Trichotillomania (TTM) is a body-focused repetitive behavior that may function as an affect regulation strategy. In bipolar-spectrum youth, persistent emotion regulation difficulties may be particularly relevant for early recognition and intervention. In a cross-sectional design, euthymic adolescents with bipolar disorder and a documented lifetime history of TTM (BD+TTM) were compared with euthymic adolescents with bipolar disorder and no lifetime TTM (BD-only) and age- and sex-matched healthy controls (40 participants per group). None of the BD+TTM participants had active hair-pulling at assessment; lifetime TTM severity was scored on the National Institute of Mental Health Trichotillomania Symptom Severity Scale (NIMH-TSS) retrospectively, anchored to the period of greatest historical severity, on the basis of structured caregiver-and-youth interviews and chart review. Participants completed clinician-rated measures of manic symptoms and self-reported measures of depressive symptoms, impulsivity, and emotion regulation difficulties. Group differences were examined with effect-size estimates, and data-driven K-means clustering was used to identify symptom profiles within the full sample. Within the BD+TTM group, correlational and regression analyses tested independent correlates of retrospectively scored lifetime TTM severity. Emotion regulation difficulties showed a graded increase from healthy controls to BD-only to BD+TTM. Retrospectively scored lifetime TTM severity was strongly associated with emotion regulation difficulties and, in multivariable models adjusted for medication load, emotion regulation difficulties were the only independent correlate. Clustering identified an affective-dysregulation profile in which lifetime TTM severity was highest. In bipolar-spectrum youth, a documented lifetime history of TTM appears to mark a clinically meaningful affective-dysregulation phenotype. Because TTM was documented historically rather than assessed during active symptoms, findings are correlational and hypothesis-generating; early dimensional assessment of emotion regulation difficulties may nonetheless help guide mechanism-focused interventions.

Objective: Nicotine use in schizophrenia remains markedly higher than in the general population, contributing to increased morbidity, relapse, and functional impairment. While biological factors have been widely studied, limited attention has been given to the psychosocial factors that sustain nicotine use in this group. This review synthesizes available evidence on these psychosocial influences to inform intervention planning and policy development. Methods: A narrative review was conducted using PubMed, Scopus, ProQuest, and Google Scholar to identify studies from 2000 to 2025 that examined psychosocial, socio-cultural, or systemic factors associated with nicotine use in schizophrenia. Thirty articles meeting the inclusion criteria were analyzed thematically across three domains: psychological, socio-cultural, and systemic influences. Results: Psychological factors such as stress regulation, cognitive enhancement, loneliness, maladaptive coping, and low self-efficacy reinforced nicotine use. Socio-cultural determinants included male gender, unmarried status, peer influence, social exclusion, stigma, and familial smoking patterns, while systemic enablers encompassed institutional permissiveness, limited cessation support, and pro-tobacco policies. Collectively, these dimensions interact to maintain nicotine dependence and impede recovery and contribute to an increased risk of relapse in schizophrenia, poorer prognosis, higher Disability- Adjusted Life Years, impaired functional recovery, and disability. Conclusions: Nicotine use in schizophrenia is reinforced by interconnected psychosocial and structural forces extending beyond biological vulnerability. A biopsychosocial approach-combining psychoeducation, family support, social rehabilitation, and institutional policy reform-offers a pathway to sustainable cessation and functional recovery in this population.

This review examines how prenatal inflammation may contribute to psychiatric and neurodevelopmental disorders, with a focus on maternal immune activation, microglial programming, and epigenetic mechanisms.

Recent studies have found that inflammation during pregnancy is associated with changes in brain development and neurodevelopmental outcomes in children. Animal research indicates that maternal immune activation can cause long-lasting changes in gene expression, neural circuitry, and microglial activity. Two-hit models suggest that prenatal inflammation may prime microglia, making the brain more vulnerable to later stress, infections, or adversity. Interventions that target microglia, reduce inflammation, or provide enriched environments may reduce downstream behavioral and neurodevelopmental effects.

Inflammation in early life may increase the risk of psychiatric disorders by altering placental signals, fetal brain development, and neuroimmune regulation. Preventing inflammation during pregnancy and reducing stress and adversity after birth may help protect against later mental health problems.

