Fine particulate matter (PM2.5) exposure and unfavourable lifestyle are both significant risk factors for mental health disorders, yet their combined effects on adolescent depression and anxiety remain poorly understood. This study aims to determine whether PM2.5 exposure and lifestyle are independently associated with adolescent depression and anxiety, and whether there are joint effects between these factors on mental health outcomes.

In this cross-sectional study, 19852 participants were analysed. PM2.5 concentrations were obtained from the ChinaHighAirPollutants (CHAP) dataset. Lifestyle factors were assessed through self-reported questionnaires, and a healthy lifestyle score was developed based on eight lifestyle risk factors. Depression and anxiety were assessed using the PHQ-9 and GAD-7 scales. Restricted cubic spline analysed dose–response relationships between PM2.5 exposure and mental health outcomes. The independent and joint effects were assessed using logistic regression models. Both multiplicative and additive interactions (relative excess risk due to interaction, RERI) were examined. Multiple classification approaches were incorporated to ensure robust results.

The study included 19852 participants with a mean age of 15.16 years (SD 1.60), comprising 9886 (49.8%) males and 9966 (50.2%) females. Depression and anxiety were identified in 3845 (19.37%) and 3230 (16.27%) participants, respectively. PM2.5 exposure showed a linear dose-response relationship with depression and anxiety. Joint effects analysis at the 75th percentile of PM2.5 with a lifestyle risk score of 4 revealed the strongest associations, with adjusted odds ratios of 4.49 (95% CI: 3.79–5.33) for depression, 4.01 (95% CI: 3.36–4.78) for anxiety and 4.24 (95% CI: 3.52–5.10) for their comorbidity. Simultaneously, significant additive interactions (RERI > 0) between high levels of PM2.5 exposure and unfavourable lifestyle factors were detected, suggesting synergistic effects on mental health outcomes. Subgroup and sensitivity analyses confirmed the robustness of these findings.

High PM2.5 exposure and unfavourable lifestyle factors demonstrated significant independent and joint effects on depression and anxiety among adolescents. These findings highlight that implementing stringent air pollution control measures, combined with promoting healthy lifestyle practices, may be crucial for protecting adolescent mental health.

The COVID-19 pandemic exacerbated psychological distress, but limited information is available on the shifts in mental health symptoms and their associated factors across different stages. This study was conducted to more reliably estimate shifts in mental health impacts and to identify factors associated with symptoms at different pandemic stages.

We performed a national repeated cross-sectional study at stable (2021), recurrence (2022), and end-of-emergency (2023) stages based on representative general national population with extensive geographic coverage. Anxiety, depression, post-traumatic stress disorder (PTSD) and insomnia symptoms were evaluated by GAD-7, PHQ-9, IES-R and ISI scales, respectively, and their associated factors were identified via multivariable linear regression.

Generally, 42,000 individuals were recruited, and 36,218, 36,097 and 36,306 eligible participants were included at each stage. The prevalence of anxiety, depression and insomnia symptoms increased from 13.7–16.4% at stable to 17.3–22.2% at recurrence and decreased to 14.5–18.6% at end of emergency, while PTSD symptom continuously increased from 5.1% to 7.6% and 9.2%, respectively (all significant, P < 0.001). Common factors associated with mental health symptoms across all stages included centralized quarantine, frontline work and residence in initially widely infected areas. Centralized quarantine was linked to anxiety, depression, PTSD and insomnia during the stable, recurrence and end-of-emergency stages. Frontline workers exhibited higher risks of anxiety, depression and insomnia throughout these stages. Individuals in initially widely infected areas were more likely to experience depression and PTSD, particularly during the stable and recurrence stages. Stage-specific risk factors were also identified. Lack of outdoor activity was associated with anxiety, depression and insomnia during the stable and recurrence stages. Residents in high-risk areas during the recurrence stage correlated with increased anxiety and insomnia. Suspected infection was tied to anxiety and insomnia in the recurrence and end-of-emergency stages, while the death of family or friends was linked to PTSD during recurrence and to depression, PTSD and insomnia at the end-of-emergency stage.

