Generalized Anxiety Disorder (GAD) and Major Depressive Disorder (MDD) are prevalent mental health conditions, and low self-esteem is considered a vulnerability factor for psychological distress. However, the relationship between self-esteem and symptom severity remains unclear, as evidence regarding the nature of this association is still insufficient. On the other hand, experiential avoidance is recognized as a transdiagnostic variable closely linked to clinical outcomes and individual characteristics, while also being associated with psychological resilience. This study investigates the serial mediating roles of experiential avoidance and psychological resilience in the relationship between self-esteem and the severity of anxiety and depressive symptoms in individuals diagnosed with GAD and MDD.

The study was conducted with 201 voluntary participants aged between 18 and 65 who had been diagnosed with either GAD (n = 90) or MDD (n = 111) and were being monitored accordingly. Participants were assessed using a sociodemographic and clinical data form prepared by the interviewer, along with the Hamilton Anxiety Rating Scale, Hamilton Depression Rating Scale, Psychological Resilience Scale, Rosenberg Self-Esteem Scale, and the Multidimensional Experiential Avoidance Questionnaire.

The results indicate an indirect relationship between self-esteem and anxiety and depressive symptoms, mediated by experiential avoidance and psychological resilience. This mediation effect was found to be complete for anxiety and partial for depression. Sensitivity analysis confirmed the robustness of the mediation findings.

The findings suggest that individuals diagnosed with GAD and MDD tend to adopt more experiential avoidance strategies in relation to low self-esteem, which in turn leads to a decrease in psychological resilience and an increase in symptom severity. Accordingly, interventions targeting experiential avoidance in the context of self-esteem may contribute to symptom reduction by enhancing psychological resilience.

Although previous studies have identified associations between insecure attachment styles and nomophobia (NMP), the underlying psychological mechanisms remain underexplored. Grounded in attachment theory, this study investigates the mediating roles of school belongingness and life satisfaction in the relationship between attachment styles and NMP in adolescents.

The study was conducted with 230 adolescents aged 12 to 18, recruited from a child and adolescent psychiatry outpatient clinic. Participants completed the Attachment Styles Scale in Interpersonal Relationships (ASSIS), Nomophobia Questionnaire (NMP-Q), School Belongingness Scale (SBS), and Life Satisfaction Scale (LSS).

Mediation analysis revealed that anxious attachment was associated with increased NMP through decreased school belongingness (β = 0.036, p = 0.043) and reduced life satisfaction (β = 0.059, p = 0.014). Similarly, secure attachment was associated with lower NMP via higher school belongingness (β = -0.054, p = 0.037) and life satisfaction (β = -0.056, p = 0.013). Avoidant attachment was not significantly associated with NMP or the proposed mediators.

The findings suggest that adolescents' attachment styles influence NMP through their senses of school belongingness and life satisfaction. Designing school-based psychosocial initiatives that cultivate relational anchoring and perceived life coherence may provide a developmentally attuned avenue to buffer NMP risk, particularly in adolescents exhibiting anxious attachment style.

Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, compromises both physical and psychological health. High levels of stress, anxiety, and depression are common yet often overlooked, negatively impacting treatment adherence and self-care. This review examines how psychological factors influence self-care behaviors in IBD and explores strategies to improve disease management. Following PRISMA guidelines and registered on PROSPERO (CRD42024575631), this systematic review applied the PICO model to identify studies involving IBD patients, self-care interventions, and outcomes related to depression, anxiety and stress. A comprehensive search was conducted in PubMed, CINAHL, Web of Science, Scopus, Cochrane Library, APA PsycInfo and Google Scholar (October-December 2024). JBI tools were used to assess risk of bias, and evidence was graded using the framework established by the Oxford Centre for Evidence-Based Medicine. Data extraction and synthesis were performed using structured tables and graphs. IBD patients frequently experience psychological distress that impairs self-care and quality of life. Depression is associated with low self-efficacy and maladaptive coping, while anxiety reduces treatment adherence, particularly in younger patients. Stress contributes to disease management difficulties, reinforcing the need for integrated psychological support. Psychological distress in IBD patients significantly affects self-care behaviors. Incorporating mental health support into standard care may enhance adherence, disease control, and overall well-being.

Rotator cuff tendinopathy (RCT) is a major contributor to over 30 million surgeries which are conducted to treat shoulder overuse injuries worldwide annually. Accumulating evidence indicates that neuropsychiatric disorders (ND) share pathogenic pathways with tendinopathy. However, unclarified causal relationships between these two disease spectra undermine the individualized design of treatment strategies benefiting patients with ND while minimizing the RCT risk. We aimed to unveil whether ND were genetically associated with increased RCT occurrence by conducting a two-sample Mendelian randomization (MR) algorithm.