This Registered Report tested perinatal predictors of infant resting respiratory sinus arrhythmia (RSA), an index of parasympathetic functioning. Maternal RSA was collected at a resting state during the third trimester of pregnancy (N = 385, 56.9% of the pregnant mothers were White, non-Hispanic/Latina). Newborn attention and arousal were assessed shortly after birth. When infants (48% are male, and 50.7% are White, non-Hispanic/Latino) were 7 months old, their resting RSA was measured, and maternal sensitivity during a free-play interaction was coded. Greater maternal prenatal RSA was found to be associated with greater infant resting RSA. This longitudinal and intergenerational association was not significantly moderated or mediated by newborn neurobehavior or maternal sensitivity. Findings suggest that infant RSA may have roots in mothers' parasympathetic functioning during pregnancy.

Genomic imprinting is a form of epigenetic regulation that leads to expression from one parental allele only and, in animals, is unique to mammals. Imprinted gene expression is predominant in the brain and their roles in neural processes are becoming more appreciated. Recent analyses have indicated an enrichment of imprinted gene expression in the 'parental hub' circuitry. Specifically, imprinted genes were over-represented in the transcriptomic profile of galanin positive (Gal⁺) neurons in the medial preoptic area (MPOA) of the hypothalamus. One of those imprinted genes showing enriched expression in Gal⁺ neurons was the maternally expressed Asb4. Here, we propose that Asb4 supports normal activation of MPOA Gal⁺ neurons required for parental care. We aim to demonstrate abnormal parental behaviours-such as decreased pup retrieval and impaired nest building-and activity of MPOA Gal⁺ neurons in brain-specific maternal Asb4 knockout mice and hypothesis knockout animals will demonstrate a deficient behavioural phenotype in one or more parental behavioural characteristics.

Open disclosure is an open discussion with a patient and/or family member about an incident(s) that resulted in harm to that patient while they were receiving healthcare. It is widely considered an ethical and moral imperative and is what patients and families want when harm occurs. However, there is a dearth of research on patient and family experiences of open disclosure and limited measures available to measure the quality of current processes. This research aimed to address this gap by using an evidence-informed approach to working with experts by experience to co-design a mechanism to measure patient experience of open disclosure.

We adopted a co-design approach, which involves partnering with stakeholders in the healthcare system to address a shared goal and working collaboratively to develop consensus about how best to address an identified challenge. A co-design team was established which included experts by experience (those with direct patient/family experience of open disclosure; n = 5), patient advocates (n = 2), patient and service user engagement lead in the health system (n = 2), quality and patient safety managers/advisors (n = 3), members of the National Open Disclosure Team (n = 3) and academics/researchers (n = 3). A one-day in-person workshop was held using the World Café approach whereby a series of small group discussions on sub-topics helped develop consensus on how to measure experience.

Participants agreed that a brief survey, focusing on key aspects of the open disclosure process would be the optimal way for patients and relevant others to provide feedback that could support learning and quality improvement. Participants acknowledged the use of open text comment boxes within the survey would be useful to allow respondents to elaborate on their experience further, if desired. Furthermore, the survey should provide the option for the respondent to indicate if they would like to speak to someone about their experience of open disclosure in more detail. The co-design team agreed that everyone who has experience of open disclosure, regardless of level of harm, should be eligible and invited to take part in providing feedback on their experiences. A draft survey was developed by the group and is presented in full.

This paper documents the co-design approach adopted on this sensitive topic and shares recommendations that emerged from the co-design process of how experiences of open disclosure should be measured for the purposes of improvement. While the survey was deemed optimal by co-design group members, it is acknowledged that this could be challenging for some to complete. This draft survey however offers a valuable starting point to understanding if the process is working as intended for patients and families who experience harm.

When care coordination meets crisis in conflict and humanitarian settings, humanitarian actors and pediatric clinicians require resources that articulate the best practices that can be used to systematically manage non-communicable diseases (NCD) in low- and middle-income countries (LMICs). This article discusses NCD burden among children in LMICs and offers a brief review of key guidelines, frameworks, and care models that can be leveraged to maximize child health and well-being in the wake of a humanitarian crisis. Special attention is paid to children less than the age of 20.