Mental health symptoms increased when pandemic recurred, and could remain after end-of-emergency, requiring prolonged interventions. Several key factors associated with mental symptoms and their variations were identified at different pandemic stages, suggesting different at-risk populations.

Schizophrenia progresses through high-risk, first-episode, and chronic stages, each associated with altered spontaneous brain activity. Resting state functional MRI studies highlight these changes, but inconsistencies persist, and the genetic basis remains unclear.

A neuroimaging meta-analysis was conducted to assess spontaneous brain activity alterations in each schizophrenia stage. The largest available genome-wide association study (GWAS) summary statistics for schizophrenia (N = 53,386 cases, 77,258 controls) were used, followed by Hi-C-coupled multimarker analysis of genomic annotation (H-MAGMA) to identify schizophrenia-associated genes. Transcriptome-neuroimaging association and gene prioritization analyses were performed to identify genes consistently linked to brain activity alterations. Biological relevance was explored by functional enrichment.

Fifty-two studies met the inclusion criteria, covering the high-risk (Nhigh-risk = 409, Ncontrol = 475), first-episode (Ncase = 1842, Ncontrol = 1735), and chronic (Ncase = 1242, Ncontrol = 1300) stages. High-risk stage showed reduced brain activity in the right median cingulate and paracingulate gyri. First-episode stage revealed increased activity in the right putamen and decreased activity in the left gyrus rectus and right postcentral gyrus. Chronic stage showed heightened activity in the right inferior frontal gyrus and reduced activity in the superior occipital gyrus and right postcentral gyrus. Across all stages, 199 genes were consistently linked to brain activity changes, involved in biological processes such as nervous system development, synaptic transmission, and synaptic plasticity.

Brain activity alterations across schizophrenia stages and genes consistently associated with these changes highlight their potential as universal biomarkers and therapeutic targets for schizophrenia.

Antimicrobial resistance (AMR) is a global health crisis exacerbated by policies like China’s Volume-Based Procurement (VBP), which may inadvertently increase antimicrobial overuse. This study evaluates a clinical pharmacist-led Antimicrobial Stewardship (AMS) program with prospective audit for special-restricted antimicrobials under VBP.

A retrospective quasi-experimental interrupted time-series analysis compared pre-intervention (2022) and post-intervention (2023–2024) data at Tongji Hospital, a tertiary hospital in Wuhan, China. Key metrics included Antimicrobial Use Density (AUD), prescription rationality, antimicrobial costs, and multidrug-resistant infection rates.

The intervention significantly improved prescription appropriateness for special-restricted antimicrobials (80.24% vs. 93.83%, P < 0.005) and reduced AUD (47.87 vs. 34.25, P < 0.001). Total antimicrobial costs decreased by 41.26%, with a reduction in the incidence of multidrug-resistant infections from 0.084% to 0.062% (P < 0.05). Carbapenem use correlated with CRKP isolation rates (R = 0.62, P < 0.05). Clinical pharmacists rejected 10.24% of prescriptions, all accepted by physicians.

Pharmacist-led prospective audits optimize antimicrobial use under VBP, mitigate resistance risks, and reduce costs, while acknowledging that concurrent infection control measures may have contributed to these trends. This model may inform similar interventions in other institutions, particularly those in resource-limited settings.

Little is known regarding the shared genetic architecture underlying the phenotypic associations between depression and preterm birth (PTB). We aim to investigate the genetic overlap and causality of depression with PTB.