Genome-wide association studies (GWAS) data of attention deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BD), epilepsy, major depressive disorder (MDD), obsessive compulsive disorder (OCD), post-traumatic stress disorder (PTSD), schizophrenia (SCZ), and RCT patients of European ancestry were retrieved for bidirectional two-sample Mendelian randomization (MR) analyses to establish causal relationships among these eight main types of ND and RCT. To detect false positive findings, MR-Egger, weighted median and causal analysis using summary effect estimates (CAUSE) were employed as sensitivity tests. Body shape, lifestyle, and socioeconomic parameters were adjusted as mediators in multivariable MR to validate the robustness of the results.

Univariable MR revealed that genetic predisposition to ADHD (odds ratio [OR] 1.14, 95% confidence interval [CI] 1.05-1.24, p = 0.001) and PTSD (OR 2.23, 95% CI 1.75-2.84, p < 0.001) significantly increased the RCT risk. MDD showed a similar association (OR 1.21, 95% CI 1.06-1.38, p = 0.004), which was attenuated after confounder adjustment (p = 0.78). Multivariable MR confirmed ADHD (OR 1.09, 95% CI 1.01-1.18, p = 0.02) and PTSD (OR 2.00, 95% CI 1.41-2.82, p < 0.001) as robust causal factors for RCT after adjusting for anthropometric, lifestyle, physical activity, and socioeconomic confounders.

Our study sheds new light on the need for early screening, targeted overuse injury prevention, and specialized clinical interventions to alleviate the RCT burden in ADHD and PTSD populations.

The clinical relevance of thyroid hormone-mediated inotropic effects in humans remains uncertain. We evaluated ventricular function in patients with severe hypothyroidism and myxedema coma using transthoracic echocardiography (TTE) and speckle-tracking echocardiography (STE).

Multicenter, retrospective cross-sectional study of adults admitted to intensive care units (ICUs) with severe hypothyroidism who underwent TTE during hospitalization. Left ventricular (LV) systolic and diastolic function and myocardial deformation, assessed by global longitudinal strain (GLS), were analyzed.

112 patients were included (mean age 53.9 ± 13.7 years; 64.3% female). Myxedema coma was present in 33 patients (29.5%), and 13 (11.6%) had severe hypothyroidism with altered mental status without hypothermia or bradycardia. Median admission TSH was 113.9 (41.9-500.0) mIU/L. Mean LV ejection fraction (LVEF) was 53.9 ± 13.7%, LV GLS -13.5%±4.2% (reference -24% to -16%), and right ventricular (RV) GLS -17.9%±6% (reference -35% to -17%). Reduced LVEF occurred in 37.5% of patients, abnormal LV diastolic function in 66.7%, and impaired LV and RV GLS in 68.2% and 34.0%, respectively. In multivariable models, beta-blocker treatment was associated with lower LVEF and worse biventricular GLS; ACE inhibitor/angiotensin receptor blocker treatment with lower LVEF; and calcium channel blocker exposure was associated with improved RV GLS. In-hospital mortality was 4.5% and occurred in patients with preserved LVEF.

Severe hypothyroidism is associated with frequent systolic and diastolic ventricular dysfunction and prevalent impairment of myocardial deformation. Associations between cardiovascular medication exposure and echocardiographic abnormalities likely reflect confounding by indication and underlying clinical phenotype rather than reflecting causal drug effects. Despite substantial myocardial abnormalities, short-term mortality was low.

