Schools are critical settings for supporting student mental health; research is needed to identify key levers for addressing the impact of Adverse Childhood Experiences (ACEs) on students' relationships.

Drawing on survey data from rural high school students (N = 2902), we examine the associations between ACEs scores and multiple developmental relationships (parenting adults, teachers, peers, neighbors, program leaders). School-level engagement and support, and teacher relationships were also examined as potential protective factors.

Higher ACEs scores were associated with weaker developmental relationships across all groups. However, positive relationships with teachers and supportive school engagement and support slightly moderated the negative influence of ACEs on youths' relationships with parenting adults.

District and school leaders should support educators in building strong relationships with students by protecting their capacity, providing trauma-informed professional development, and ensuring access to mental health services for students and staff.

Building strong relationships with teachers and fostering a supportive and engaging school environment can be key strategies for buffering the risks associated with adversity and ultimately supporting young people's development of strong, healthy relationships.

Periodontitis, a chronic inflammatory disease, is increasingly prevalent among young people and impairs their quality of life. Adverse childhood experiences (ACE), depressive symptoms, and suboptimal health status (SHS) are linked to health risks and chronic diseases, but their interrelationships with periodontitis in Chinese young adults remain unclear. This study aimed to explore associations among these factors.

From December 2024 to May 2025, 2,888 participants (aged 18-35) from Tongji Hospital completed surveys on demographics, ACE, depressive symptoms, and SHS. Periodontitis was diagnosed according to the 2018 criteria. Simple, parallel, and chain mediation models were used, controlling for age, sex, marital status, and smoking.

Periodontitis prevalence was 25.00% and higher in married individuals (P < 0.001) and smokers (P = 0.004). ACE correlated positively with depressive symptoms (r = 0.28, P < 0.001), SHS (r = 0.19, P < 0.001), and periodontitis (r = 0.16, P < 0.001). Mediation analyses showed: Simple model: Depressive symptoms and SHS partially mediated the effect of ACE on periodontitis (indirect effect = 0.011 for both). Parallel model: Only SHS significantly mediated the effect (indirect effect = 0.011). Chain model: ACE was related to periodontitis via "depressive symptoms → SHS" (indirect effect = 0.010), with significant direct and indirect effects.

ACE associated with higher periodontitis risk in young people. This association included both a direct link between ACE and periodontitis, and an indirect link through the chain pathway of "depressive symptoms → SHS"; among these pathways, SHS was a key mediator.

The study was registered in the Chinese Clinical Trial Registry (ChiCTR) with the registration number ChiCTR2500103464.

Incarcerated populations face greater health challenges, including higher rates of communicable and mental diseases. However, traditional health measures like disease prevalence and life expectancy do not capture their physical, mental, emotional, and social well-being. This scoping review will summarize the health-related quality of life (HRQoL) outcomes in incarcerated populations using preference-based HRQoL instruments (and measures that can be used to derive utility scores), providing insights for health policies and economic evaluations.

A scoping review was conducted following PRISMA-ScR guidelines. Six electronic databases and three health technology assessment agencies were searched for peer-reviewed studies reporting preference-based HRQoL or HRQoL scores that can be used to generate health state utility values in incarcerated populations. Eligibility and data extraction were performed by two independent researchers.Findings were synthesized to identify knowledge gaps.

Twenty-two articles met the inclusion criteria, primarily focusing on male and white populations. Ten studies targeted disease-specific populations, with mental health disorders (n = 7) being the most prevalent. Across studies, inmates generally reported lower HRQoL scores than the general population, especially those with mental health issues. Female and Indigenous inmates had lower HRQoL scores than male and non-Indigenous inmates.

The variety in HRQoL instruments used, with each assessing different domains, hinders direct comparisons between studies. Validating instruments specific to incarcerated populations may be needed for future research. Overall, incarcerated populations, especially women and Indigenous inmates, demonstrate poorer HRQoL than the general population. There is a need for more diverse, inclusive studies to address these gaps.

