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Diabetes mellitus encompasses disorders characterized by hyperglycemia due to pancreatic β-cell dysfunction. Type 2 diabetes (T2D) constitutes over 90% of cases, with a background of genetic, metabolic, and environmental risk factors. Knowing that sex differences impact insulin resistance and glycemic control, this review aims to identify differences in adherence to dietary patterns between women and men with T2D. This systematic review aims to evaluate sex differences in dietary pattern adherence among individuals with T2D and the implications of these differences for glycemic control. The protocol was developed using the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. Studies published until July 2026 will be identified by searching the following electronic databases: MEDLINE, Scopus, Cochrane Library, and Web of Science. Three investigators will independently screen articles based on titles and abstracts followed by a thorough analysis of selected full-text articles of interest. Articles on T2D and dietary pattern scores that include biological sex data will be included. The estimation of risk of bias will be performed using the Standard Quality Assessment Criteria for Evaluating Primary Research Papers From a Variety of Fields. To synthesize the results, a narrative analysis will be performed based on the GRADE (Grading of Recommendations Assessment, Development, and Evaluation) framework. The search strategy was developed and refined between July 2025 and July 2026 through scoping and pilot searches. The comprehensive database search will be conducted in August 2026, covering records from database inception to July 2026. Study selection and data extraction are expected to be completed by December 2026, with publication anticipated in late 2027. This systematic review will provide a comprehensive overview of the role of sex in dietary adherence among individuals with T2D. Identifying sex-specific and gender differences may inform the development of tailored nutritional strategies and interventions aimed at improving glycemic outcomes. Ultimately, this work highlights the importance of incorporating sex-based approaches in the management of T2D to optimize long-term health outcomes. PROSPERO CRD42024340213; https://www.crd.york.ac.uk/PROSPERO/view/CRD42024340213. DERR1-10.2196/98958.

Empathetic responses, including socially-transferred pain hypersensitivity (STPH) and the targeted caring behaviors shown as allolicking (injury site targeted licking) and allogrooming (body grooming) toward a familiar demonstrator with pain, can be quantified in rodents using a dyadic social interaction (DSI) paradigm. These responses exhibit sex differences. Although our prior research established that β-estradiol is selectively required for allolicking, but not allogrooming in female mice, the overall scope of sex hormones remains unclear. Here, we discovered androgen deficiency following bilateral orchiectomy (ORC) in male observers impaired engagement of allolicking and allogrooming, STPH and social sniffing, but not self-grooming towards a familiar demonstrator. A 7-day replacement therapy with testosterone propionate (TP; 0.5, 1.0, 2.0 mg/kg bw, s.c.) prevented these deficits, but β-estradiol (E2; 0.5, 1.0, 2.0 mg/day, s.c.) failed. Moreover, E2 administration significantly suppressed both allolicking and allogrooming in intact male observers. In intact female observers, TP selectively enhanced both sniffing and allogrooming in terms of time and bouts, however, it suppressed the bouts of allolicking although the total time of allolicking remained unchanged. TP had no effects on STPH or self-grooming in intact female observers. Thus, we demonstrate that testosterone is essential for sniffing, allolicking and allogrooming behaviors in male and allogrooming (but not allolicking) in intact female, while estrogen inhibits empathetic behaviors in intact male. This fundamental sexual dimorphism in hormonal regulation offers promising insights for developing sex-specific hormone therapies following gonadectomy.

Sex- and gender-based differences significantly influence cardiovascular disease presentation, diagnosis, treatment response, and outcomes, contributing to persistent health disparities. Despite this, gender-focused education remains inconsistently integrated into cardiovascular nursing curricula. Our aim, in this discussion paper was to examine the benefits and challenges of incorporating sex- and gender-focused care into cardiovascular nursing education and to highlight its role in improving clinical practice and promoting health equity. Integrating gender-focused education enhances nurses' ability to recognize both sex- and gender-specific differences, improves clinical decision-making, and supports more equitable care delivery. However, implementation is limited by curriculum constraints, lack of faculty expertise, and the risk of reinforcing stereotypes. Structured, evidence-based approaches are needed to ensure effective integration. Embedding sex- and gender-focused care into nursing education can improve diagnostic accuracy, optimize treatment strategies, and foster patient-centered and culturally responsive care. This approach is essential to reduce disparities and enhance outcomes in cardiovascular health.

