Significant changes in Taiwan’s psychiatric services over recent decades include expansion of community-based clinics and implementation of the Schizophrenia Pay-for-Performance programme.

This study aimed to assess the trend of the quality of healthcare for individuals with schizophrenia, using various indicators of the treatment process and outcomes between 2010 and 2019.

Individuals with schizophrenia were identified using Taiwan’s National Health Insurance claims database. The quality of healthcare for individuals with schizophrenia was assessed using treatment process and outcome indicators, including antipsychotic types, medication adherence, daily dose for antipsychotics and concurrent use of other psychotropic agents. Outcome indicators included all-cause mortality, suicide deaths, psychiatric hospitalisation, emergency department visits and employment status.

Antipsychotic medication usage has shifted towards second-generation antipsychotics (SGAs) and long-acting injectable antipsychotics (LAIs), with declines in first-generation antipsychotics. The percentage of medication adherence declined, while that of individuals with an adequate daily dose increased. Concurrently, anticholinergic and benzodiazepine use decreased while antidepressant and mood stabiliser use increased. Outcome indicators showed no significant change in all-cause mortality or suicide rates over time, but there were reductions in psychiatric hospitalisations and emergency department visits. Employment rates increased overall, particularly in urban areas.

The quality of healthcare for individuals with schizophrenia, as measured by treatment process and outcome indicators, improved alongside changes in Taiwan’s psychiatric services; however, causality cannot be inferred from our findings. Future research should evaluate the effectiveness of psychiatric service policies and continuously monitor healthcare quality to further enhance the lives of individuals with schizophrenia.

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.

Euthymic bipolar disorder (euBD) patients exhibit deficits in neurocognitive and social cognitive functioning compared to healthy controls (HCs). Our prior research has shown that the excitatory/inhibitory (E/I) imbalance in the default mode network (DMN) is linked to executive function in euBD. Neurocognitive impairments are associated with social cognition deficits in individuals with mental disorders. Given this connection, this study posits E/I imbalance within the DMN is associated with social cognition, with executive function as a mediator.

Seventy-five HCs and 49 euBD individuals were recruited. Using the emotion recognition task, Diagnostic Analysis of Nonverbal Accuracy 2-Taiwan version (DANVA-2-TW) and cognitive flexibility task, Wisconsin Card Sorting Test (WCST), we assessed emotion recognition and prefrontal function. Proton magnetic resonance spectroscopy (1H-MRS) measured metabolites in the posterior cingulate cortex (PCC) and medial prefrontal cortex/anterior cingulate cortex (mPFC/ACC), quantifying excitatory glutamate+glutamine (Glx) and inhibitory GABA to calculate the E/I ratio.

euBD patients showed poorer emotion recognition (p = 0.020) and poorer cognitive flexibility (fewer WCST categories completed, p = 0.002). A negative association was found between emotion recognition and the E/I ratio in the mPFC/ACC of the BD patients (r = −0.30, p = 0.034), which was significantly mediated by cognitive flexibility (Z = −2.657, p = 0.007).

The BD patients demonstrate deficits in emotion recognition, linked to an altered E/I balance in the prefrontal cortex, and the cognitive flexibility, a key aspect of executive function, mediates the impact of the E/I ratio on emotion recognition accuracy in euBD patients.

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.

Methadone maintenance treatment (MMT) and protracted abstinence (PA) effectively reduce the craving for heroin among individuals with heroin use disorder (HUD). However, the difference in their effects on brain function, especially the coupling among the large-scale brain networks (default mode [DMN], salience [SN], and executive control [ECN] networks), remains unclear. This study analyzed the effects of the MMT and PA on these networks and the predictive value of the bilateral resource allocation index (RAI) for craving for heroin.

Twenty-five individuals undergoing the MMT, 22 undergoing the PA, and 51 healthy controls underwent resting-state functional magnetic resonance imaging (rs-fMRI). Independent component analysis identified the ECN, DMN, and SN. The SN-ECN and SN-DMN connectivity and the bilateral RAI were evaluated. The relationships between network coupling and clinical and psychological characteristics were analyzed. The multiple linear regression model identified significant variables for predicting craving scores.

The MMT group showed significantly stronger SN-left ECN (lECN) coupling and left RAI than the PA group. In the MMT group, SN-lECN connectivity and bilateral RAI were positively correlated with the total methadone dose. In both treatment groups, SN-right ECN (rECN) connectivity and right RAI were negatively correlated with craving. The models revealed that the bilateral RAI and the MMT and PA were associated with the craving.

The MMT enhances SN-lECN coupling and the left RAI more than the PA, possibly due to higher control modulation. The RAI could help predict heroin craving in individuals with HUD undergoing either treatment program.

This study aimed to examine the relationship between fibroblast growth factor 19 (FGF19) and depressive symptoms, measured by Beck’s Depression Inventory (BDI) scores and investigate the moderating role of smoking.

This study involved 156 Chinese adult males (78 smokers and 78 non-smokers) from September 2014 to January 2016. The severity of depressive symptoms was evaluated using the BDI scores. Spearman rank correlation analyses were used to investigate the relationship between cerebrospinal fluid (CSF) FGF19 levels and BDI scores. Additionally, moderation and simple slope analyses were applied to assess the moderating effect of smoking on the relationship between the two.

FGF19 levels were significantly associated with BDI scores across all participants (r = 0.26, p < 0.001). Smokers had higher CSF FGF19 levels and BDI scores compared to non-smokers (445.9 ± 272.7 pg/ml vs 229.6 ± 162.7 pg/ml, p < 0.001; 2.7 ± 3.0 vs 1.3 ± 2.4, p < 0.001). CSF FGF19 levels were positively associated with BDI scores in non-smokers (r = 0.27, p = 0.015), but no similar association was found among smokers (r = −0.11, p = 0.32). Linear regression revealed a positive correlation between FGF19 and BDI scores (β = 0.173, t = 2.161, 95% CI: 0.015–0.331, p < 0.05), which was negatively impacted by smoking (β = −0.873, t = −4.644, 95% CI: −1.244 to −0.501, p < 0.001).

These results highlight the potential role of FGF19 in individuals at risk for presence of or further development of depressive symptoms and underscore the importance of considering smoking status when examining this association.