Objective: Increased point prevalence rates of oppositional defiant disorder and conduct disorder have been reported in American Indian and Canadian First Nations children and adolescents. To date, in Australia, there has been no published examination of standardized mental disorder diagnoses in First Nations children and adolescents, determined after addressing key cultural methodological issues.
Methods: In all, 113 First Nations children and adolescents and 217 non-First Nations young people, aged 6-16 years, age, gender, mental disorder symptom severity, symptom-linked distress and impairment matched were recruited in a case control study. Also, 112 typically developing non-First Nations participants, age and gender matched to the other two clinical groups as a second comparison group were recruited. mental disorder diagnoses via semi-structured clinical interview, social adversity status and full scale IQ were determined in all participants with cultural validity and reliability of the impairing patterns of symptoms in First Nations young people determined by First Nations mental health staff and Aboriginal Health Liaison Officers. Full scale IQ and social adversity status were appropriately controlled in the Logistic Regression analyses of mental disorder diagnoses between the two clinical groups.
Results: Oppositional defiant disorder was the only diagnostic and statistical manual mental disorder diagnosis that differed between the First Nations and non-First Nations clinical groups, adjusting for confounding by social adversity status and full scale IQ in the multivariable model. The point prevalence of oppositional defiant disorder was 2.94 times higher (95% confidence interval: 1.14-7.69) among the First Nations compared to the non-First Nations clinical group.
Conclusion: Key known risk factors for oppositional defiant disorder can be identified early and holistically managed in First Nations young people. This will prevent oppositional defiant disorder decreasing their access to mental health services and increasing their involvement in the criminal justice system. In addition, the resilience building aspects of oppositional defiant disorder that may enhance self-respect need to be nurtured.
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http://dx.doi.org/10.1177/00048674211063819 | DOI Listing |
Sci Rep
December 2024
Department of Psychiatry and Behavioral Sciences and Weill Center for Neurosciences, University of California, San Francisco, CA, 94107, USA.
Telomere attrition is a hallmark of biological aging, contributing to cellular replicative senescence. However, few studies have examined the determinants of telomere attrition in vivo in humans. Mitochondrial Health Index (MHI), a composite marker integrating mitochondrial energy-transformation capacity and content, may be one important mediator of telomere attrition, as it could impact telomerase activity, a direct regulator of telomere maintenance.
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December 2024
Department of Drug Prohibition and Public Security, Criminal Investigation Police University of China, Shenyang, 110035, China.
Methamphetamine use disorder has emerged as a significant public health concern globally. This study endeavors to elucidate the alterations in expression changes of miRNAs in the plasma of methamphetamine use disorder and elucidate the alterations in miRNA expression in the plasma of individuals with methamphetamine use disorder and investigate the relationship between these differentially expressed miRNAs and the disorder itself, cravings for methamphetamine, and associated mental disorders. Furthermore, the study seeks to clarify the expression of downstream target molecules of specific miRNAs in the plasma of methamphetamine use disorder, assess the diagnostic utility of these miRNAs and their target molecules, explore their potential as biomarkers, and identify potential targets for the diagnosis and treatment of methamphetamine use disorder.
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December 2024
Department of Neuroscience, Baylor College of Medicine, Houston, TX, 77030, USA.
The bipolar disorder (BD) risk gene ANK3 encodes the scaffolding protein AnkyrinG (AnkG). In neurons, AnkG regulates polarity and ion channel clustering at axon initial segments and nodes of Ranvier. Disruption of neuronal AnkG causes BD-like phenotypes in mice.
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December 2024
Department of Molecular Pharmacology and Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
The mechanism(s) underlying gut microbial metabolite (GMM) contribution towards alcohol-mediated cardiovascular disease (CVD) is unknown. Herein we observe elevation in circulating phenylacetylglutamine (PAGln), a known CVD-associated GMM, in individuals living with alcohol use disorder. In a male murine binge-on-chronic alcohol model, we confirm gut microbial reorganization, elevation in PAGln levels, and the presence of cardiovascular pathophysiology.
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December 2024
Department of Theory and Bio-Systems, Max Planck Institute of Colloids and Interfaces, 14476, Potsdam, Germany.
Neurodegeneration in Huntington's disease (HD) is accompanied by the aggregation of fragments of the mutant huntingtin protein, a biomarker of disease progression. A particular pathogenic role has been attributed to the aggregation-prone huntingtin exon 1 (HTTex1), generated by aberrant splicing or proteolysis, and containing the expanded polyglutamine (polyQ) segment. Unlike amyloid fibrils from Parkinson's and Alzheimer's diseases, the atomic-level structure of HTTex1 fibrils has remained unknown, limiting diagnostic and treatment efforts.
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