Harassment, including sexual harassment, in the workplace poses a significant threat to workers' wellbeing and contributes to social inequities. Organizations play a pivotal role in both enabling and preventing workplace harassment. We use a grounded theory approach to understand how workers experience workplace sexual harassment. Drawing on semi-structured interviews with thirty U.S. workers, most from the service industry in the San Francisco Bay Area, who have experienced sexual harassment at work, we describe organizational practices that workers believe effectively prevent and respond to harassment. Findings demonstrate that workplaces may better support workers by (1) setting clear expectations that harassment will not be tolerated and (2) responding effectively to incidents of harassment by establishing an independent entity to whom victims can report incidents, providing verbal support, and taking appropriate actions to support and protect victims.

While exposure to individual non-essential metals (NEMs) links to abdominal obesity (AOB), the NEM mixture effects and mechanisms remain unclear, particularly in vulnerable aging populations. We included 3795 community-dwelling Chinese older adults (age ≥ 60 years), measured 6 urine NEMs [gallium (Ga), arsenic (As), cesium (Cs), barium (Ba), thallium (Tl), and uranium (U)] via ICP-MS, defined AOB by sex-specific waist circumference, assessed insulin resistance (IR) via triglyceride-glucose (TyG) index, and determined vitamin D status by serum 25-hydroxyvitamin D [25(OH)D]. Multivariable logistic regression, mixture models [weighted quantile sum (WQS), quantile g-computation (QGC), and Bayesian kernel machine regression (BKMR)], mediation and moderation analyses, and network toxicology analyses were performed. Multivariable logistic regression showed a positive association between urinary Tl and AOB (OR = 1.18, 95% CI: 1.05-1.32). Mixture analyses consistently revealed a significant overall effect of NEMs on AOB, with Tl identified as the primary contributor (WQS weight = 0.481; QGC weight = 0.428; conditional PIP = 0.918). The TyG index was identified as a potential mediator, accounting for 10.18-7.84% of the associations between Tl and AOB and the NEM mixture and AOB, respectively. Vitamin D sufficiency [serum 25(OH)D ≥ 75 nmol/L] significantly attenuated TyG index-AOB association. Network toxicology identified the AGE-RAGE signaling pathway and several hub genes as candidate biological pathways for future investigation of the association between NEM exposure and AOB. These findings highlight the metabolic implications of NEMs, particularly Tl, and suggest that Vitamin D sufficiency may influence metabolic responses associated with AOB, offering novel insights into AOB prevention in the context of NEMs exposure.

Acid-sensing ion channels (ASICs) are proton-gated members of the degenerin/epithelial sodium channel family that are emerging as multifaceted regulators of cardiovascular function. ASICs expressed in baroreceptor, cardiac, and skeletal muscle afferents contribute to reflex control of blood pressure, cardiac function, and sympathetic outflow. In vascular smooth muscle and endothelial cells, ASICs integrate mechanical, metabolic, and humoral signals to regulate vascular tone. In the systemic circulation, ASIC2 contributes to pressure-dependent vasoconstriction of renal and cerebral arteries, supporting blood flow autoregulation and protection against organ injury. In contrast, ASIC1a promotes vasodilation, contributing to nitric oxide-dependent dilation in the cerebral arteries and to endothelium-dependent hyperpolarization and vasodilation in mesenteric arteries. In the pulmonary vascular smooth muscle cells, ASIC1a plays a central role in acute hypoxic- and receptor-mediated vasoconstriction, a role that becomes increasingly important in chronic hypoxia-induced pulmonary hypertension. Under these conditions, metabolic reprogramming drives extracellular acidification and enhances ASIC1a trafficking to the plasma membrane, promoting sustained depolarization, augmented store-operated calcium entry, and a hyperproliferative, apoptosis-resistant smooth muscle phenotype. ASIC1a additionally regulates mitochondrial homeostasis by modulating mitochondrial membrane potential, redox balance, and apoptotic susceptibility. Chronic hypoxia redistributes ASIC1a from mitochondria to the plasma membrane, leading to mitochondrial dysfunction and cell survival signaling, key features of pulmonary vascular disease. This review summarizes current understanding of ASIC function in the systemic and pulmonary vasculature and highlights non-proton-mediated signaling mechanisms, emerging mitochondria-specific mechanisms, sex-related differences, and therapeutic opportunities and challenges in targeting ASIC-dependent signaling pathways in vascular disease.

