Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by persistent itch and a prolonged clinical course and can affect mental health and impair quality of life. Stress and anxiety exacerbate the symptoms of itch, leading to a vicious cycle that influences patient scratching behaviors and worsens disease prognosis. Dermatologists should consider psychosomatic correlations in patients with AD and provide psychosomatic intervention. However, standardized, consensus-based non-pharmacological psychosomatic approaches for patients with AD have not been established in Japan. This study sought to establish a Japanese consensus on non-pharmacological psychosomatic approaches to patients with AD. Japanese experts in psychosomatic dermatology stated their level of agreement with 28 items in round 1 plus one added in round 2 (29 items in total) regarding psychosomatic approaches as non-pharmacological approaches among patients with AD over Delphi rounds. Consensus was defined a priori as agreement from ≥ 75% of participants. The response rate was 17/21 (81.0%) in the first round and 17/17 (100%) in the second round. Twenty-five statements were adopted over both rounds. Performance of medical interviews and physical examinations, recognition of patient efforts, and respect for the interpretive model of the patient categorized to establish a good therapeutic relationship showed agreement. Evaluation of pathology from physical and psychological perspectives (addictive scratching, building a bio-psycho-social [BPS] model and pathophysiological hypothesis) showed high-level agreement. Indirectly promoting patient awareness of aggravating factors of AD and sharing the BPS model and pathophysiological hypothesis with the patient showed consensus. Further, 14 statements about the application of psychosomatic correlations to therapy showed agreement. In the second round, group therapy also gained consensus as a useful intervention. Our Delphi panel provides recommendations about psychosomatic interventions for patients with AD to standardize approaches in clinical practice and research.

Loneliness is a frequent yet understudied consequence of acquired brain injury (ABI), associated with poorer psychological adjustment and social participation. This study examined the relative contributions of executive dysfunction, emotional reactivity, and concealment to loneliness in individuals with chronic ABI.

Cross-sectional observational study of 103 adults with ABI (61.2% men; mean age ≈ 51 years; mean time since injury ≈ 80 months). Measures included the UCLA Loneliness Scale, Frontal Systems Behaviour Scale, Perth Emotional Reactivity Scale, and Anticipated Stigma/Concealment Questionnaire. Analyses comprised correlations and hierarchical regressions.

Loneliness was significantly associated with greater negative emotional reactivity (ρ = .74, p < .001) and concealment (ρ = .56, p = .001). Executive dysfunction showed a small positive association with loneliness (ρ = .20, p = .04). The final regression model explained 58% of variance in loneliness (R² = .58, F(3,99) = 46.27, p < .001). Negative emotional reactivity and concealment remained significant independent predictors, whereas executive dysfunction did not.

Post-ABI loneliness is primarily associated with negative emotional reactivity and concealment. Findings support screening for loneliness, emotional reactivity, and concealment, and interventions targeting emotional hyperreactivity and tendencies to conceal information routinely in clinical rehabilitation settings following acquired brain injury.

Maternal immune activation (MIA) during pregnancy has been implicated in offspring neurodevelopment, but evidence linking maternal gestational immune mediators with autism spectrum disorder (ASD) remains heterogeneous. This systematic review and meta-analysis evaluated whether maternal circulating cytokine and chemokine levels during pregnancy are associated with autism in offspring.

Five databases were searched for human observational studies measuring maternal blood cytokines or chemokines during pregnancy and reporting autism outcomes in offspring. Eligible studies included autism versus control comparisons using maternal serum or plasma samples. Random-effects meta-analyses were conducted using odds ratios (ORs) as the primary effect measure. Standardised mean differences (SMDs) were also analysed where group-level concentration data were available. Heterogeneity was assessed using I² statistics, and small-study effects were explored using Egger's test where estimable.

Seven studies met the eligibility criteria. In OR-based analyses, nominal associations with autism were observed for IL-10 (OR 1.34, 95% CI 1.06-1.69), CXCL10 (OR 1.62, 95% CI 1.24-2.11), IL-1α (OR 1.42, 95% CI 1.23-1.65), IL-5 (OR 1.49, 95% CI 1.18-1.89), and IL-17A (OR 0.81, 95% CI 0.70-0.94). CCL4 showed a borderline association. Supportive SMD analyses indicated higher IL-6 and lower IL-1β concentrations in autism-associated pregnancies. Heterogeneity varied across analytes and was substantial for IL-10 and CCL4.

Maternal gestational immune profiles may differ in pregnancies later associated with autism, but current evidence does not support a single robust cytokine biomarker. Progress requires larger prospective cohorts with repeated sampling, harmonised assays, pathway-level analyses, and integrated placental-fetal neurodevelopmental phenotyping.