Dietary modification is an important strategy for the prevention of type 2 diabetes, with fibre intake recognised as a key factor in promoting metabolic health. Resistant starch (RS), a type of fermentable dietary fibre, has emerged as a promising therapeutic approach due to its association with weight loss, enhanced insulin sensitivity and improved glucose metabolism. As nutritional research progresses, the focus has shifted from individual nutrients to overall dietary patterns. Based on this concept, this study aims to investigate the metabolic effects of a dietary pattern that optimises carbohydrate structure by increasing RS intake and reducing rapidly digestible carbohydrate in adults with pre-diabetes.

This is a multicentre, randomised, parallel-controlled clinical trial, which will enrol 250 adults diagnosed with pre-diabetes. Eligible participants will undergo randomisation to receive either a guideline-based conventional diet or an optimised carbohydrate diet (OCD). In the OCD intervention, daily RS intake will be increased to approximately 40 g, with fibre intake rising to 20-40 g per 1000 kcal. At the same time, the intake of rapidly digestible starch and free sugars will be reduced. The intervention will last for 6 months, followed by a 3-month post-intervention follow-up period. The primary outcome is the change in postprandial glycaemic response, assessed using the incremental area under the curve (iAUC) for plasma glucose during the oral glucose tolerance test (OGTT). Secondary outcomes include the proportion of participants achieving remission to normoglycaemia or progressing to type 2 diabetes, changes in other glucose- and lipid-related metabolic parameters and changes in lifestyle-related behavioural factors. Exploratory outcomes will include changes in appetite-related hormones, circulating cytokines, immune function and multi-omics profiles.

This study was approved by the Ethics Committee of Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine (Approval No. 2025-122; Protocol V.1.0, 20250811) and the Ethics Committee of Shenzhen Center for Chronic Disease Control (Approval No. SZCCC-2024-011-01-PJ) and registered in the Chinese Clinical Trial Registry. Findings from this study will be disseminated in peer-reviewed journal publications.

ChiCTR2500113583.

Pre-diabetes is becoming increasingly prevalent in adolescent populations. We recently reported a high prevalence of pre-diabetes among rural adolescent girls from the DERVAN cohort study established in the predominantly undernourished KONKAN region of India. We aimed to investigate the heterogeneity of pre-diabetes by identification of distinct subtypes.

Anthropometry (body mass index (BMI) and waist circumference) and body composition (adiposity), as well as glycemic parameters (glucose, insulin, and glycated hemoglobin), were measured at the recruitment stage. Indices for insulin resistance (homeostatic model assessment (HOMA)-IR), β-cell function (HOMA-β), insulin sensitivity (HOMA-S), and compensatory β-cell response for prevailing insulin insensitivity were calculated using the homeostasis model. Pre-diabetes was diagnosed using the American Diabetes Association criteria. Unsupervised K-means clustering and a subgrouping algorithm were applied to characterize pre-diabetes. We used BMI, waist circumference, and adiposity for characterization. Glycemic parameters and HOMA indices were compared between clusters, as well as subgroups.

Among 1382 girls, 809 (58.5%) were thin and 550 (39.8%) were pre-diabetic. We identified five clusters based on phenotypic characteristics: Cluster 1: young lean (YL), Cluster 2: old lean (OL), Cluster 3: low BMI-high waist, Cluster 4: normal BMI-low waist, and Cluster 5: obese. The cluster frequencies were 145 (26.4%), 131 (23.8%), 146 (26.5%), 74 (13.5%), and 54 (9.8%). Clusters YL and OL had the lowest fasting insulin concentrations, HOMA-IR, and HOMA-β but high HOMA-S and a compensatory β cell response for prevailing insulin insensitivity. Subgroup analysis further revealed a distinct lean pre-diabetic phenotype (n=314) with the lowest BMI (<18.5 kg/m²), no central obesity and adiposity, and the lowest fasting insulin concentration, HOMA-IR, and HOMA-β compared with remaining subgroups.

We demonstrated the existence of a distinct lean pre-diabetic phenotype in adolescent girls whose characteristics seem to mirror those of adult type 5 diabetes, which has been recently recognized as a distinct entity. This suggests a need for precise strategies for primordial prevention.