Stress beliefs-general expectations about the nature and consequences of stress-have been linked to health and performance, yet their role in shaping responses to everyday stress remains less understood. This study examined whether stress beliefs moderate affective reactivity and stress regulation strategies in response to naturally occurring stressors in daily life. In a 7-day ecological momentary assessment study, 104 university students completed thrice-daily reports (1,939 observations) on social and work-related stressors, positive and negative affect, and two stress regulation strategies-situation selection and response modification-as proposed in the stress optimization model (Crum et al., 2020). At baseline, stress beliefs were assessed alongside variables to characterize the sample. Negative stress beliefs moderated the association between daily stressors and positive affect: Individuals with high negative stress beliefs showed reduced positive affect during social stress and no increase in positive affect under higher workload. By contrast, those with low or moderate negative stress beliefs maintained positive affect during social stress and showed increased positive affect under higher workload-consistent with a challengelike appraisal. Additionally, controllability beliefs buffered increases in negative affect in response to daily social stress, with lower beliefs linked to stronger affective reactivity. By contrast, stress beliefs did not moderate associations between daily stressors and the investigated stress regulation strategies. These findings suggest that stress beliefs tune affective reactivity to everyday social and work stressors, identifying them as a potential intervention target given the established links between affect and long-term health. The generalizability of these findings should be confirmed across broader populations. (PsycInfo Database Record (c) 2026 APA, all rights reserved).

Immune dysregulation, particularly inflammation, may contribute significantly to the pathophysiology of schizophrenia (SZ). Autophagy is an essential cellular process that maintains neuroimmune homeostasis, but its relationship with inflammation in SZ remains unclear. Eicosapentaenoic acid (EPA), an omega (n)-3 polyunsaturated fatty acid (PUFA), was reported to exert therapeutic effects by modulating inflammation. Here, we hypothesized that EPA alleviates SZ-related behavioral and neurochemical abnormalities via autophagy regulation. Transcriptomic analysis of peripheral blood from SZ patients revealed reduced autophagic markers (BECLIN1, LC3B), which were negatively correlated with symptom severity, while P62 levels were increased, which was positively correlated with symptoms severity. SZ patients also showed an altered n-3 PUFA profile (reduced EPA and DHA, while elevated n-6/n-3 ratio). In a mouse model of SZ induced by maternal immune activation, lower Beclin1, an autophagic marker, was observed in the brains of mice. EPA treatment ameliorated SZ-like behaviors, upregulated Beclin1 expression, rebalanced glial activation toward anti-inflammatory and neuroprotective states. EPA also suppressed pro-inflammatory cytokines (IL-6, TNF-α), increased IL-10 and decreased DA/5-HT ratio in the prefrontal cortex and restored the n-6/n-3 PUFA ratio. Notably, EPA effects were largely blocked by co-administration of an autophagy inhibitor 3-methyladenine (3-MA), whereas these effects were recovered following treatment with the autophagic activator rapamycin. EPA supplementation also increased brain DHA levels, suggesting that downstream DHA-related mechanisms may additionally contribute to the observed effects. Together, these findings indicate that autophagic impairment is associated with neuroimmune and neurochemical abnormalities in SZ and support the autophagic function involved in EPA therapeutic effects on SZ-like changes.

Poricoic acid A (PAA) is a bioactive triterpenoid from the fungus Poria cocos. Nevertheless, whether it exerts antidepressant-like effects and whether the gut microbiota and immune regulation are involved remain unknown.

Male C57BL/6J mice were subjected to chronic unpredictable stress (CUS) and treated with PAA treatment. Behavioral tests were performed, and hippocampal damage was evaluated by H&E and TUNEL staining. Gut microbiota composition was analyzed using 16S rRNA sequencing, and hippocampal transcriptomic profiling was performed using RNA-seq, followed by immune cell infiltration, correlation, and functional enrichment analyses.