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with exposure to repetitive head impacts (RHIs), characterized by tau tangles around small blood vessels at the depths of the sulci. Currently, CTE can be diagnosed only postmortem, but can present with an array of cognitive, behavioral, mood, and motor symptoms. However, traumatic brain injury is also associated with increased risk of Alzheimer's disease (AD) and may lead to comorbid neuropathology. Characterization of the in vivo biomarkers of CTE is a necessary next step to facilitate accurate diagnoses. We examined the profile of cerebrospinal fluid (CSF) biomarkers of amyloid-β, total tau (tTau), and phospho-tau (pTau) in a cohort of former professional (PRO, n = 100) and college (COL, n = 40) football players at high risk of CTE compared to asymptomatic unexposed controls (UE, n = 43). CSF was collected under controlled conditions using collection, processing, and cryostorage kits provided by the DIAGNOSE CTE Research Project Biomarker Core, and concentrations of Aβ₄₀, Aβ₄₂, tTau, and pTau (pTau₁₈₁, pTau₂₁₇, pTau₂₃₁) were measured at the University of Gothenburg, Sweden, using immunoassays. Associations between CSF biomarker levels with football history, and diagnosis of traumatic encephalopathy syndrome (TES) were examined using linear regression, and corrected for age, education, APOE-ε4 allele status, race, and body mass index. Our analysis revealed that football exposure affected both CSF Aβ₄₀ (p = 0.039) and Aβ₄₂ (p = 0.038), particularly among those under 60 years of age in the PRO compared to the UE exposure group. Among former football players, estimates of RHI exposure were not generally associated with CSF Aβ, tTau, and pTau biomarker levels. CSF Aβ₄₀ (p = 0.0041) and Aβ₄₂ (p = 0.011) were lower in former football players with TES diagnosis compared to unexposed participants, although CSF Aβ, tTau, and pTau biomarker levels did not differ between former players with and without a TES diagnosis. Among former football players, reduced CSF Aβ₄₀ (p = 0.011) and Aβ₄₂ (p = 6e-04) were observed in those with cognitive impairment compared to those with neurobehavioral dysregulation. The findings of significant associations of reduced CSF Aβ levels with RHI in elite football players are in line with recent postmortem studies; however, the lack of relationship with CSF tTau and pTau species observed to be altered in the setting of AD suggests that the pathological features of CTE reflected in fluid biomarkers are complex and require further study. The overlapping comorbid age-dependent features of neurodegeneration that occur in those at risk for CTE suggest that tau pathology in CTE is not reliably reflected by currently available fluid biomarkers and that the use of multiple biomarkers related to the compound characteristics of CTE may be required for early detection.

Clinical high risk for psychosis (CHR-P) is associated with distress, impairment, and elevated risk for developing full-threshold psychosis. Early intervention can improve prognostic outcomes, but limited research has investigated associations between social determinants and mental health care utilization among people at CHR-P. The authors aimed to explore whether distressing positive symptoms, race-ethnicity, immigration, racial discrimination, and social support correlate with mental health care utilization in this population.

Data were drawn from a parent study in which community-based participants completed questionnaires and clinical interviews. Participants included in the present analyses were ages 16-30 and met interview-based criteria for CHR-P (N=171).

Asian and Black participants were significantly less likely than White participants to report past use of mental health care. Black participants were significantly less likely than White participants to report current use of services. Differences in past service use for Asian and Black participants versus Hispanic/Latinx participants and in current service use for Asian versus White participants approached statistical significance. Trend-level associations suggesting a lower likelihood of service use among immigrant participants were attenuated when household income was accounted for. Across the full sample, distressing positive symptoms significantly predicted current use of services.

Associations between self-reported race-ethnicity and mental health care utilization persisted even when analyses accounted for distressing positive symptoms, social support, and discrimination. As CHR-P research and practice increasingly focus on early intervention, study findings underscore the importance of better understanding contextual factors and social determinants that are associated with mental health service use among youths at CHR-P.

Major depressive disorder (MDD) in adolescents is increasingly prevalent and associated with high recurrence, suicide risk, and disease burden. Family caregivers, typically parents or close relatives, often internalize public stigma, resulting in affiliate stigma-shame and distress arising from their association with patients. This stigma impairs caregivers' mental health, quality of life, and patients' recovery. However, few studies have explored how psychosocial factors such as social support, coping style, and family functioning influence affiliate stigma. This study therefore examines its score level, influencing factors, and the mediating roles of family functioning and coping style.

A cross-sectional study we conducted at a mental health center in Inner Mongolia, China. A total of 308 family caregivers of adolescents diagnosed with MDD were recruited. Demographic information, affiliate stigma, social support, family functioning, and coping styles were assessed using validated instruments. Data we analyzed using IBM SPSS Statistics 26.0 and AMOS 24.0 to examine the influencing factors of affiliate stigma and the underlying mechanisms through structural equation modeling.

The average affiliate stigma score among caregivers was74.922 ± 9.834. Multiple regression analysis showed that social support, family functioning, positive and negative coping styles, gender, education level, household income, and whether the adolescent was experiencing a first depressive episode independently predicted of affiliate stigma (P < 0.05), explaining 65.5% of the variance (R² = 0.655). The structural equation model showed acceptable fit with room for improvement (χ² = 2431.24, df = 1394,; χ²/df = 1.744; RMSEA = 0.075; CFI = 0.905; GFI = 0.914;IFI = 0.916;TLI = 0.913). Social support had indirect effects on affiliate stigma via family functioning (-6.5%) and coping styles (-9.5%), with all pathways being statistically significant (P < 0.01).