Leveraging summary statistics from the largest genome-wide association studies for broad depression (Ntotal = 807,533), major depression (Ntotal = 173,005), bipolar disorder (Ntotal = 414,466), and PTB (Ntotal = 226,330), we conducted a large-scale genome-wide cross-trait analysis to assess global and local genetic correlations, identify pleiotropic loci, and infer potential causal relationships

Positive genetic correlations were observed between PTB and broad depression (rg = 0.242), major depression (rg = 0.236), and bipolar disorder (rg = 0.133) using the linkage disequilibrium score regression, which were further verified by the genetic covariance analyzer. Local genetic correlation was identified at chromosome 11q22.3 (harbors NCAM1-TTC12-ANKK1-DRD2) for PTB with depression. Cross-trait meta-analysis identified two loci shared between PTB and broad depression, two loci shared with major depression, and five loci shared with bipolar disorder, among which three were novel (rs7813444, rs3132948 and rs9273363). Mendelian randomization demonstrated a significantly increased risk of PTB for genetic liability to broad depression (odds ratio [OR]=1.30; 95% confidence interval [CI]: 1.11-1.52) and major depression (OR=1.27; 95%CI: 1.08-1.49), and the estimates remained significant across the sensitivity analyses.

Our findings demonstrate an intrinsic link underlying depression and PTB and shed novel light on the biological mechanisms, highlighting an important role of early screening and effective intervention of depression in PTB prevention, and may provide novel treatment strategies for both diseases.

MicroRNAs (miRNAs) alterations in patients with bipolar disorder (BD) are pivotal to the disease’s pathogenesis. Since obtaining brain tissue is challenging, most research has shifted to analyzing miRNAs in peripheral blood. One innovative solution is sequencing miRNAs in plasma extracellular vesicles (EVs), particularly those neural-derived EVs emanating from the brain.

We isolated plasma neural-derived EVs from 85 patients with BD and 39 healthy controls (HC) using biotinylated antibodies targeting a neural tissue marker, followed by miRNA sequencing and expression analysis. Furthermore, we conducted bioinformatic analyses and functional experiments to delve deeper into the underlying pathological mechanisms of BD.

Out of the 2,656 neural-derived miRNAs in EVs identified, 14 were differentially expressed between BD patients and HC. Moreover, the target genes of miR-143-3p displayed distinct expression patterns in the prefrontal cortex of BD patients versus HC, as sourced from the PsychENCODE database. The functional experiments demonstrated that the abnormal expression of miR-143-3p promoted the proliferation and activation of microglia and upregulated the expression of proinflammatory factors, including IL-1β, IL-6, and NLRP3. Through weighted gene co-expression network analysis, a module linking to the clinical symptoms of BD patients was discerned. Enrichment analyses unveiled these miRNAs’ role in modulating the axon guidance, the Ras signaling pathway, and ErbB signaling pathway.

Our findings provide the first evidence of dysregulated plasma miRNAs within neural-derived EVs in BD patients and suggest that neural-derived EVs might be involved in the pathophysiology of BD through related biological pathways, such as neurogenesis and neuroinflammation.

Social determinants of health (SDHs) exert a significant influence on various health outcomes and disparities. This study aimed to explore the associations between combined SDHs and mortality, as well as adverse health outcomes among adults with depression.

The research included 48,897 participants with depression from the UK Biobank and 7,771 from the US National Health and Nutrition Examination Survey (NHANES). By calculating combined SDH scores based on 14 SDHs in the UK Biobank and 9 in the US NHANES, participants were categorized into favourable, medium and unfavourable SDH groups through tertiles. Cox regression models were used to evaluate the impact of combined SDHs on mortality (all-cause, cardiovascular disease [CVD] and cancer) in both cohorts, as well as incidences of CVD, cancer and dementia in the UK Biobank.

In the fully adjusted models, compared to the favourable SDH group, the hazard ratios for all-cause mortality were 1.81 (95% CI: 1.60–2.04) in the unfavourable SDH group in the UK Biobank cohort; 1.61 (95% CI: 1.31–1.98) in the medium SDH group and 2.19 (95% CI: 1.78–2.68) in the unfavourable SDH group in the US NHANES cohort. Moreover, higher levels of unfavourable SDHs were associated with increased mortality risk from CVD and cancer. Regarding disease incidence, they were significantly linked to higher incidences of CVD and dementia but not cancer in the UK Biobank.

Combined unfavourable SDHs were associated with elevated risks of mortality and adverse health outcomes among adults with depression, which suggested that assessing the combined impact of SDHs could serve as a key strategy in preventing and managing depression, ultimately helping to reduce the burden of disease.