The role of environmental factors in college students' learning adaptation has been widely examined. However, few studies have adopted a more micro-level perspective by focusing on the dormitory context to investigate the relationship between dormitory exclusion and learning adaptation, and its underlying mechanisms. This study investigates the chain mediating roles of loneliness and psychological distress in the relationship between dormitory exclusion and college students' learning adaptation, as well as the gender differences in these mediating pathways based on the Temporal Need-threat Model of Social Exclusion, Social Support Theory and Gender Role Theory. Using a convenience sampling method, 940 college students were surveyed using the dormitory exclusion scale, the loneliness scale, the depression-anxiety-stress scale, and the learning adaptation scale. The results showed that: (1) Dormitory exclusion significantly negatively predicted learning adaptation; (2) Dormitory exclusion predicted college students' learning adaptation through the single and chain mediation of loneliness and psychological distress; and (3) The chain mediation model exhibits gender differences. Specifically, for males, loneliness mediated the relationship between dormitory exclusion and learning adaptation; for females, loneliness and psychological distress serve as both independent mediators and sequential mediators in the relationship between dormitory exclusion and learning adaptation. The findings revealed the underlying mechanism of college students' dormitory exclusion and learning adaptation, providing valuable insights for interventions.

Sexing the skeletal remains of young individuals is crucial yet notoriously difficult in archaeology. Children, who cannot be reliably sexed morphologically, are often excluded from gender-related research, limiting our understanding of past childhood. This issue is compounded in contexts lacking grave goods, such as early Christian burials. We conducted genomic screening of 142 individuals from Sweden dating from the late Viking Age to the Medieval period, including 68 subadults and 74 adults from 27 single and 50 multiple burials. To investigate the treatment of children in death and the role of collective graves, we applied genomic sexing and kinship analyses to individuals from three sites. Contrary to the assumption that collective burials reflect close kinship, our results show that children interred with adults rarely shared close biological ties. Burial patterns indicate that gender roles were established early, with both boys and most girls mirroring adult spatial patterns. However, flexibility existed, and extended kinship likely played a central role in structuring these communities.

Dating violence is an important public health and psychosocial concern among young adults. Gender role attitudes may be associated with whether violent behaviors within intimate relationships are recognized, tolerated, or normalized. Evidence regarding gender differences and subscale-level associations between attitudes toward dating violence and gender role attitudes among university students remains limited. This study aimed to examine university students' attitudes toward dating violence and gender roles, compare total and subscale scores by gender, and investigate associations between the two constructs. This cross-sectional study included 1,866 students at a state university. Data were collected using a sociodemographic form, the Dating Violence Attitude Scale, and the Gender Roles Attitude Scale. Gender comparisons were performed using parametric or non-parametric tests as appropriate. Associations between attitudes toward dating violence, gender role attitudes, and age were analyzed using Spearman correlation coefficients. The observed Dating Violence Attitude Scale scores suggested relatively low reported acceptance of dating violence; however, this interpretation was descriptive because the scale has no established categorical cut-off point. Male students had higher total Dating Violence Attitude Scale scores than female students, indicating lower reported acceptance, although the effect was very small and was the only gender difference on this scale that remained significant after Bonferroni correction (r&#x2009;=&#x2009;0.06, p&#x2009;=&#x2009;0.006). Differences in physical and economic violence subscales did not remain significant after correction. Male students had higher total Gender Roles Attitude Scale scores and higher female, marital, traditional, and male gender role subscale scores, whereas female students had higher egalitarian gender role subscale scores. Total Dating Violence Attitude Scale and Gender Roles Attitude Scale scores were moderately and positively correlated (r&#x2009;=&#x2009;0.35, p&#x2009;<&#x2009;0.001). Gender role attitudes were associated with attitudes toward dating violence. Because of the cross-sectional and correlational design, these findings do not establish causal, predictive, or behavioral effects. Future longitudinal and experimental studies are needed to clarify the direction and practical relevance of these associations.