Diabetes mellitus is a rapidly growing global health challenge and a major driver of atherosclerotic cardiovascular disease (ASCVD). Dyslipidaemia, highly prevalent in both type 1 and type 2 diabetes, plays a central role in this excess cardiovascular risk and often persists despite statin therapy. Although statins remain the cornerstone of lipid management, many patients with diabetes do not achieve recommended low-density lipoprotein cholesterol (LDL-C) goals. Therefore, there is a need for effective, safe, and practical adjunctive therapies. Bempedoic acid is a first-in-class oral ATP-citrate lyase inhibitor with liver-specific activation, resulting in significant LDL-C reduction without relevant muscle-related adverse effects. Across clinical trials, including the CLEAR programme, bempedoic acid has demonstrated consistent LDL-C lowering, as well as reductions in apolipoprotein B and non-HDL-C, and favourable effects on the inflammatory marker high-sensitivity C-reactive protein (hs-CRP), with similar efficacy in patients with and without diabetes. Importantly, the CLEAR Outcomes trial showed a significant reduction in major adverse cardiovascular events in statin-intolerant patients, almost half of whom had diabetes, without adverse effects on glycaemic control. This article summarises the evidence supporting the use of bempedoic acid in people with diabetes, proposes its therapeutic positioning within contemporary lipid-lowering algorithms, and highlights its role as an effective oral option, aiming to provide practical and nationally relevant guidance for lipid management in people with diabetes. By helping to reduce residual cardiovascular risk and bridge treatment gaps in patients who may not be eligible for or have access to PCSK9 inhibitors, bempedoic acid represents a valuable addition to personalised lipid management strategies aimed at lowering cardiovascular morbidity and mortality in this high-risk population.

Diabetic foot ulcer (DFU) is a severe complication of diabetes mellitus characterized by impaired wound healing and high amputation risk. Current treatments remain unsatisfactory, necessitating exploration of novel molecular mechanisms. The transcription factor CCAAT enhancer binding protein delta (CEBPD) regulates inflammatory responses and cellular stress pathways implicated in diabetic complications. However, its specific role and mechanism in DFU pathogenesis are poorly understood. Human umbilical vein endothelial cells (HUVECs) were exposed to high glucose (HG) to mimic diabetic conditions. C-X-C motif chemokine ligand 10 (CXCL10) and CEBPD mRNA expression were analyzed by quantitative real-time polymerase chain reaction. The protein expression of CXCL10, CEBPD, and glutathione peroxidase 4 (GPX4) was detected by western blotting assay. Cell viability was analyzed by a cell counting kit-8 assay. Cell proliferation was analyzed by a 5-ethynyl-2'-deoxyuridine assay. Cell apoptosis was detected by flow cytometry. Cell migration was analyzed by a wound-healing assay. Tube formation was analyzed by a tube formation assay. Fe²⁺ and malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity were analyzed by colorimetric assays. Reactive oxygen species (ROS) levels were analyzed by fluorometric assay and flow cytometry. The chromatin immunoprecipitation (ChIP) assay and dual-luciferase reporter assay were used to analyze the association of CXCL10 and CEBPD. The effect of CEBPD knockdown on HG-induced cell injury was further analyzed using a DFU rat model. CXCL10 and CEBPD expression were significantly upregulated in DFU patients and HG-stimulated HUVECs. CXCL10 knockdown reversed HG-induced cellular damage, restoring proliferation, migration, and tube formation while suppressing apoptosis and altering ferroptosis-related indicators (evidenced by reduced Fe²⁺/MDA/ROS and elevated SOD/GPX4). Crucially, CEBPD transcriptionally activated CXCL10, confirmed by promoter binding (ChIP) and luciferase activity. Silencing CEBPD replicated the protective effects of CXCL10 knockdown, and CXCL10 overexpression attenuated CEBPD knockdown-induced effects in HG-treated HUVECs. In vivo, CEBPD knockdown accelerated diabetic wound closure in rats, enhancing collagen deposition and tissue regeneration. CEBPD exacerbated human umbilical vein endothelial cell dysfunction at least partly through the transcriptional regulation of CXCL10, and CEBPD knockdown accelerated diabetic wound healing in vivo, suggesting that targeting the CEBPD/CXCL10 interplay may serve as a potential therapeutic strategy for DFU.

