Muslim mental health is an emerging field of inquiry in the global South. Understanding how mental health conditions are interpreted within diverse Muslim communities is important for culturally responsive psychological care.

This qualitative study explored psychologists' experiences of providing services to Muslim clients in the Western Cape, South Africa, and explored psychologists' accounts of explanatory models of mental health conditions encountered in therapeutic practice. Semi-structured interviews were conducted with 15 clinical and counseling psychologists practicing in the Western Cape. Data were analyzed using Reflexive Thematic Analysis.

Three themes were constructed. First, psychologists emphasized the importance of understanding Muslim clients within their broader sociocultural and historical context, particularly the enduring influence of Apartheid, migration histories, intergenerational trauma, and institutional mistrust. Second, psychologists reported encountering diverse explanatory models among Muslim clients, including interpretations of distress in relation to religiosity, supernatural influences, stigma, personal weakness, and biomedical understandings. These explanatory models were described as shaping emotions such as fear, guilt, and shame, as well as pathways to help-seeking and engagement with treatment. Third, psychologists highlighted the importance of culturally responsive practice, including reflexive engagement with clients' religious worldviews, ongoing self-education, culturally informed supervision, and ethical collaboration with Muslim religious leaders.

The findings suggest that explanatory models are not solely individual beliefs about MHC but are embedded within broader religious, familial, historical, and sociopolitical contexts. By exploring psychologists' accounts of therapeutic encounters with Muslim clients in the Western Cape, this study extends explanatory-model scholarship by highlighting how collective histories and relationships with systems of care shape understandings of mental health and help-seeking.

Type 2 diabetes mellitus (T2DM) is frequently accompanied by complex brain microstructural abnormalities and cognitive decline. Conventional diffusion tensor imaging (DTI) metrics can reflect both tissue diffusion properties and extracellular free-water effects, complicating the interpretation of T2DM-related brain changes. We aimed to characterize free-water-corrected diffusion alterations in white matter (WM) and cortical gray matter (GM) and examine their associations with cognitive performance and fasting blood glucose.

We enrolled 48 patients with T2DM and 48 healthy controls (HCs). Diffusion measures included conventional fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD), together with free-water-corrected FA (FAt), free-water-corrected MD (MDt), free-water-corrected AD (ADt), and free-water-corrected RD (RDt), as well as the free-water fraction (FW), estimated using a free-water elimination (FWE) DTI model. Tract-based spatial statistics (TBSS) was used to evaluate all nine diffusion metrics in WM, whereas gray matter-based spatial statistics (GBSS) was used to evaluate six metrics in the cortical GM skeleton (AD, MD, RD, ADt, MDt, and RDt). Voxel-wise association analyses were performed using FMRIB Software Library (FSL) randomise based on a general linear model with nonparametric permutation testing to examine the relationships of imaging metrics with fasting blood glucose and Mini-Mental State Examination (MMSE) scores, while adjusting for age, sex, and total intracranial volume in the primary models; sensitivity models additionally included diagnostic group as a covariate.

Compared with HCs, patients with T2DM showed widespread diffusion abnormalities across the WM and GM skeletons, including lower FAt and higher MDt, ADt, and RDt. No skeleton-wide between-group difference in the estimated FW was detected. In the primary analyses, higher fasting blood glucose was associated with higher FW in selected WM regions and greater cortical GM diffusivity, whereas lower MMSE scores were associated with widespread WM and GM diffusion abnormalities.

T2DM-related diffusion abnormalities persisted after free-water correction, whereas no skeleton-wide between-group difference in the estimated FW was detected. Integrating FWE with complementary spatial analyses of WM and cortical GM may help characterize diffusion-derived brain phenotypes and their clinical correlates in T2DM.

Adult ADHD and autism assessment services increasingly receive clinically heterogeneous referrals in which the sequelae of childhood adversity may overlap with neurodevelopmental presentations. The distribution and clinical significance of adverse childhood experiences (ACEs) in this referral population remain insufficiently characterized.

This retrospective cross-sectional cohort study analyzed routinely collected clinical data from 389 adults who attended either the ADHD or the autism diagnostic pathway of a regional National Health Service (NHS) Adult ADHD and Autism Service. The analytic sample consisted of 233 adults with a definitive diagnostic outcome at data extraction; 149 were awaiting an outcome, six had an inconclusive outcome, and one underage case was excluded. ACE exposure was measured with the 10-item ACE Questionnaire. Psychiatric symptom burden was assessed with routinely administered screening instruments (PHQ-9, GAD-7, AUDIT, DAST-10, MDQ, HELPS and IPDS). The primary analysis examined the association between ACE score, analyzed as a continuous variable, and diagnostic outcome, with adjustment for age, gender and assessment pathway in binary logistic regression; all other analyses were exploratory.

