Although extensive research has been conducted on the impact of the COVID-19 pandemic on global mental health, a systematic synthesis of the cross-time dynamics of suicidal ideation (SI) remains lacking. This study aims to systematically synthesise the global aggregated prevalence of SI before and after the pandemic, investigate the potential association between pandemic exposure and the SI risk through meta-regression analysis of longitudinal studies, and explore key moderating factors.

A systematic search was conducted in Web of Science, PubMed, PsycINFO and ProQuest databases up to August 2025. Observational studies were included if they employed cross-sectional or longitudinal designs and reported the prevalence of SI before and after the pandemic across global regions.

The analysis included 354 cross-sectional studies (N = 8,247,875) and 27 longitudinal studies. In cross-sectional studies, the pooled prevalence of SI was 13.20% [95% CI 12.06%–14.42%]. Pre-pandemic prevalence was 12.52% [95% CI 8.46%–18.14%], and post-pandemic prevalence was 13.24% [95% CI 12.07%–14.50%], with no significant difference. Meta-regression analysis identified three moderators. Specifically, larger sample sizes (n) were associated with lower prevalence (β = −0.232, P < 0.0001); higher study quality predicted lower prevalence (β = −0.278, P < 0.001); and studies on adults reported significantly lower prevalence than adolescents (β = −0.366, P < 0.05). Conversely, time progression during the pandemic, development level, geographical area, gender and measurement method did not show significant independent effects. Interaction analyses also found no significant moderating effect of economic development level or geographical area on the temporal trend of SI prevalence. Longitudinal analysis found no significant increase in prevalence from the pre-pandemic to the post-pandemic period (P = 0.101). However, a small but significant increase occurred between early and late stages within the pandemic (β = 0.265, P = 0.021). Subgroup analyses showed no significant moderation of these temporal changes.

The COVID-19 pandemic’s impact on SI was dynamic. While no significant prevalence change was found between pre- and post-pandemic periods, a significant increase occurred as the crisis progressed. This deteriorating trend was more pronounced in adolescents, identifying them as a key vulnerable group. Methodologically, findings were moderated by the measurement instrument, study quality and sample size, with evidence suggesting potential small-study effects. These findings underscore the need for robust mental health surveillance and targeted interventions for at-risk populations during prolonged public health crises.

The protocol was registered on PROSPERO (CRD42024603151).

Cognitive impairment in major depressive disorder (MDD) may be driven by neuro-inflammatory processes involving pro-inflammatory cytokines.

This study aimed to examine the relationship between serum tumour necrosis factor-alpha (TNF-α) levels and cognitive performance across different domains in individuals with MDD.

Sixty patients with MDD and 60 healthy controls were recruited. Cognitive function was assessed using the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), and serum TNF-α levels were measured via flow cytometry.

After adjusting for covariates, RBANS total and subscale scores were significantly lower in MDD patients compared with controls (P < 0.001), while log10-transformed TNF-α levels were significantly higher in the MDD group (P = 0.006). In MDD patients, log10TNF-α levels were inversely correlated with immediate memory scores after adjusting for confounding factors (r = −0.35, P = 0.009); however, this relationship was not observed in healthy controls (r = −0.02, P = 0.90). Stepwise multivariate regression analysis further confirmed the negative association of log10TNF-α with immediate memory scores in MDD patients (β = −14.58, t = −4.14, P < 0.001), but not in healthy controls (β = −0.02, t = −0.14, P = 0.89).

These findings suggest that elevated serum TNF-α may contribute to the pathophysiology of MDD and is specifically associated with deficits in immediate memory.

Accurate and up-to-date epidemiological data on the prevalence and treatment of common mental disorders are essential for evidence-based healthcare policy and resource allocation. However, large-scale, representative epidemiological surveys on common mental disorders in China—particularly those incorporating insomnia disorder and applying the latest diagnostic criteria alongside validated assessment tools—remain notably lacking.

We conducted a population-based, cross-sectional epidemiological survey to assess the prevalence and treatment of common mental disorders among adults in Beijing, China, using a multistage clustered probability sampling design (n = 10,778). Licensed psychiatrists administered standardized diagnostic interviews based on DSM-5 criteria to assess both lifetime and current mental disorders through a single-stage assessment protocol.

Among all lifetime mental disorders assessed, depressive disorders constituted the most prevalent diagnostic category (7.7%), with major depressive disorder representing the most common specific diagnosis (5.4%). Individuals aged 65 years and older exhibited significantly higher 1-month prevalence of both depressive disorders and insomnia disorder compared with younger age groups. Alcohol-related disorder was more prevalent in men than in women, and in urban residents than in rural residents. Help-seeking patterns revealed a predominant reliance on informal support over professional services among individuals with lifetime mental disorders. Only 13.4% sought help from mental health professionals, and 12.7% received mental health professional treatment.

The improved access to treatment did not translate into a reduction in population-level mental disorder prevalence, which may be attributable to the low rate of professional mental health treatment. Governments must optimize mental healthcare access.

To investigate the association of midlife and late-life undiagnosed mood symptoms, especially their comorbidity, with long-term dementia risk among multi-regional and ethnic adults.

The prospective study used data from the UK Biobank (N = 142,670; mean follow-up 11.0 years) and three Asian studies (N = 1,610; mean follow-up 4.4 years). Undiagnosed mood symptoms (manic symptoms, depressive symptoms and comorbidity of depressive and manic symptoms) and diagnosed mood disorders (depression, mania and bipolar disorders) were classified. Plasma levels of 168 metabolites were measured. The association between undiagnosed mood symptoms and 12-year dementia (including subtypes) risk and domain-specific cognitive function was examined. The contribution of metabolites in explaining the association between symptom comorbidity and dementia risk was estimated.