To examine the role of maternal lipid metabolism before and during pregnancy in the development of gestational diabetes mellitus, and to evaluate its clinical implications for maternal and offspring outcomes.

Shifts in lipid metabolism represent key physiologic adaptations of pregnancy, and, when dysregulated, may contribute to the pathogenesis of gestational diabetes. Lipid abnormalities typically precede conception, underscoring a continuum between pre-pregnancy metabolic health and pregnancy outcomes. Low HDL-C, elevated triglycerides, and small dense LDL-C particles have been repeatedly associated with increased gestational diabetes risk across several cohorts and meta-analyses, although the strength of these associations varies according to study design and population characteristics. During pregnancy, women with gestational diabetes display a reproducible lipid phenotype defined by higher triglycerides, lower HDL-C, and increased triglycerides/HDL-C ratios. These perturbations exacerbate insulin resistance, trigger inflammatory and oxidative stress pathways, and act as contributors to disease progression rather than secondary consequences of hyperglycemia. Clinically, maternal dyslipidemia has been associated with adverse outcomes including pre-eclampsia, gestational hypertension, severe hypertriglyceridemia-related pancreatitis, and neonatal complications such as macrosomia, large-for-gestational-age birth weight, and preterm delivery. Beyond pregnancy, lipid disturbances have been linked to unfavourable cardiometabolic trajectories in the offspring, suggesting transgenerational effects.

Integrating mechanistic and clinical evidence, this review emphasizes the need for early lipid assessment, personalized nutritional counseling, and targeted interventions alongside glucose-centered care to improve maternal and offspring outcomes.

In patients presenting with intestinal symptoms who undergo colonoscopy with mucosal sampling, the pathologist plays a central role in identifying the underlying etiology in order to guide appropriate clinical management. However, common intestinal symptoms such as diarrhea are shared by a broad spectrum of conditions, including infectious diseases, functional disorders (e.g., irritable bowel syndrome), inflammatory bowel disease (IBD), drug-induced injury, and metabolic disorders (e.g., diabetes mellitus). Although serological biomarkers may support the diagnostic workup, they are frequently insufficient to establish a definitive diagnosis. Moreover, endoscopic examination may fail to detect significant mucosal abnormalities even when histology reveals disease-specific patterns, as occurs in lymphocytic and collagenous colitis (i.e., microscopic colitis). In this complex diagnostic landscape, histomorphological evaluation represents a crucial element, allowing integration of microscopic findings with clinical and endoscopic data to reach an accurate interpretation. In recent years, accumulating evidence has demonstrated that similar histological patterns of intestinal injury-such as IBD-like architectural and inflammatory changes or eosinophil-rich infiltrates-may be associated with different underlying etiologies. This overlap is particularly relevant in patients treated with novel oncologic therapies, including tyrosine kinase inhibitors (TKIs), immune checkpoint inhibitors (ICIs), and emerging treatments such as chimeric antigen receptor T-cell (CAR-T) therapy. In addition, in daily practice, pathology request forms often lack essential clinical, endoscopic, and laboratory information, further increasing the risk of diagnostic misinterpretation and inappropriate disease attribution. To address these challenges, the Italian Group of Digestive Disease Pathology (GIPAD) proposes a pattern-based histological approach for reporting mucosal damage in patients with colitis. In this first paper, we focus on non-chronic patterns of mucosal injury and discuss their principal differential diagnoses, with the aim of supporting standardized reporting and improving clinicopathological correlation.