Forty-seven participants (20.2%) received a diagnosis of ADHD or autism and 186 (79.8%) did not meet DSM-5 criteria. The mean ACE score was 3.10 (SD = 2.59), and 39.7% of participants reported four or more ACEs, compared with 8.3% in an English national household survey. Participants who were not diagnosed reported higher ACE scores than participants who were diagnosed (3.37 vs. 2.04; Hedges g = 0.52, 95% CI 0.19-0.84, p = 0.002). In the adjusted model, each additional ACE was associated with lower odds of receiving a neurodevelopmental diagnosis (odds ratio 0.85, 95% CI 0.73-0.99, p = 0.040). The proportion diagnosed declined across ACE categories from 35.6% (no adversity) to 6.2% (six or more ACEs). ACE scores correlated positively with depressive symptoms (r = 0.37), anxiety symptoms (r = 0.28) and drug use scores (r = 0.27), but not alcohol use, and were higher among participants screening positive for possible personality disorder, head injury and mood disorder. In an exploratory model additionally adjusting for depressive symptoms and personality disorder screening status, the ACE association attenuated and was no longer statistically significant, indicating that it is not independent of concurrent psychiatric symptom burden.

ACE exposure in this referral cohort was substantially higher than English population estimates and was associated with diagnostic non-confirmation and with greater psychiatric symptom burden. These findings support consideration of childhood adversity within trauma-informed formulation during adult neurodevelopmental assessment. Prospective studies incorporating direct measures of trauma-related psychopathology are needed to determine whether trauma-related mechanisms contribute to neurodevelopmental-like presentations. The cross-sectional retrospective design precludes causal inference.

Effective management of drug-resistant tuberculosis requires molecular assays that not only detect Mycobacterium tuberculosis but also identify resistance-associated variants, support drug-level interpretation, and indicate when broader confirmatory testing is needed. This narrative review applies a mutation-to-drug-to-decision framework to distinguish assay validity, exact-variant detection, drug-level inference, and decision impact. We synthesize evidence on target accessibility, minority-allele preservation, multiplexing, direct-specimen testing, and sequencing enrichment, emphasizing how these factors shape clinical interpretability. Current evidence remains dominated by analytical studies, isolate-based evaluations, and small direct-specimen investigations, with prospective multicenter treatment-impact validation still lacking. Population-level benchmarks indicate incomplete biological coverage for compact target regions, reaching approximately 92.6% for rpoB RRDR-based rifampicin detection, 85.4% for katG codon 315 plus the inhA promoter for isoniazid, and 84.7%-88.2% for gyrA/gyrB-based fluoroquinolone detection. Allele-specific CRISPR is therefore best suited to rapid rule-in of selected resistance-associated variants, while dispersed or heterogeneous mechanisms require broader molecular or phenotypic assessment. CRISPR should complement WHO-recommended rapid molecular testing and targeted next-generation sequencing rather than replace established molecular or phenotypic methods.

Schizophrenia is a chronic psychiatric disorder that leads to substantial disability, impaired quality of life, and reduced life expectancy. In addition to its profound impact on affected individuals, the disorder places a considerable financial burden on health care systems, caregivers, and society. Although the cost of schizophrenia has been studied in several individual countries, comprehensive global estimates across multiple cost categories remain scarce. This study aimed to estimate the global socioeconomic burden of schizophrenia using health economic modelling.

We conducted a prevalence-based cost-of-illness analysis for 204 countries in 2019, focusing on adults aged 20 years and older. Data on direct (medical and nonmedical), indirect (productivity losses), and informal (nonprofessional, unpaid) care costs were systematically retrieved through a PubMed-based literature search covering records published between 02/2010 and 04/2023. Extracted per-patient costs were standardized to 2019 purchasing power parity (PPP) USD, and missing data were imputed using a stratification approach based on four gross national income (GNI) groups. Costs were scaled to the national level by multiplying the per-patient costs by country-specific prevalence estimates from the Global Burden of Disease Study. Costs were additionally expressed as a proportion of gross domestic product (GDP). To ensure data validity from a clinical perspective, all estimates were scrutinized by a panel of psychiatry experts.

