White matter (WM) abnormalities are implicated in major depressive disorder (MDD), yet the organization of white matter morphometric similarity networks (WM-MSNs) – which capture interregional similarity in voxel-wise WM morphology – and the transcriptional mechanisms associated with their disruption remain insufficiently understood.

Using T1-weighted MRI from a large multisite sample (1,154 individuals with MDD and 1,026 healthy controls), we constructed individualized WM-MSNs. Group differences were assessed at the edge, global, and nodal levels. To identify molecular pathways underlying these alterations, nodal abnormalities were linked to regional gene expression profiles from the Allen Human Brain Atlas using spatially informed transcriptomic association, followed by functional, cell-type-specific, and developmental enrichment analyses.

MDD showed distributed but selective reorganization of WM-MSNs. Network-based statistics revealed two significant components, with 118 edges exhibiting increased morphometric similarity and 45 showing decreased similarity. Globally, MDD demonstrated higher small-worldness, clustering coefficient, global efficiency, and local efficiency, together with shorter characteristic path length. Nodal disruptions were concentrated in major commissural and association tracts – including the corpus callosum, cingulum, uncinate fasciculus, and tapetum. Transcriptomic integration indicated enrichment for gene signatures related to oligodendrocyte function, myelination, lipid metabolism, axonal organization, and cellular stress-related molecular processes, with implicated genes showing broad developmental-stage expression.

MDD is associated with robust alterations in individualized WM-MSNs that converge with transcriptional signatures linked to myelination, metabolic processes, axonal structure, and cellular stress, linking macroscale network disruption to underlying molecular architecture and providing cross-scale insights into WM pathology in depression.

To examine the association between dietary patterns and metabolic syndrome (MetS) in western China, which has not been previously reported.

A population based cross-sectional study design. Dietary intake was assessed using a semi-quantitative FFQ. Principal component analysis identified dietary patterns and multivariate logistic regression evaluated their associations with MetS.

Population-based Cohort Study of Chronic Diseases in Xinjiang (PCCDX), conducted in 2022.

A total of 3208 individuals from PCCDX (mean age: 53·1 (sd 10·8) years; 49·1 % male).

MetS was diagnosed in 1762 participants (54·9 %). Four distinct dietary patterns were identified, with the refined grain–animal products dietary pattern being the dominant one. After adjusting for general demographic and lifestyle factors, a higher score in the refined grain–animal product pattern was associated with an increased risk of MetS. The OR for the second, third and fourth quartiles of the dietary score were 1·07 (95 % CI: 0·860, 1·322), 1·14 (0·923, 1·413) and 1·48 (1·189, 1·853), with a statistically significant trend (P = 0·003). Higher dietary scores in this pattern were also associated with increased risks of elevated waist circumference, high TAG and low HDL cholesterol (P < 0·05). Mediation analysis showed that visceral fat percentage partially mediated the association between the refined grain–animal product dietary pattern and low HDL-cholesterol, accounting for 17·2 % of the total effect (indirect effect = 0·005, P = 0·006). The other three dietary patterns showed no significant associations with MetS or its components.

This study highlights the high prevalence of MetS in western China and links a refined grains-animal products diet to poorer metabolic health, emphasising the need for region-specific dietary strategies.

Considerable effort has been devoted to investigate the neuroimaging correlates and predictors of antidepressant response to ketamine, yet inconsistency in the location and nature of the regional brain effects makes it difficult to unify this research. Despite the revolutionary notion that psychiatric therapeutics show network-level brain representations, investigations into network localization of brain functional effects of ketamine treatment are still lacking.

We initially identified the locations of longitudinal brain functional alterations (increase and decrease separately) induced by ketamine treatment from 16 published studies with 508 depressed patients. By integrating these affected brain locations with large-scale functional MRI datasets from 1113 healthy and 255 depressed individuals, we then leveraged a novel functional connectivity network mapping approach to construct ketamine-induced hyper-functional and hypo-functional networks respectively.

The hyper-functional network mainly involved the subcortical (caudate nucleus and thalamus) and default (medial prefrontal cortex) networks, while its hypo-functional counterpart predominantly implicated the limbic (temporal pole), subcortical (hippocampus and amygdala), and default (lateral temporal cortex) networks.