PAA treatment eased CUS-induced depression- and anxiety-like behaviors. It also cut down hippocampal neuron damage and cell death. Besides, PAA fixed gut bacteria balance by lowering harmful germs like L. murinus and boosting good germs like A. muciniphila and L. reuteri. Hippocampal transcriptomic analysis revealed that PAA modulated immune cell infiltration by reducing M1 macrophages and restoring M2 macrophages, with significant correlations between gut microbial taxa and hippocampal immune-related gene expression. Functional enrichment analyses indicated that PAA regulates pathways related to synaptic plasticity, neuroinflammation, and neuronal development. qPCR and western blotting confirmed that PAA restored the hippocampal expression of key molecules involved in neuroinflammation (HSP90B1), synaptic plasticity (RPS6KB2 and IGF2BP2), and blood-brain barrier integrity (COL4A5) CONCLUSIONS: PAA alleviates depression-like Behaviors in CUS mice by remodeling the gut microbiota and modulating the hippocampal M1/M2 macrophage balance via the gut-brain axis. These findings support the potential of PAA as a prebiotic-like nutritional agent for major depressive disorder.

To investigate the causal relevance of melatonin metabolism, which provides the biological basis for circulating melatonin levels, to specific depression symptom subtypes, we performed a targeted systematic review of melatonin metabolism pathways in the human brain and liver. Using two-sample Mendelian randomization (MR), we assessed the causal effects of metabolism pathways and/or individual genes on major depressive disorder (MDD) and nine symptom subtypes derived from Patient Health Questionnaire-9 (PHQ-9). Instrumental variables (IVs) were expression quantitative trait loci (eQTL) for eight individual genes, one synthesis route, and three degradation routes. Results were assessed using Bayesian colocalization and phenome-wide association analyses. At the pathway-level, the genetically proxied synthesis-route signal was associated with PHQ-9 Assessment 5 (PHQ9A5, OR: 0.89, 95% CI: 0.85-0.93), but sensitivity analyses suggested this association was primarily driven by TPH1 and may reflect serotonin-related biology. In contrast, higher brain melatonin degradation raised the risk of both PHQ9A1 (OR: 1.03, 95% CI: 1.02-1.04) and PHQ9A7 (OR: 1.03, 95% CI: 1.02-1.03). Within degradation, up-regulation of the kynurenine sub-pathway increased the odds of PHQ9A3 (OR: 1.05, 95% CI: 1.02-1.07), PHQ9A4 (OR = 1.04, 95% CI: 1.02-1.06) and PHQ9A7 (OR: 1.05, 95% CI: 1.02-1.07). Gene-level analyses were largely concordant, except for SULT1A1, whose higher expression was genetically protective for PHQ9A3 but risk-increased for PHQ9A1 and PHQ9A4. Overall, these results demonstrate that melatonin metabolism exerts symptom-specific and pathway-specific causal effects on depression. A stratified view of melatonin's role may help optimize the application of exogenous melatonin supplementation.

Nigeria's rapidly expanding older adult population, mirroring a global demographic shift, is driving a surge in dementia cases. Currently 4.9% of Nigerian older adults have dementia and this figure is set to increase. Fragmented care delivery, weak institutional infrastructure, and pervasive social stigma severely hinder effective diagnosis, treatment, and structural support. This paper proposes a Modern Service Framework for Dementia Care in Nigeria; a proactive, evidence-based national strategy designed to overhaul Nigerian healthcare delivery through six critical, intersecting pillars. The proposed framework establishes a coordinated intervention pathway by: (1). Creating integrated, communicative health systems, (2). Promoting healthy ageing and life-course prevention, (3). Driving diagnostic innovation and primary-care screening, (4). Raising targeted community, traditional, and religious awareness, (5). Scaling workforce capacity alongside sustainable funding mechanisms, and (6). Fostering cross-sectoral partnerships to safeguard vulnerable individuals. Rapid, formal adoption of this comprehensive framework is vital to mitigate the immense economic and caregiving burdens placed on families and the broader healthcare system, ultimately ensuring that every Nigerian living with dementia receives equitable, dignified, and rights-based support.