To explore how first-time fathers articulated their caregiving roles for preterm infants following admission to neonatal intensive care units (NICUs) and to identify the dominant discourses shaping their caregiving identities. A qualitative study informed by Fairclough's three-dimensional framework for critical discourse analysis, grounded in social constructivist and poststructuralist perspectives. Four focus group interviews were conducted with 17 Danish first-time fathers of preterm infants between October 2022 and January 2023. Transcripts were coded and thematized using an emic, data-driven approach. Fairclough's framework guided analysis at the textual, discursive, and social levels. Butler's theory of performativity informed interpretation of how fathers reproduced, reinforced, and challenged gender norms through caregiving practices and language use. Three themes were identified in the textual analysis: (1) first-time fathers' practical and emotional involvement in caregiving; (2) first-time fathers' expressions of protection and responsibility; and (3) shared parenting practices and negotiations of caregiving roles. These themes intersected with broader discourses: paternity leave, caregiving, the father's role, and gender roles. Fathers expressed strong emotional and practical engagement but were sometimes positioned as secondary caregivers by organizational routines. First-time fathers actively constructed identities as competent and involved caregivers while negotiating institutional and societal expectations. Findings highlight opportunities for neonatal nurses to foster father-inclusive, family-centered care by actively involving fathers in caregiving tasks and addressing implicit gender assumptions. Promoting inclusive caregiving cultures that recognize both parents as competent caregivers may advance gender equity and improve outcomes for preterm infants.

Women exhibit sex-specific differences in their responses to nicotine, with sex hormones like estrogen and progesterone playing key roles in nicotine addiction among women. Nicotine disrupts neuronal firing in the brain's reward system, an effect regulated by estrogen. In this study, we hypothesized that exposing human female neurons to both nicotine and estrogen would activate distinct signaling pathways. We treated human female SH-SY5Y neurons with nicotine and estrogen, and compared these to treatments with each substance alone or vehicle control. Using PamGene PamStation technology, we created an atlas of over 500 kinase activities per sample. We found that nicotine modulates MAP kinase pathways in a dichotomous manner. Estrogen showed unique kinase effects, and in combination with nicotine, elicited diverse pathway responses-some kinases becoming hyperactive and others hypoactive. Bioinformatics analysis highlighted several kinases as central to this combined signaling, including PKC&#x269; and TAO, which showed higher kinase activity only with combined treatment and have known links to behavior in rodent models. Conversely, kinases such as the insulin receptor (INSR), HER2, FAK1, and ABL1 exhibited decreased activity under combined treatment. These findings reveal nicotine-specific kinase mechanisms and suggest potential targets for pharmacotherapy aimed particularly at females with high estrogen levels and nicotine use disorder.

Few programs exist to train learners in advancing equity in perioperative care. In response, the UCSF Center for Health Equity in Surgery and Anesthesia (CHESA) launched the CHESA Fellowship in 2021. This 18-month, non-ACGME fellowship uses asynchronous modules, expert-led seminars, mentored research, and community building to equip fellows with the skills to advance perioperative equity worldwide. This report describes the fellowship's structure and evaluates its early impact on alumni career development. We conducted a mixed-methods fellowship evaluation comprising alumni and end-of-year surveys, focus groups, and a list of fellow-authored publications. Surveys assessed skill development, scholarly output, and satisfaction with curriculum elements. Qualitative data from focus groups were coded to highlight fellows' experiences and identify areas for improvement. Since 2021, CHESA has trained 80 fellows across 18 countries and 12 specialties; 71.3% are from LMICs and 48.8% are female. Surveys demonstrated strong satisfaction with faculty mentorship, project work, and community-building. Fellows reported acquiring skills in academic writing, mentorship, and leadership, with 53.8% developing new collaborations with co-fellows and 75.0% integrating fellowship learning into their clinical practice. Among alumni, 76.5% reported advancement into new leadership roles or clinical positions. Across cohorts, alumni published 364 manuscripts during or after the fellowship, with 58.8% focusing on health equity. Fellow and faculty feedback identified needs for enhanced research support and faculty development, which were incorporated into subsequent program iterations. The CHESA Fellowship offers an innovative model for building global perioperative leadership. The part-time, virtual format allows fellows to complete the program alongside clinical duties, while seed grants for LMIC fellows support locally driven scholarly projects. By prioritizing cross-border collaborations between fellows, building long-term partnerships with LMIC institutions, and ensuring diversity across geography, specialty, and sex, the fellowship balances accessibility with mentorship and community-building. Alumni report high satisfaction and translate their training into academic, clinical, and advocacy outcomes that advance perioperative equity.