Our findings may shed light on the neurobiological effects of ketamine from a network perspective, which might represent a crucial step toward fostering the clinical application of ketamine in antidepressant treatment.

To investigate the variations of serum ghrelin levels in children with left-to-right shunt CHD, and analyse the correlation with the geometric structure of the heart. It may provide some clinical guidance for evaluating the early changes of cardiac structure and function in CHD children.

A total of 93 children with left-to-right shunt CHD who were hospitalised to Children’s Hospital of Soochow University from September 2021 to February 2023 were included in the CHD group (of which 58 were ventricular septal defect and 35 were patent ductus arteriosus). In addition, 57 cases (mainly inguinal hernia) were selected as the control group. The corresponding clinical data were recorded, and the fasting serum ghrelin levels of the two groups were detected by enzyme-linked immunosorbent assay on the day of admission. Then, the clinical data and serum ghrelin levels of the two groups were compared, and the Spearman correlation was analysed.

The serum ghrelin level in CHD group was higher than that in control group, and the difference was statistically significant (P < 0.05). Z score of weight for age and Z score of height for age in CHD group were lower than those in control group were statistically significant difference (P < 0.05). But there was no correlation between serum ghrelin and BMI, weight-for-age Z-score, and height-for-age Z-score (P > 0.05). Ghrelin in the enlarged heart group was lower than that in the non-enlarged heart group, and there were statistical significance of among those groups (P < 0.05). There were no significant differences in left ventricular ejection fraction and left ventricular fractional shortening among different cardiac load groups (P > 0.05). The left ventricular end-systolic diameter Z-scores, left ventricular mass Z-scores, left ventricular mass index, and left ventricular end-diastolic volume-scores in the cardiomegaly groupwere higher than those in the non-cardiomegaly group, and those two groups were significantly different (P < 0.05). The relative wall thickness and left ventricular remodelling index in the cardiomegaly group were lower than those in the non-cardiomegaly group, and the differences between the groups were statistically significant (P < 0.05). Serum ghrelin was negatively correlated with left ventricular end-diastolic diameter Z-scores, left ventricular end-systolic diameter Z-scores, and left ventricular end-diastolic volume Z-scores in cardiac indexes (P < 0.05), positively correlated with left ventricular remodelling index (P < 0.05), and had no correlation with relative wall thickness, left ventricular mass Z-scores, and left ventricular mass index (P > 0.05).

The levels of serum ghrelin are increased in CHD children, and serum ghrelin is negatively correlated with left ventricular end-diastolic diameter and left ventricular end-diastolic volume in cardiac geometric structure, and positively correlated with left ventricular remodelling index. Additionally, patients with cardiac enlargement present with a low serum ghrelin level. These findings collectively suggest that serum ghrelin may play a potential role in cardiac remodelling.

Major depressive disorder (MDD) patients exhibit a mood-congruent emotional processing bias within the amygdala toward negative facial stimuli at both unconscious and conscious levels. Therefore, our study aimed to investigate the temporal and spatial dynamics of amygdala along with its interactions with the whole brain during implicit and explicit conditions in MDD.

Thirty MDD patients and 26 healthy controls (HCs) underwent magnetoencephalography (MEG) recordings and performed implicit and explicit emotional face recognition tasks with happy, sad, and neutral facial expressions. Using the amygdala as a seed region, time frequency representations (TFR) and functional connectivity (FC) were calculated. Pearson correlation analyses measured the relationship between TFR and FC values with clinical symptoms.

During implicit processing, MDD patients exhibited left amygdala activation in the gamma power (60–70 Hz) before 250 ms in response to sad facial stimuli compared to HCs. In the implicit mode, there were increased FC between the right amygdala and several brain regions in the occipitoparietal lobes, as well as higher FC between the left amygdala and putamen in MDD patients. Additionally, the right amygdala was positively correlated with the severity of depression and anxiety during implicit processing.

MDD patients had lateralized amygdala activation in response to sad facial expressions during unconscious emotional recognition of facial stimuli. Our study provided valuable insights into the spatiotemporal dynamics of facial emotional recognition associated with depressive and anxiety-related cognitive bias during implicit and explicit processing.