Given the differences between Chinese T2DM patients and those of other ethnicities, understanding the metabolic contributions in this population is essential. This study aimed to identify T2DM-associated metabolic biomarkers through clinical untargeted metabolomics and mendelian randomization (MR).

This study included 120 Chinese participants, including 60 patients with T2DM and 60 control subjects. We employed ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) for non-targeted metabolomics analysis of plasma metabolites. Orthogonal partial least squares discriminant analysis (OPLS-DA) was used to identify T2DM-related metabolites. Integration of metabolomics and MR data identified novel key biomarkers for T2DM.

LC-MS/MS-based untargeted metabolomics identified 71 up-regulated and 37 down-regulated metabolites in the Chinese T2DM patients. In MR analysis, 52 metabolites exhibited causal associations with the risk of T2DM. Integrating metabolomic analysis with genetic evidence-based causal inference collectively confirmed that higher adrenic acid (AdA) were associated with increased risk of T2DM and positively correlated with fasting blood glucose (FBG). The main metabolic impacted pathways were unsaturated fatty acids biosynthesis, linoleic acid metabolism.

Increased plasma AdA level was associated with higher FBG and an elevated risk of T2DM, suggesting that AdA represents a probable biomarker for T2DM.

To examine postural control in people with type 2 diabetes mellitus (T2DM) with and without diabetic neuropathy (DN) using center of pressure (CoP) measures under varying sensory and cognitive conditions.

In this cross-sectional study, adults aged ≥ 40 years with T2DM for at least one year. Neuropathy was classified as severe peripheral neuropathy (DPN) or autonomic neuropathy (DAN), defined by vibration perception threshold ≥ 50 V, ≥2 abnormal cardiac autonomic reflex tests, or orthostatic hypotension. Postural control was assessed by CoP^Area and CoP^Velocity under different sensory and cognitive conditions. Regression analyses were adjusted for demographic factors, physical performance, and fall-associated medication. Exploratory analyses were performed by neuropathy subtype.

99 participants were included, 49 with DN and 50 without. The DN group was older (66.8 vs. 60.8 years) and more often male (75.5% vs. 52%). DN was associated with greater CoP^Area (β = 0.56, p = 0.006). Exploratory analyses suggested larger CoP^Area in participants with DAN alone (β = 0.76, 95% CI 0.36-1.16) or combined with DPN (β = 0.70, 95% CI 0.13-1.34), whereas DPN alone was not associated with CoP^Area.

DN was linked to impaired postural control, with indications of differences by neuropathy subtype. CoP assessment may help identify people with T2DM at increased risk of falls.

Diabetic wounds are a common complication and a debilitating condition of diabetes mellitus, which are characterized by chronic inflammation, persistence, and aggravation. Evidence suggests the beneficial influence of Loganin on diabetic complications and inflammation. However, the effectiveness of Loganin on diabetic wounds remains uninvestigated.

Network pharmacology was applied to identify the potential targets of Loganin in diabetic wound healing. Employing a streptozotocin (STZ)-induced diabetic mouse model, we conducted evaluations pertaining to the effects of Loganin on wound healing and assessment of macrophage-related phenotypes via ELISA, immunohistochemistry, Western blot and qPCR. In vitro, we used J774A.1 mouse macrophage cell line and induced differentiated Th17 cells for experiments. Molecular docking, biotin-labeled pull-down assays and cellular thermal shift assays were applied to investigate direct mechanisms.

Loganin topical application accelerated wound healing in diabetic mice, reduced local inflammation, and inhibited NLRP3 inflammasome activation. The IL-17/NF-κB signaling pathway was suppressed by Loganin, thus inhibiting NLRP3 inflammasome. In particular, Loganin inhibited IL-17 A/F production in Th17 cells and targeted the NF-κB p50 subunit in macrophages, thus blocking its nuclear translocation and pro-inflammatory activation.

Loganin may be considered as an adjuvant or a new therapeutic agent in the management of chronic non-healing diabetic wounds.