Nearly all individuals with Down syndrome (DS) develop Alzheimer's disease (AD) dementia, primarily due to overexpression of the APP gene. Although specific cerebrospinal fluid (CSF) and plasma tau biomarkers have been investigated in DS-AD, how different tau species change in the DS-AD continuum in comparison to sporadic AD remains uncertain. In this cross-sectional study, we analysed CSF and plasma tau biomarkers in 461 samples from the DABNI and SPIN cohorts, including individuals with DS, cognitively normal euploid participants, and patients with sporadic AD. Biomarker differences were assessed using linear regression with Tukey post hoc comparisons. LOESS modelling was applied to estimate the age at which tau biomarkers became abnormal. We analysed 461 participants from the DABNI and SPIN cohorts. Both CSF and plasma tau biomarkers increased during the asymptomatic stages of DS and in euploid controls, coinciding with A&#x3b2; positivity; across the DS clinical spectrum the largest increases were observed for CSF NTA-tau (fold-change [fc] = 6.46-6.94), CSF p-tau217 (fc = 6.43-6.74) and plasma p-tau217 (fc = 4.63-6.54) (linear regression adjusted for age, sex and APOE-&#x3b5;4 with Tukey post-hoc tests; all p < 0.001). During the dementia stages, CSF tau biomarkers showed only modest further increases (no CSF biomarker differed between pDS and dDS; all p &#x2265; 0.268), whereas plasma tau biomarkers retained a broader dynamic range across symptomatic phases (pDS vs dDS: plasma p-tau217 p = 0.001, p-tau181 p = 0.002, p-tau231 p = 0.004). Plasma p-tau217 showed the highest diagnostic accuracy, with areas under the curve (AUC) of 0.91-0.97 for biological categorisations and numerically higher values than CSF in symptomatic stages (pDS vs dDS: plasma p-tau217 AUC = 0.69 [95% CI 0.58-0.80] vs CSF p-tau217 AUC = 0.53 [95% CI 0.41-0.65]; DeLong test p = 0.019). In LOESS analyses, tau biomarkers diverged from age-matched controls in the late 30s to early 40s (e.g., plasma p-tau217 &#x2248; 37.3 years, CSF p-tau181 &#x2248; 38.1 years) and reached abnormality (+2 SD) over an approximately 20-year span between the fourth and sixth decades, outlining differential but temporally compressed increases. Finally, during symptomatic stages, tau biomarker levels remained stable in DS-AD, in contrast to sporadic AD, where levels declined with advancing age. These findings highlight the complementary roles of CSF and plasma tau biomarkers in tracking disease progression: CSF biomarkers capture early pathological changes, whereas plasma biomarkers more effectively reflect disease progression within symptomatic stages. Furthermore, tau biomarkers might support disease staging and monitor clinical progression in DS-AD, but with the need to adapt biomarker frameworks to this specific population. La Caixa Foundation, Instituto de Salud Carlos III, Generalitat de Catalunya, National Institute on Ageing, Wellcome Trust, J&#xe9;r&#xf4;me Lejeune Foundation, Medical Research Council, Alzheimer's Association, National Institute for Health Research, EU Joint Programme-Neurodegenerative Disease Research, Alzheimer's Society.