Schizophrenia (SCZ) is a chronic mental disorder with unknown etiology and complex pathophysiology. Circular RNAs (circRNAs) have emerged as important regulators in neuropsychiatric disorders. This study investigated the clinical relevance, functional role, and potential mechanism of hsa_circ_0005567 in SCZ.

hsa_circ_0005567 expression was measured by qRT-PCR in peripheral blood mononuclear cells (PBMCs) from 160 patients with SCZ and 160 healthy controls. Associations with clinical symptoms and laboratory parameters were explored. Functional studies were conducted in MK-801-treated SH-SY5Y cells after hsa_circ_0005567 knockdown or overexpression. Cell viability, apoptosis, and inflammatory cytokines were assessed. Candidate hsa_circ_0005567-interacting proteins were explored using chromatin isolation by RNA purification (CHIRP), mass spectrometry, RNA immunoprecipitation, and Western blotting.

hsa_circ_0005567 expression was significantly increased in PBMCs from patients with SCZ (P < 0.001) and in SH-SY5Y cells following MK-801 treatment (P = 0.026). Higher hsa_circ_0005567 expression remained associated with SCZ status after adjustment for age and sex. Exploratory analyses of PANSS scores and laboratory parameters showed only nominal associations, none of which remained significant after FDR correction. In vitro, hsa_circ_0005567 manipulation affected cell viability, apoptosis, and TNF-α expression in MK-801-treated SH-SY5Y cells. RPL7A was identified as a candidate hsa_circ_0005567-interacting protein, and its protein expression was altered following hsa_circ_0005567 knockdown or overexpression.

hsa_circ_0005567 is upregulated in PBMCs from patients with SCZ and is independently associated with SCZ status. Functional experiments suggest that hsa_circ_0005567 may participate in cellular responses under MK-801-induced stress conditions, while RPL7A represents a candidate interacting protein. Further clinical and mechanistic validation is needed.

To characterize the clinical, functional, and educational characteristics of adolescents with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and compare selected illness domains with adults in the Multi-Site Clinical Assessment of ME/CFS (MCAM) study.

Baseline cross-sectional data from adolescents aged 10-17 years enrolled in MCAM were analyzed. Standardized measures included the Short Form-36 (SF-36v2), CDC Symptom Inventory (CDC-SI), Multidimensional Fatigue Inventory (MFI-20), and selected domains of the DePaul Questionnaire. Descriptive statistics characterized the pediatric cohort and bivariate analyses compared adolescents with adults enrolled in MCAM.

Forty adolescents (mean age 15.3 years; 52.5% female) were included. Mean illness duration was 4.0 years. Educational disruption was substantial: 64% received homebound or homeschool instruction, 89% missed school because of illness, and participants missed a mean of 10.8 school days during the preceding month. Physical health-related quality of life was substantially impaired. Persistent post-exertional malaise (PEM), unrefreshing sleep, fatigue, and neurocognitive symptoms were common. Compared with adults (n = 595), adolescents had shorter illness duration and better physical functioning, vitality, and social functioning, whereas mental health scores were similar. Adults reported greater burden across several physical symptom domains although many between-group differences were small.

Adolescents with ME/CFS experience substantial multisystem symptom burden, impaired physical functioning and educational disruption. Many core clinical features were similar to those in adults, supporting the need for early recognition and appropriate clinical and educational support.

Bipolar disorder is a disabling psychiatric condition affecting approximately 2% of the population, for which identifying modifiable risk factors prior to illness onset is a research priority. Cannabis use is highly prevalent, yet its role in the development of bipolar-spectrum outcomes remains unclear. Previous reviews have included few studies or combined distinct bipolar-spectrum outcomes, limiting outcome-specific inference.

To evaluate the association between cannabis exposure and subsequent incident BD and manic/hypomanic symptoms separately and examine potential moderating factors.

Registered (https://osf.io/s38x4/), PRISMA/MOOSE-compliant systematic review and meta-analysis of PubMed and Web of Science from inception to October 2025. We included longitudinal observational studies comparing cannabis-exposed and unexposed individuals without prior BD and assessing subsequent bipolar-spectrum outcomes. We meta-analysed studies with extractable data, calculating the unadjusted risk ratios (RRs) for incident BD and manic/hypomanic symptoms. Random-effects meta-analyses, heterogeneity analyses, subgroup analyses and meta-regressions were performed. Study quality was appraised using the Newcastle-Ottawa Scale (NOS).

Nineteen studies were included (total N = 6,960,517; mean age 23.8 ± 11.8 years; 49% female). Cannabis use was associated with increased risk of BD (RR = 2.46, 95% CI = 1.57-3.84; k = 8; N = 206.572) and manic/hypomanic symptoms (RR = 2.11, 95% CI = 1.07-4.18; k = 6; N = 57,243). Moderator analyses identified significant clinical and methodological sources of heterogeneity. NOS scores ranged from 6 to 9, indicating good to high methodological quality.

Cannabis use was associated with an increased risk of subsequent bipolar-spectrum outcomes. Routine evaluation of cannabis use alongside prevention strategies, to delay initiation and reduce use, may warranted.