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.

Data on aortic valve outcomes following surgical repair of doubly committed subarterial ventricular septal defect remain limited.

This retrospective study included doubly committed subarterial ventricular septal defect patients who underwent surgical repair at our centre from 2013 to 2023. The primary outcome was the incidence of new-onset aortic regurgitation during follow-up.

A total of 320 patients were included, with a median age of 2.0 (0.9–7.2) years. Among them, 289 patients underwent surgical repair alone (repair group), and 31 received additional aortic valve surgery (repair + aortic valve surgery group). Preoperatively, 58 (18.1%) patients exhibited aortic regurgitation ≥ mild (10.7% in the repair group vs 87.1% in the repair + aortic valve surgery group, P < 0.001). The overall median follow-up was 40.5 (16.0–72.0) months. At the last follow-up, 23 (7.4%) patients had aortic regurgitation ≥ mild (3.8 vs 52.2%, P < 0.001), and 6 (1.9%) had aortic regurgitation > mild (0.3 vs 21.7%, P < 0.001). Sixteen (5.1%) patients developed new-onset aortic regurgitation during follow-up (1.7 vs 47.8%, log-rank P < 0.001), and 6 (1.9%) of them developed new-onset aortic regurgitation > mild (0.3 vs 21.7%, log-rank P < 0.001). Age, ventricular septal defect size, preoperative aortic regurgitation > mild, and maximum aortic valve flow velocity (AVmax) were related to concurrent aortic valve surgery and new-onset aortic regurgitation.

Based on our retrospective data, the mid-term aortic valve outcomes after doubly committed subarterial ventricular septal defect repair were relatively satisfactory, with a low incidence of new-onset aortic regurgitation during follow-up. However, aortic valve outcomes for patients who received concurrent aortic valve surgery were less satisfactory.

Antimicrobial resistance (AMR) is a global health challenge, highlighting the need for antibiotic stewardship policies. We evaluated the impact of the National Action Plan to Contain Antimicrobial Resistance (2022–2025) on antibiotic use among primary healthcare institutions (PHIs) in Central China.

A segmented interrupted time-series analysis from January 2021 to December 2023.

We collected data from 1510 PHIs, by region, types of healthcare institutions and medication type, assessing antibiotic consumption using defined daily doses per 1000 inhabitants per day and the quality by the percentage of broad-spectrum antibiotics.

Post-intervention, antibiotic consumption declined by −35.96% (95%CI: –49.34 to –22.57), and the proportion of broad-spectrum antibiotic use decreased by –41.97% (–61.74 to –22.20). Consumption dropped significantly in both moderately developed areas and underdeveloped areas, while highly developed areas saw the largest reduction in broad-spectrum antibiotic use. Rural PHIs also showed notable declines in both overall antibiotic consumption and broad-spectrum usage.

The policy was associated with a reduction in antibiotic use across PHIs, though regional disparities in its implementation suggest uneven benefits.

Studies highlight the thalamus as a key region distinguishing early- from late-onset obsessive-compulsive disorder (OCD). While structural thalamic correlates with OCD onset age are well-studied, resting-state functional connectivity (rsFC) remains largely unexplored. This study examines thalamic subregional rsFC to elucidate pathophysiological differences in OCD based on different onset times.

The study comprised 85 early-onset OCD (EO-OCD) patients, 94 late-onset OCD (LO-OCD) patients, and 94 age- and sex-matched healthy controls (HCs). rsFC analysis was conducted to assess thalamic connectivity across seven subdivisions among the groups.

Both EO-OCD and LO-OCD patients exhibited increased rsFC between the primary motor thalamus and the posterior central gyrus and between the thalamic premotor and the supplementary motor areas. EO-OCD patients showed significantly stronger rsFC between the prefrontal thalamus (Ptha) and the middle frontal gyrus (MFG) compared to both LO-OCD patients and HCs. In contrast, LO-OCD patients demonstrated reduced rsFC between the Ptha and the inferior parietal lobule (IPL) compared to EO-OCD patients and HCs. Additionally, the rsFC between the Ptha and both the MFG and IPL was negatively correlated with age of onset, with earlier onset linked to stronger connectivity.