The hypothalamic radial-glia-like tanycyte population plays important and intertwined roles in metabolism, reproduction, and seasonality. Although these processes are circadian-regulated, the role of the molecular clock in tanycytes themselves has not yet been examined. We report that clock genes cycle with much higher amplitude in ventral tanycytes compared to more dorsal ependymocytes and that adult, tanycyte-specific knockout of core clock gene Bmal1 reduces diet-associated weight gain and fat mass in female mice. Fate mapping studies show that female mice have higher baseline tanycyte-derived neurogenesis than males, with many of the resulting neurons localizing to the feeding-relevant arcuate nucleus. Female but not male mice show reduced tanycyte-derived arcuate neurogenesis after adult Bmal1 deletion, with an increased proportion of newborn neurons acquiring a feeding-suppressing POMC neuropeptidergic fate. Together, our data support a role for tanycyte BMAL1 as a sex-specific regulator of body composition and hypothalamic adult neurogenesis.

While dopamine is a monoamine neurotransmitter best known for its roles in reward, motivation, and motor function in the central nervous system, its actions extend beyond neurons and can influence non-neuronal cells via epigenetic mechanisms. An increasing body of literature demonstrates that dopamine signaling is important in immune cells, which express dopamine receptors (DRD1-DRD5) as well as the molecular machinery for dopamine synthesis and metabolism. Dopamine can regulate inflammatory activity, cell trafficking, and disease pathology, yet the epigenetic mechanisms underlying these effects remain poorly understood. Primary human monocyte-derived macrophages were treated with dopamine, and DNA methylation at the IL-1&#x3b2; proximal promoter was evaluated alongside IL-1&#x3b2; and epigenetic enzyme gene expression. Associations between donor characteristics, dopamine receptor expression, and dopamine-induced epigenetic responses were also examined. Dopamine increased DNA methylation at the IL-1&#x3b2; proximal promoter in a DNMT-dependent manner while concurrently increasing IL-1&#x3b2; gene expression. Dopamine treatment also upregulated the expression of several key epigenetic regulators, including TET2, HDAC2, and HDAC6, suggesting coordinated regulation of both DNA methylation and histone modifications that shape inflammatory transcription. Furthermore, baseline dopamine receptor expression and donor demographics, including sex and age, influence the magnitude of these epigenetic responses, highlighting inter-individual variability in macrophage sensitivity to dopaminergic signaling. These findings establish dopamine as a modulator of macrophage inflammation via epigenetic remodeling and provide a mechanistic framework for understanding how peripheral immune cells respond to dopaminergic cues. By linking dopamine signaling, epigenetic regulation, and innate immunity, this work identifies potential targets for therapeutic intervention and supports the use of accessible human immune cells to investigate dopaminergic dysregulation in neuroimmunological disorders.

Depressive disorders and obesity are highly comorbid conditions sharing genetic, metabolic, and immunological substrates. In a cross-sectional analysis of 53 participants across the obesity spectrum (lean n = 12; overweight n = 9; obese n = 32), a depression genetic risk score (d-GRS) correlated positively with BMI (&#x3c1; = 0.379, p = 0.005) and with serum CRP (&#x3c1; = 0.322, p = 0.031), consistent with the known genetic coarchitecture between depression and inflammatory traits. The d-GRS was tested against 116 flow-cytometry-derived immune parameters using Spearman rank correlation. The most consistent immune association at nominal significance (p < 0.05, uncorrected) involved the immunoregulatory CD56brightCD16- natural killer (NK) cell subset across two independent gate representations (&#x3c1; = 0.444, p = 0.004), remaining significant after sequential adjustment for BMI, sex, age, and physical activity (adjusted &#x3c1; range: 0.439-0.469), with no equivalent association for a genetically independent obesity GRS. In silico analysis of d-GRS SNP-tagged genes identified several with documented roles in NK cell trafficking, activation, and cytokine production, providing a putative mechanistic basis for this association. These findings nominate the CD56brightCD16- NK cell subset as a candidate immunological link between depression genetic susceptibility and neuroimmune mechanisms, warranting independent replication and functional characterisation in prospective cohorts.