Traditional epidemiological surveillance methods are often limited by delays in reporting and fragmented data systems. Saudi Arabia faces additional public health challenges from mass gatherings during Hajj and Umrah, an increasing burden of noncommunicable diseases and rapid urbanization, highlighting the need for investing in digital epidemiology.

Saudi Arabia has accelerated digital transformation in health care through Vision 2030 initiatives. The strategies include health information exchange platforms, analytics driven by artificial intelligence, telemedicine services and digital monitoring systems used during Hajj. We review current initiatives to invest in digital epidemiology in Saudi Arabia, implementation challenges and policy priorities.

Saudi Arabia's health system operates under a predominantly public model. The health ministry is the main provider, regulator and finance provider of most health-care services. Health-care coverage is nearly universal, with citizens receiving services free of charge through the public system. Ongoing reforms aim to gradually decentralize certain functions.

The initiatives under Vision 2030 have supported disease surveillance, data integration and public health response capacities. Existing digital health reforms have created a foundation for integrating digital epidemiology into routine public health practice. However, challenges remain, including fragmented interoperability between institutions, workforce shortages, unequal digital access, and concerns about data governance, privacy and algorithmic bias.

Saudi Arabia's experience suggests that digital epidemiology is more effective when integrated within broader digital health reforms. Successful implementation requires not only digital infrastructure, but also workforce development, ethical governance, transparency and mechanisms for integrating digital data into public health decision-making.

Purpose: Most children with autism live in resource-limited settings with limited access to timely interventions. To address this gap, the World Health Organization developed Caregiver Skills Training (CST) to support caregivers and expand intervention access globally. This study examined the feasibility and preliminary outcomes of a modified CST in mainland China. Methods: Using the ecological validity model and qualitative interviews, the CST materials were culturally adapted and modified for the Chinese context. A pre- and post-test controlled trial was conducted with caregivers of children with autism aged 2-9 years, who were assigned to either the CST intervention group (N = 15) or a caregiver education control group (N = 15). Clinical outcomes for caregivers and children were evaluated at baseline and after a 10-week intervention period. Results: Cultural adaptation and modifications focused on language adjustments, localization of case examples and demonstrations, and optimization of teaching methods and training schedules. Supplementary within-group analyses indicated pre-post changes in caregiver knowledge and skills, parenting stress, and selected child outcomes, including speech/language/communication, sensory/cognitive awareness, and overall autism symptoms. However, most between-group differences were not statistically significant after baseline adjustment. Conclusions: The findings provide preliminary evidence for the feasibility of culturally adapted and modified CST in mainland China. Given the pilot nature of the study and the absence of statistically significant between-group effects for most outcomes, the outcome findings should be interpreted as exploratory and hypothesis-generating rather than evidence of efficacy. Further large-scale studies with greater statistical power and objective outcome measures are needed to evaluate effectiveness and implementation feasibility.

The intricate balance between angiotensin-converting enzyme 1 (ACE1) and 2 (ACE2) in the pulmonary vasculature is pivotal for the pathogenesis of pulmonary arterial hypertension (PAH). Catalysing the K48-linked deubiquitination, ubiquitin carboxyl-terminal hydrolase 10 (USP10) is involved in tumour suppression, autophagy, and cell proliferation. This study aims to determine whether a positive feedback loop of USP10 and AMP-activated protein kinase (AMPK) in pulmonary endothelium is protective against PAH.

In silico data analyses and in vitro culture cell experiments were used to investigate the role of USP10 in human idiopathic PAH (IPAH) and rodent pulmonary hypertension (PH) as well as the underlying mechanism involving a positive feedback loop of AMPK and USP10 in lung endothelium. Endothelial cell (EC)-specific USP10 transgenic (Tg) mice and mice administered liraglutide were used to explore the efficacy of the AMPK/USP10 loop in mitigating PH in rodents.