An estimated 22.1 million adults were living with schizophrenia in 2019 (0.39% prevalence). Total economic costs across upper-middle, lower-middle, and high-income regions reached $243.2 billion (PPP), with direct costs representing 47%, indirect costs 29%, and informal care costs 24%. Upper-middle-income countries bore the greatest burden relative to GDP, whereas high-income countries had the highest per-patient and national costs.

This study provides the most comprehensive global assessment to date of the economic burden of schizophrenia. Per-patient costs were identified as the main driver of the absolute global burden, underscoring the importance of effective disease management strategies. Policy-makers and other stakeholders should prioritize interventions that enhance patient functioning and societal participation.

As artificial intelligence (AI) expands across mental health services, questions arise about whether it can replace digital health navigators (DHNs), including those with lived experience. The DHN role generally resists automation because lived experience deepens specific dimensions that AI cannot replicate. Drawing on emerging evidence of AI's limitations in contextual reasoning, cultural sensitivity, and clinical safety, the authors identify where DHNs with lived experience are least substitutable: real-world knowledge of services, cultural grounding in the communities they serve, and relational trust. A practical model is also outlined in which AI augments DHN workflows through triage, documentation, and engagement monitoring.

The fast development of social media platforms has changed the way Generation Z communicates, sharing information and consuming digital material. One of such innovations is Instagram Reels, a popular short and long video-sharing functionality that helps with communication, knowledge exchange, and content usage. The feature was first introduced as Instagram TV (IGTV) in 2018 and subsequently integrated into Instagram Reels during the 2022 product consolidation of Instagram, however, the user behaviors underlying this topic, including video content consumption, creator engagement, and trust building, are still the center of the existing video ecosystem on the platform. Although the use of video-based content on Instagram is becoming increasingly popular, scarce studies have considered which factors affect its use and the consequences of this usage on the mental health and psychological wellbeing of users.

The paper examines the predictors of Instagram Reels use and the connection between Instagram Reels and mental health outcomes in Generation Z users. Based on Social Influence Theory, Expectation Confirmation Theory and the Technology Acceptance Model (TAM), a conceptual framework was created with consideration of Social Influence, Expectation Confirmation, Behavioral Intention, Idea Sharing, Building trust, Instagram Reels Usage, and Mental Health Outcomes.

The quantitative research design was used and a survey with 422 Generation Z users in Jordan was carried out using a structured questionnaire. Partial Least Squares Structural Equation Modeling (PLS-SEM) and Artificial Neural Network (ANN) were the methods that were used to analyze the data.

The results showed that, Social Influence and Expectation Confirmation play significant roles in Idea Sharing and Building Trust which consequently leads to the increased use of Instagram Reels. Behavioral Intention was cited and found to predict the relationship between Idea Sharing, Trust Building and platform engagement. Moreover, the Usage of Instagram Reels was also revealed to have a substantial impact on Mental Health Outcomes, with both positive and negative wellbeing indicators demonstrating varying effects. The Importance-Performance Map Analysis (IPMA) has determined Idea Sharing to be the most significant driver of Instagram Reels Usage, then Social Influence and Expectation Confirmation.

The paper finds that interactive features and perceived benefits of social media platform have a pivotal role in determining users engagement and psychological experiences. The results add to the body of literature on social media adoption and digital wellbeing and offer some practical implications to educators, policymakers, and platform developers interested in creating healthier digital spaces in which Generation Z users can operate.

Borrelia miyamotoi is a relapsing-fever spirochete that conventional tick-borne testing does not detect. We report a case notable for two findings not emphasized in prior series: creatine kinase elevation to 1464 U/L and glucose concentrations above 500 mg/dL without ketoacidosis in a pump-treated patient with type 1 diabetes mellitus. A 36-year-old man with frequent wooded exposure presented with fever, headache, myalgias, and rash, along with leukopenia, thrombocytopenia, and mild transaminitis. Lyme serology, Babesia smear, Anaplasma and Ehrlichia PCR, spotted-fever group Rickettsia serology, and blood cultures were negative; blood real-time PCR identified B. miyamotoi after discharge. The hyperglycemia was attributable to infection-related insulin resistance and interruption of pump delivery. Seventeen days of doxycycline produced full clinical and laboratory recovery. Exercise and dehydration may have contributed to the hyperCKemia. This case supports early blood PCR during the febrile illness in culture-negative tick-borne disease and illustrates that insulin requirements may rise sharply when infection coincides with failure of insulin-delivery technology.