Intermittent theta-burst stimulation (iTBS) is widely used for its rapid antidepressant efficacy in clinical practice. However, its underlying neuroimmune mechanisms and objective biomarkers of treatment response remain largely unexplored. High mobility group box 1 (HMGB1), a critical driver of neuroimmune interactions in stress-related disorders, may link peripheral inflammation to central pathological processes in depression and may serve as a potential therapeutic target. Therefore, we aimed to explore the functional involvement of HMGB1 in depression and whether HMGB1-related inflammatory signaling is modulated by iTBS.

We measured circulating HMGB1 levels in patients with Major depressive disorder (MDD). In mice exposed to chronic restraint stress (CRS) or LPS, HMGB1/TLR4/NF-κB signaling and neuroinflammatory responses in the prefrontal cortex were assessed. Glycyrrhizic acid (GA), a well-established HMGB1 antagonist, was used to determine the functional relevance of HMGB1. iTBS-mediated antidepressant effects were assessed via behavioral tests and HMGB1-related inflammatory signaling analysis.

HMGB1 was markedly upregulated in patients and in depressive‑like mouse models, accompanied by activation of the HMGB1/TLR4/NF-κB signaling pathway and increased neuroinflammation. GA alleviated depressive-like behaviors. iTBS reversed behavioral deficits and suppressed HMGB1-associated inflammatory signaling.

HMGB1 is functionally involved in depression, and the therapeutic effects of iTBS are associated with suppression of HMGB1-related neuroinflammatory signaling. These findings suggest that HMGB1 may have potential as a biomarker for monitoring the biological effects of iTBS and may provide a basis for further investigation of HMGB1 in treatment response.

A recent arts exposome framework identified 50 transdiagnostic causal mechanisms (emotional, cognitive, self-referential, arousal-stress, inflammatory-epigenetic, social, and behavioural) by which arts engagement may affect mental health, organised around patterned daily exposure to active ingredients across diverse modes of arts engagement. Translating this structure into testable predictions depends on two operational prerequisites that current research has under-addressed. First, the active ingredients must be decomposed into mechanism-aligned exposure dimensions: aggregating activities as varied as receptive consumption, active participation, and cultural attendance under "arts engagement" averages mechanistically different effects and yields findings that the framework cannot localise to specific processes. Second, mechanism tractability is unevenly distributed across measurement modalities. Stress-HPA-immune mechanisms are well-served by peripheral measurement, including transcriptomic markers such as the Conserved Transcriptional Response to Adversity. Aesthetic and reward mechanisms are tractable through central measurement and autonomic indices of aesthetic emotion, but not through peripheral biomarkers. Affiliative mechanisms face validity challenges in peripheral measurement that may require pharmacological probes or behavioural proxies. Neither prerequisite suffices alone: a valid biomarker linked to a heterogeneous exposure measures something the framework cannot interpret, and a well-specified exposure linked to an inappropriate modality deteriorates evidence quality. These refinements are best understood as minimum conditions for identifying the core ingredients that matter most for each mechanism, since individual and contextual variation continue to moderate activation in real-world settings. Together, they identify where mechanism research can deliver near-term advances, where alternative methods are needed, and how the framework can move from theoretical mapping toward ecologically grounded testable inference.

Chronic conditions, such as NonCommunicable Diseases (NCDs) and impairments in body structures, may limit activities of daily living. The quality of care of NCD patients in Malawi is low, leading to a high prevalence of complications of NCD in Malawi.

The study aimed at exploring the experiences of NCD patients living with complications in Mzuzu, Malawi.

This qualitative study recruited nine NCD patients with complications. The participants were selected purposively, and where applicable, we used the snowballing technique. Data were collected via in-depth interviews. The recorded data were transcribed and coded into themes and subthemes via thematic analysis.

The study found that two main attributes were common among NCD patients living with complications, namely, a lack of access to sanitation, including poor design of sanitation, loss of dignity, and lack of education on sanitation. They also faced challenges accessing health care, including long waiting times and a shortage of staff.

In conclusion, the study confirms that people living with NCD complications in resource-limited settings require special care to improve quality of life and dignity.

Gestational diabetes mellitus (GDM) is an increasing public health challenge in Africa, contributing substantially to maternal and neonatal morbidity. Evidence from our systematic review, meta-analysis, and bibliometric analysis shows that inconsistent screening practices, reliance on selective rather than universal testing, and limited health system capacity contribute to underdiagnosis and poor pregnancy outcomes. GDM is associated with adverse maternal and neonatal complications and increases the long-term risk of type-2 diabetes for mothers and offspring. Our bibliometric findings reveal uneven research capacity, limited regional collaboration, and evidence gaps across Africa. We propose five policy priorities: standardising GDM screening, strengthening prevention, expanding access to diagnostics and treatment, improving workforce capacity and follow-up, and increasing investment in African-led research to improve maternal health and reduce the intergenerational burden of diabetes.