USP10 level was decreased in the lung endothelium of human IPAH and rodent PH. AMPK/USP10 loop activation increased ACE2 Ser-680 phosphorylation and Lys-788 deubiquitination, thus contributing to the homeostatic level of ACE2 and lung vascular patency. Mice with liraglutide administration phenocopied the mitigated PH in EC-specific USP10 Tg mice, in part because of the activated AMPK/USP10 loop in the pulmonary endothelium.

Genetic or pharmacologic [via glucagon-like peptide-1 receptor agonists (GLP-1 RAs)] interventions in the AMPK/USP10 loop can augment ACE2 level in lung endothelium. This type of ACE2 enhancement garners protection against PAH in humans and PH in rodents, which provides a rationale for using GLP-1 RAs to alleviate PAH.

Fragmented primary health care in China fails to tackle the growing burden of noncommunicable diseases. Despite substantial investment, fewer than half of patients with diabetes achieve glycaemic control.

Tianjin's 2020-2023 reform established a public-private partnership model where WeDoctor managed community health centres under a capitation scheme. This strategy integrated: (i) monthly prepaid capitation covering all diabetes-related outpatient services; (ii) claims auditing and clinical decision support using artificial intelligence (AI); (iii) dedicated health managers for care coordination; and (iv) redesigned services incorporating complication screening and digital medication management. A pilot study including 494 945 patients with diabetes compared three care models from 2022 to 2023: WeDoctor-community health centre care, hospital care and usual care.

Tianjin city serves 15 million residents through 177 hospitals and 266 community health centres. Chronic disease management is fragmented: the Health Commission regulates care standards, while the Insurance Bureau controls funding.

Visits for diabetes at WeDoctor health centres increased 2.6% (0.7/26.6) but declined 10.6% (-3.8/35.7) for hospital-based care and 2.3% (-0.8/34.1) for usual care. All groups reduced outpatient expenditure. The WeDoctor model generated a 37.62 million United States dollars (US$) surplus, boosted health centre diabetes revenue by 65% (US$ 154 577/237 805) and raised physician annual salaries by 30% (US$ 5172/17 241). More than three quarters of patients expressed satisfaction with and trust in the WeDoctor model.

Integrating capitation financing with third-party governance and AI support can strengthen primary health care, contain costs and enhance patient-centred care.

Background/Objectives: Bilateral thoracoscopic sympathectomy (BTS) is the definitive treatment for primary focal hyperhidrosis, yet postoperative pain remains an undertreated consequence with no established analgesic consensus. This study compared three analgesic regimens on pain trajectory, opioid consumption, and functional recovery following BTS. Methods: In this prospective observational cohort study, 300 patients undergoing BTS were allocated in a non-randomized manner reflecting institutional practice to three parallel cohorts (n = 100 each): Group 1 received systemic opioids alone; Group 2 received opioids plus pre-emptive local anesthetic wound infiltration; and Group 3 received opioids plus thoracoscopic-guided intercostal nerve block (ICNB). Primary outcomes included pain intensity on the Numerical Rating Scale and total opioid consumption. Results: ICNB patients reported significantly lower mean peak pain scores (3.8 ± 1.7) versus local infiltration (4.6 ± 1.9) and opioid-only groups (5.2 ± 2.1; p < 0.001). Total opioid consumption was reduced by 38% in the ICNB group (12.4 ± 4.8 mg vs. 20.1 ± 6.3 mg; p < 0.001). Moderate-to-severe pain occurred in 42.0% of ICNB patients versus 74.0% of controls (p < 0.001). ICNB was independently associated with reduced moderate-to-severe pain (adjusted odds ratio (AOR) 0.31; 95% confidence interval (CI) 0.17-0.56; p < 0.001). ICNB patients returned to normal activities faster (median 3 vs. 5 days; p = 0.008) with higher satisfaction (91.0% vs. 78.0%; p = 0.044). Conclusions: In this observational cohort, ICNB was associated with significantly lower postoperative pain scores, reduced opioid consumption, and faster functional recovery following BTS. These findings suggest that ICNB may be an effective adjunct analgesic strategy for ambulatory BTS, pending confirmation in randomized controlled trials.