Osteoarthritis (OA) is a highly heritable joint disease. Genome-wide association studies have linked single nucleotide polymorphisms (SNPs) within the collagen beta(1-O) galactosyltransferase 2 (COLGALT2) gene region, notably rs11583641 and rs1046934, to OA risk. Their roles in Chinese populations, clinical phenotypes, and gene expression remains unclear. This case-control study, 230 primary OA patients and 230 matched healthy controls were genotyped for rs11583641 and rs1046934 using the TaqMan assay. OA was diagnosed per American College of Rheumatology (ACR) and Kellgren-Lawrence (K-L) grading. Logistic regression assessed independent associations with OA. COLGALT2 expression in peripheral blood mononuclear cells (PBMC) was measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Allele and genotype distributions of rs11583641 and rs1046934 differed significantly between case and control groups (P<0.025). Multivariate regression adjusted for age, sex, and BMI showed that rs11583641 and rs1046934 remained associated with OA susceptibility (P<0.05). Cross-sectional subgroup analyses showed that rs11583641 polymorphism significantly associated with disease duration (P<0.025) and imaging severity (P<0.025). COLGALT2 expression was higher in OA patients than controls (P< 0.05). Its expression associated with risk genotypes, with the same trend at both loci: highest in rs11583641 CC and rs1046934 AA carriers, followed by CT and AC carriers, and lowest in TT and CC carriers. This study provides additional evidence supporting the association of COLGALT2 SNPs with OA susceptibility in a Chinese population. Cross-sectional subgroup analyses suggested that rs11583641 may be associated with severity-related clinical phenotypes. Increased PBMC COLGALT2 expression and its association with risk genotypes offer preliminary correlative evidence warranting further investigation, as these findings may be influenced by systemic inflammation, leukocyte composition, or other confounding factors. Further longitudinal and functional studies are required to clarify its clinical and biological significance. These findings provide additional insights into the genetic and molecular heterogeneity of OA.

Professor Carolyn S.P. Lam is a senior consultant cardiologist at the National Heart Centre Singapore, where she founded Singapore's first women's heart clinic, and a tenured full professor at Duke-NUS Medical School. She is co-founder of Us2.ai, an award-winning startup applying artificial intelligence to echocardiography, with regulatory clearance across more than 35 countries. Her research spans heart failure with preserved ejection fraction, sex differences in cardiovascular disease, and Asian heart failure phenotypes. She is principal investigator of the ASIAN-HF registry and chairs several large international trials, including SURMOUNT-MMO, LIBREXIA-AF, HF-POLARIS, and CASTLE-HFpEF. She is co-chair of the 2024 KDIGO Controversies Conference and a leading voice on women's heart health and AI-enabled cardiovascular care.

Human Pleural Mesothelioma (HPM) is an aggressive asbestos-related tumor with limited treatment options and a poor prognosis. MicroRNAs (miRNAs), known to play key roles in the pathogenesis of HPM, have emerged as promising candidates for both diagnostic and therapeutic applications. Among them, miR-197-3p has been previously identified as dysregulated in sera from HPM patients and workers ex-exposed to asbestos fibers. To investigate the functional role of miR-197-3p, loss- and gain-of-function studies were performed in HPM cell lines and human mesothelial cells (HMC) using miR-197-3p-specific antagomiR and mimic. The effects of miR-197-3p modulation on cell proliferation, viability, migration, and apoptosis were evaluated. In addition, bioinformatics analyses were performed to identify potential miR-197-3p target genes, which were subsequently evaluated at both mRNA and protein levels. MiR-197-3p tested significantly upregulated in HPM cells. Its inhibition led to a marked reduction of the HPM cell proliferation, whereas its overexpression in HMC promoted a proliferative phenotype, supporting a potential role in cell growth regulation. Among the predicted targets, TGF-&#x3b2;1 and p120 showed modulation at the mRNA level, although protein-level changes were limited or only partially consistent. These findings suggest that miR-197-3p may contribute to HPM pathogenesis by promoting cell proliferation and influencing critical molecular pathways. However, the underlying molecular mechanisms remain to be fully elucidated, and the interaction with candidate targets, such as TGF-&#x3b2;1 and p120, should be considered putative. Further investigations, including functional and mechanistic validation in more representative experimental models, will be required to clarify the role of miR-197-3p in HPM pathobiology.