These findings reveal both shared and distinct thalamic connectivity patterns in EO-OCD and LO-OCD patients. Sensory-motor networks exhibiting thalamic hyperconnectivity are critical for the manifestation of OCD, regardless of age of onset. The frontal–parietal network and thalamic hyperconnectivity may present a compensatory mechanism in EO-OCD patients, while hypoconnectivity with the frontoparietal network may reflect a neural mechanism underlying LO-OCD.

Posttraumatic stress disorder (PTSD) exhibits marked heterogeneity, with relational (R; interpersonal) and nonrelational (NR; environmental) trauma subtypes demonstrating distinct psychopathological trajectories. Despite clinical recognition of these differences, their neurobiological underpinnings of emotion processing remain poorly understood. Guided by the Nested Hierarchical Model of Self (NHMS) – which posits trauma-type-specific disruptions in hierarchical self-processing systems – this study investigated neural mechanisms differentiating among PTSD subtypes during implicit emotion regulation.

A sample of 122 participants, including patients with PTSD (R: n = 51; NR: n = 29) and trauma-exposed controls matched by trauma type (R: n = 22; NR: n = 20), underwent functional magnetic resonance imaging while performing the Shifted Attention Emotion Appraisal Task. Behavioral assessments and trauma typology coding were complemented by regions of interest (ROI)-based and whole-brain analyses.

Results revealed that PTSD-R showed hypoactivation in right superior frontal gyrus (during implicit emotion regulation; BA9; p = 0.049, ηp2 = 0.033), whereas PTSD-NR exhibited hyperactivation in fusiform (during emotion modulation by attention shifting; p = 0.036, ηp2 = 0.037). Symptom severity inversely correlated with social support (r = −0.353 to −0.417, p < 0.01), with relational PTSD reporting the lowest support (p < 0.001). Across conditions, dorsolateral prefrontal clusters (BA8/9) demonstrated anticorrelations with default-mode regions (r = −0.272 to −0.549, p < 0.01) aligning with NHMS’ predictive coding framework.

These findings validate trauma-type-specific neural hierarchies, suggesting relational trauma disrupts top-down self-identity schemas, while NR trauma amplifies bottom-up threat detection. The study advances precision psychiatry by linking implicit regulation biomarkers to targeted interventions – cognitive restructuring for PTSD-R and interoceptive recalibration for PTSD-NR.

Depression and anxiety are prevalent mental health disorders. While sleep duration has been extensively studied, sleep regularity may play a critical role. We aimed to examine associations between objectively measured sleep regularity and incident depression and anxiety and to investigate whether meeting recommended sleep duration modifies these associations.

In 79,666 UK Biobank participants without baseline depression or anxiety, wrist accelerometers worn for 7 days yielded a sleep regularity index (SRI) and average sleep duration. SRI was categorized as irregular (≤51), moderately irregular (52–70), or regular (≥71). Sleep duration was classified by age-specific recommendations (7–9 hours for ages 18–64 years; 7–8 hours for over 65 years). Cox regression models assessed associations between sleep parameters and mental health outcomes.

During a median follow-up of 7.5 years, 1,646 participants developed depression, and 2,097 developed anxiety. Compared to irregular sleepers, regular sleepers had a 38% lower depression risk (hazard ratio [HR], 0.62; 95% confidence interval [CI], 0.52–0.73) and a 33% lower anxiety risk (HR, 0.67; 95%CI, 0.58–0.77). Participants with both irregular sleep and nonrecommended duration exhibited the highest risks (depression HR, 1.91; 95%CI, 1.55–2.35; anxiety HR, 1.61; 95%CI, 1.35–1.93). Notably, irregular sleepers who met duration guidelines still faced elevated risks (depression HR, 1.48; 95%CI, 1.18–1.86; anxiety HR, 1.35; 95%CI, 1.11–1.64).

Greater sleep regularity is independently associated with lower depression and anxiety risk regardless of sleep duration, suggesting that sleep–wake consistency should be considered in mental health promotion strategies alongside traditional sleep duration recommendations.