogenesis of pancreatic cancer.

Freshwater fish is widely consumed, yet raw or undercooked freshwater fish can transmit foodborne zoonotic pathogens. Clonorchiasis, caused by Clonorchis sinensis, is a major foodborne parasitic disease associated with hepatobiliary injury and fibrosis. The biological functions and mechanisms underlying liver injury mediated by C. sinensis-derived extracellular vesicles (EVs) encapsulated microRNAs in fibrogenic remodeling remain poorly defined. Here, we isolated and characterized EVs from adult C. sinensis, confirmed their uptake by hepatic stellate cells (HSCs), and identified Csi-bantam as a CsEV-enriched microRNA. Csi-bantam enhances HSC activation and upregulates fibrogenic markers, including α-SMA, COL1A1, and COL3A1, both in vitro and in a mice infection model. Bioinformatic prediction and dual-luciferase assays validated TRIM35 as a target of Csi-bantam. TRIM35 silencing phenocopied Csi-bantam overexpression and increased PI3K/AKT phosphorylation, whereas Csi-bantam inhibition restored TRIM35 and attenuated fibrogenic markers. Collectively, CsEV-associated Csi-bantam promotes HSC activation via the TRIM35-PI3K/AKT axis, suggesting a potential target for antifibrotic intervention in clonorchiasis. These findings provide mechanistic insight into how infection acquired from raw or undercooked freshwater fish harboring infective C. sinensis metacercariae can lead to hepatobiliary injury and fibrogenic remodeling, supporting food safety risk assessment and future prevention of fish-borne parasitic hazards.

Relationship between the microplastics in typical marine organisms and the environment: A case study in Bohai Bay, China.

Rational design and synthesis of flavonolactam derivatives as potent topo I inhibitors with antitumor activity.

New insights into the ambivalent role and clinical implications of tripartite motif family proteins in colorectal cancer.

With global population aging, sarcopenia and osteoporosis have become critical public health challenges. Muscles and bones are closely interconnected anatomically and functionally, but the biological mechanisms connecting sarcopenia and osteoporosis have not yet been fully elucidated. This study systematically investigated the bidirectional relationship and shared mechanisms between sarcopenia and osteoporosis through multi-omics analysis integrating genomic, proteomic, and metabolomic data from the UK Biobank. Our findings indicated that the two conditions may act as reciprocal risk factors. Higher lean mass index (hazard ratio [HR] = 0.830, 95% confidence interval [CI]: 0.788-0.874), greater hand grip strength (HR = 0.544, 95% CI: 0.531-0.558) and faster usual walking pace (HR = 0.735, 95% CI: 0.723-0.746) were significantly associated with lower osteoporosis incidence, with multiple plasma proteins and metabolites identified as mediators in these associations. Conversely, higher bone mineral density of left heel (HR = 0.613, 95% CI: 0.394-0.946) and right heel (HR = 0.591, 95% CI: 0.380-0.912) were associated with reduced sarcopenia risk. We also observed a positive genetic correlation (r = 0.25, p = 1.6 × 10-5) between sarcopenia and osteoporosis, as well as substantial overlaps in risk-associated genes and circulating biomarkers between the two conditions with consistent effect directions. Furthermore, modifiable factors including smoking, sleep duration, and physical activity exhibited similar effect patterns between sarcopenia and osteoporosis, with more than 30% overlap in mediating proteins and metabolites. These discoveries highlight common pathophysiological pathways potentially underlying both conditions and are expected to advance the understanding of muscle-bone interdependence.