Family caregivers of adolescents with MDD experience moderately high levels of affiliate stigma. Social support not only directly influences stigma but also exerts indirect effects through family functioning and coping strategies. Interventions should focus on improving family functioning and promoting adaptive coping to reduce affiliate stigma.

Vascular damage, including cerebral amyloid angiopathy (CAA) and non-amyloid cerebral small vessel disease (CSVD), has been linked to glymphatic dysfunction, which may contribute to Alzheimer's disease (AD) pathology and cognitive decline. We investigated the associations among vascular damage, glymphatic function measured by the DTI-ALPS (Diffusion Tensor Imaging-Analysis Along the Perivascular Space) index, AD plasma biomarkers, and cognitive decline.

This study includes 1,249 participants recruited from Samsung Medical Center. We performed linear regression analysis to identify factors associated with the DTI-ALPS index. Further, linear regression analysis with vascular imaging markers, including CAA and CSVD summary scores, as predictors and DTI-ALPS index as an outcome was performed to investigate the effect of vascular pathology on glymphatic function. We conducted mediation analyses to investigate whether the DTI-ALPS index mediates the effect of vascular imaging markers on plasma biomarkers (phosphorylated tau 217 [p-tau 217], glial fibrillary acidic protein [GFAP], and neurofilament light chain [NFL]). Additionally, mediation analyses with the DTI-ALPS index as a predictor, each plasma biomarker as a mediator, and annual MMSE or CDR-SOB change as an outcome to investigate whether plasma biomarkers mediate the effect of the DTI-ALPS index on longitudinal cognitive decline.

First, the DTI-ALPS index was negatively associated with both CAA (β [95% CI] = -0.163 [-0.214, -0.112], p < 0.0001) and CSVD (β [95% CI] = -0.195 [-0.247, -0.143], p < 0.0001) summary scores after controlling for age, sex, BMI status, and APOE genotype. Second, the DTI-ALPS index fully mediated the relationship between these vascular markers and p-tau 217 (CSVD summary score, indirect effect β [95% CI] = 0.016 [0.010, 0.023], p < 0.001; CAA summary score, indirect effect β [95% CI] = 0.013 [0.008, 0.020], p < 0.001) and GFAP (CSVD summary score, indirect effect β [95% CI] = 0.015 [0.008, 0.022], p < 0.001; CAA summary score, indirect effect β [95% CI] = 0.012 [0.007, 0.019], p < 0.001), while partially mediating the relationship for NFL, regardless of Aβ uptake on PET. Finally, the DTI-ALPS index was significantly associated with cognitive decline and this association was partially mediated by plasma biomarkers.

These findings highlight glymphatic dysfunction as a key mechanism linking vascular pathology with tau, inflammation and neurodegeneration, independent of Aβ uptakes.

Patients with self-harm and suicidal ideation are increasingly presenting in emergency departments (ED) in the UK. Self-harm is the strongest risk factor for suicide. Currently, there are no evidence-based interventions for self-harm offered in the context of general hospitals in the UK. This trial, funded by the National Institute for Health and Care Excellence (NIHR), aims to assess the clinical and cost-effectiveness of the ASSURED intervention. The ASSURED intervention includes up to five rapid follow-up contacts, comprising a narrative interview and enhanced safety planning session and three solution-focused sessions. The trial is sponsored by Devon Partnership NHS Trust and City St George's, University of London.

ASSURED is a multicentre, two-arm, parallel-group, individually randomised, controlled trial comparing the ASSURED intervention with usual care. The primary outcome is whether study participants re-attend ED and are referred to liaison psychiatry within 18 months from the date of randomisation. Secondary outcomes include suicidality, self-reported self-harm, psychological wellbeing, social outcomes, experiences of attending the ED, and suicide. The study will also evaluate the cost-effectiveness of the intervention. The aim of this study was to recruit and randomise 620 patients across 14 acute hospital sites in London, Devon, Somerset, and the Midlands. Participants are invited to complete research assessments at baseline and 3, 9, and 18 months. The first participant was enrolled in the study in August 2022, and the recruitment target was met in December 2024.

This will be the first UK trial to test the effectiveness and cost-effectiveness of a rapid intervention for patients presenting to EDs with self-harm and suicidal ideation and has the potential to improve outcomes for these patients.

ISRCTN 13472559. Registered on 18 of November 2021.