Subcutaneous insulin resistance (SIR) is a rare condition characterized by impaired responsiveness to subcutaneous insulin despite preserved intravenous insulin efficacy. The coexistence of SIR with rapid loss of endogenous insulin secretion following exogenous insulin exposure has rarely been reported.

A 47-year-old Chinese man initially classified as having type 2 diabetes (T2D) had preserved endogenous insulin secretion (random C-peptide, 4.59 ng/mL) and negative insulin autoantibody (IAA), glutamic acid decarboxylase antibody, and insulinoma-associated protein 2 antibody at diagnosis. Shortly after initiation of subcutaneous insulin therapy, he developed pruritic, erythematous, and indurated injection-site lesions with progressive hyperglycemia and subsequently presented with diabetic ketoacidosis. C-peptide became undetectable, whereas IAA increased to >175 IU/mL. Intravenous insulin consistently restored glycemic control, while several subcutaneous insulin preparations were initially ineffective, indicating a marked route-dependent difference in insulin responsiveness. Subcutaneous insulin responsiveness later recovered, first with biphasic protamine human insulin 40/60 and subsequently with insulin analogues, despite persistent IAA positivity. At recent follow-up, 14-day continuous glucose monitoring showed a mean glucose of 7.6 mmol/L, time in range of 80%, and time below range of 3%. A heterozygous WFS1 variant (NM_006005.3:c.2147C>G, p.Ala716Gly) was identified as an exploratory finding of uncertain clinical significance.

This case highlights the coexistence of rapid loss of endogenous insulin secretion and severe but reversible SIR following exogenous insulin exposure. Preserved intravenous insulin responsiveness and recovery of subcutaneous insulin efficacy despite persistent IAA positivity underscore the dynamic and route-specific nature of this phenotype. The underlying mechanism remains uncertain, and no causal relationship with the WFS1 variant can be inferred. Recognition of this pattern may facilitate appropriate insulin delivery and longitudinal monitoring.

Maturity-onset diabetes of the young (MODY) comprises a heterogeneous group of autosomal dominant monogenic diabetes disorders; accurate molecular diagnosis is essential, as different subtypes require fundamentally distinct management strategies.

In a Chinese pedigree initially misdiagnosed as MODY10 based on an incidental INS variant, we aimed to identify the true genetic etiology through comprehensive genetic analysis (including copy number variation [CNV] detection) and continuous glucose monitoring (CGM), and to illustrate the clinical consequences of rigorous variant interpretation.

Detailed clinical evaluation, whole-exome sequencing (WES), whole-genome sequencing (WGS), multiplex ligation-dependent probe amplification (MLPA), segregation analysis, and CGM monitoring were performed across three generations of the pedigree.

We identified a 1, 171 bp GCK deletion (chr7:44, 228, 224-44, 229, 394 [GRCh37], encompassing the β-cell promoter, exon 1, and part of intron 1) that co-segregated with diabetes across three generations. This deletion removes the β-cell promoter while leaving the hepatic promoter intact, predicting selective loss of the pancreatic glucokinase isoform. The deletion was classified as pathogenic under ACMG/AMP criteria using the ClinGen Monogenic Diabetes Expert Panel specifications. Segregation analysis revealed that an INS variant (NM_000207.3:c.4G>A, p.Ala2Thr; rs535989053) did not co-segregate with diabetes: it was inherited from the euglycaemic maternal grandfather (fasting glucose 5.0 mmol/L, HbA1c 5.2%) and was absent in the proband. Under ACMG/AMP criteria, the INS variant meets criteria for a benign allele (BS1, BP2). The proband (isolated MODY2) exhibited a characteristic "plateau-like" stable mild hyperglycemia (coefficient of variation [CV] 14.35%). The elder brother, who carries both variants, showed a similar stable pattern (CV 13.41%). The mother, who also carries both variants, had been treated with insulin for ten years under the erroneous MODY10 diagnosis; upon discontinuation of insulin, her glycemic control remained stable, with CGM metrics comparable to those of her children.

This case underscores the critical importance of CNV analysis and segregation studies in monogenic diabetes diagnostics. The identification of a large GCK deletion corrected the initial misdiagnosis of MODY10-based on an incidental INS variant-and enabled appropriate genetic counseling and discontinuation of unnecessary insulin therapy. CGM emerges as a valuable ancillary tool for distinguishing MODY2 from MODY10 and for reassuring patients that pharmacological treatment is not required.