Undiagnosed mood symptoms were prevalent (11.4% in the UK cohort and 31.2% in Asian cohorts) among 1,462 (1.0%) and 74 (19.4%) participants who developed dementia. Comorbidity of undiagnosed mood symptoms was associated with higher dementia risk (sub-distribution hazard ratios = 9.46; 95% confidence interval = 4.07–21.97), especially Alzheimer’s disease, and with worse reasoning ability, poorer numeric memory and metabolic dysfunction. Glucose and total Esterified Cholesterol explained 9.1% of the association between symptom comorbidity and dementia, with most of the contribution being from glucose (6.8%).

Comorbidity of undiagnosed mood symptoms was associated with a higher cumulative risk of dementia in the long term. Glucose metabolism could be implicated in the development of mood disorders and dementia. The distinctive pathophysiological mechanism between psychiatric and neurodegenerative disorders warrants further exploration.

Mitochondrial dysfunction has been implicated in the pathogenesis of major depressive disorder (MDD); however, the causal contributions of specific mitochondrial genes across regulatory layers remain unclear.

We integrated genome-wide association study summary statistics from the Psychiatric Genomics Consortium and FinnGen with quantitative-trait-locus (QTL) datasets for DNA methylation, gene expression (eQTL), and protein abundance. Mitochondrial genes were annotated using the MitoCarta3.0 database. Summary-based Mendelian randomization and Bayesian colocalization were applied to assess causal relationships, with colocalization determined by the posterior probability of a shared causal variant (PPH4), and the false discovery rate used for multiple-testing correction. Brain-specific effects were evaluated using Genotype-Tissue Expression eQTL data. Prioritized genes were ranked based on cross-omics consistency and replication evidence.

Five mitochondrial genes were prioritized. TDRKH showed consistent associations across methylation, transcription, and protein levels, with hypermethylation at cg24503712 linked to reduced expression and a lower risk of MDD (Tier 1). METAP1D (Tier 2) demonstrated protective effects at both the transcript and protein levels. LONP1, FIS1, and SCP2 (Tier 3) exhibited consistent but complex regulatory patterns. Several signals were replicated in brain tissues, including TDRKH in the caudate and METAP1D in the cortex.

This study provides multi-omics evidence for the causal involvement of mitochondrial genes in MDD. TDRKH and METAP1D emerged as key candidates, offering promising targets for future mechanistic research and therapeutic development.

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.

Clinical outcomes of a standardised enhanced recovery after surgery protocol, including thoracic epidural analgesia, were studied in children undergoing trans-atrial cardiac surgery via the right mid-axillary thoracotomy approach.

This single-centre retrospective study examined 42 paediatric patients who underwent trans-atrial cardiac surgeries via the mid-axillary approach (2018 to 2020), of whom 30 received epidural catheters. The standardised enhanced recovery after surgery protocol included transesophageal echo-guided thoracic epidural catheter placement, multimodal analgesia, reduced opioid use, and planned early extubation and discharge. Clinical outcomes assessed included extubation times, postoperative analgesic requirements, ICU pain scores, hospital length of stay, and any complications related to regional anaesthesia or surgery.

Thirty patients received an epidural placed between the third and sixth thoracic interspace levels under transesophageal ultrasonography guidance. The median age was 42 months (range 3–156), and the median weight was 15.7 kg (range 4.9–61 kg). Epidural infusions were continued for a median of 52 hours postoperatively. The intraoperative fentanyl usage was a median of 4.5 mcg/kg (interquartile range (IQR) 2–9). Intraoperative extubation was achieved in 28 of the 30 patients. Median post-extubation pain scores in the first 6 and 12 hours were 0 (IQR 0), and postoperative rescue opioid requirements were low in epidural patients. There were no instances of tracheal reintubation, neuraxial blockade-related complications, or other anaesthesia-related adverse events.

Through our standardised and reproducible anaesthetic protocol, we achieved excellent and nearly pain-free recovery in paediatric patients undergoing trans-atrial cardiac surgeries via the mid-axillary approach.

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.

Psychomotor disturbance (PmD) is prevalent in major depressive disorder (MDD), with neural substrates implicated in disrupted motor circuits and the interaction to non-motor cortex. Our objective is to explore the functional connectivity pattern underlying PmD using functional magnetic resonance imaging (fMRI).

A total of 150 patients with MDD and 91 healthy controls (HCs) were included in this study. The patients were categorized into psychomotor (pMDD, n = 107) and non-psychomotor (npMDD, n = 43) groups based on the Hamilton Depression Rating Scale. Seed-based connectivity (SBC) analysis was conducted using predefined somatomotor and cerebellar network (SMN and CN) coordinates as seeds, to assess group differences and symptom correlations. Subsequently, we correlated the group-contrast SBC map with existing neurotransmitter maps to explore the neurochemical basis.

In pMDD patients compared to HC, we observed decreased connectivity, especially between the SMN and frontal cortex, within the bilateral SMN, and between the CN and right precentral cortex. Meanwhile, connectivity increased between the SMN and the middle cingulate cortex and between the CN and left precentral cortex in pMDD relative to npMDD and HC. Connectivity between the SMN and angular gyrus was positively correlated with the severity of PmD. Additionally, the aberrant SBC patterns in pMDD were linked to the distribution of dopamine D1 and D2 receptors.

This study provides insights into the aberrant connectivity within the motor circuits and its interactions with non-motor regions in PmD. It also suggests a potential role for dopaminergic dysregulation in the connectivity abnormalities associated with PmD.