Association of adverse and positive childhood experiences with health-related quality of life in adolescents.

OBJECTIVES: To investigate the independent impacts of adverse childhood experiences (ACEs) and positive childhood experiences (PCEs) on the health-related quality of life (HRQOL) of Chinese adolescents, and to explore the potential moderating role of PCEs in the association between ACEs and HRQOL. STUDY DESIGN: This was a cross-sectional study. METHODS: We surveyed 6982 students aged 11-20 in Guangzhou, China, from November to December 2021. Adolescents self-reported their ACEs, PCEs, and HRQOL by the Childhood Trauma Questionnaire Short Form, the Adverse Childhood Experiences-International Questionnaire, the Benevolent Childhood Experiences Scale, and the Paediatric Quality of Life Inventory Version 4.0, respectively. Multivariable linear regressions were performed to examine the associations between ACEs, PCEs, and HRQOL controlled for adolescents' age, gender, single-child status, boarding school attendance, primary caregivers, as well as parental age and occupational status. Likelihood-ratio tests were further applied to explore the moderating role of PCEs. RESULTS: In the models that considered both ACEs and PCEs, ACEs were significantly associated with lower HRQOL scores in all dimensions, summary scales, and total scale (ß = -13.88, 95% confidence interval [CI]: -14.82, -12.94 for total scale). Conversely, exposure to an above-average number of PCEs was associated with higher HRQOL scores in all measured aspects (ß = 7.20, 95%CI: 6.57, 7.84 for total scale). PCEs significantly moderated the association between ACEs and all HRQOL dimensions, summary scales, and total scale, except school functioning. CONCLUSION: ACEs and PCEs exert independent and opposite impacts on adolescents' HRQOL. PCEs could mitigate the negative impacts of ACEs. Enhancing resilience, like PCEs, may contribute to improving the HRQOL among adolescents who have exposed to ACEs.

Hypertriglyceridaemic-waist phenotype and risk of diabetes in people with impaired fasting glucose in primary care: a cohort study.

AIM: We aimed to determine the prospective association between baseline triglyceridaemic-waist phenotypes and diabetic mellitus incidence in individuals with impaired fasting glucose seen in primary care. METHODS: A cohort of 1101 participants (84.4% of the recruited individuals) with impaired fasting glucose were recruited from three primary care clinics during regular follow-ups to monitor their chronic conditions. Baseline triglyceridaemic-waist phenotypes were divided into four groups: (1) normal waistline and triglyceride level (n = 252); (2) isolated central obesity (n = 518); (3) isolated high triglyceride level (n = 80); and (4) central obesity with high triglyceride level (i.e. hypertriglyceridaemic-waist phenotype) (n = 251). The presence of diabetes at follow-up was determined by fasting plasma glucose (≥ 7.0 mmol/l) and/or 2-h 75-g oral glucose tolerance test (≥ 11.1 mmol/l) and/or HbA1c (47.5 mmol/mol; ≥ 6.5%) according to American Diabetes Association diagnostic criteria. Multivariable Cox proportional hazards regressions were established to assess the impact of different triglyceridaemic-waist phenotypes on time to diabetes onset. RESULTS: After a mean follow-up period of 6.5 months (sd 4.7 months), the number of diabetes cases was significantly higher in the group with hypertriglyceridaemic-waist phenotype (52.2%) compared with the other three phenotype groups (group 1: 28.2%; group 2: 34.6%; group 3: 30.0%). Only the hypertriglyceridaemic-waist phenotype showed an increased risk of developing diabetes (hazard ratio 1.581, 95% CI 1.172-2.134; P = 0.003) compared with the group with normal waistline and triglyceride level after controlling for confounders. CONCLUSIONS: The combination of central obesity and hypertriglyceridaemia is associated with > 50% risk of progression to diabetes within 6 months among individuals with impaired fasting glucose seen in primary care.

Aquaporin-4 autoantibodies cause asymptomatic aquaporin-4 loss and activate astrocytes in mouse.

BACKGROUND: Neuromyelitis optica (NMO) is a central nervous system inflammatory demyelinating disorder. Up to 90% of patients are seropositive for aquaporin-4 autoantibodies (AQP4 Ab). The pathogenetic mechanisms underlying clinical onset and relapse of NMO are uncertain. OBJECTIVE: Study the pathogenicity of AQP4 Ab in the absence of complement activation. METHODS: Female C57BL/6N mice (human IgG cannot activate mouse complements) pretreated with complete Freund's adjuvant (CFA, day 0) and pertussis toxin (PTx, day 0 and day 2) were transferred with IgG isolated from serum of healthy subjects or NMO patients (AQP4 Ab-positive or negative) intraperitoneally (day 7-9). Mice were observed for signs of experimental autoimmune encephalomyelitis (EAE) by standard 6-grade EAE scores. Spinal cord was obtained at day 11 for immunohistochemistry. RESULTS: None of the mice had clinical signs of encephalomyelitis, inflammatory cells infiltration or demyelination of spinal cord. CFA and PTx induce BBB breakdown evidenced by leakage of human IgG into cord parenchyma. Patchy areas of AQP4 loss were observed in spinal cord of mice transferred with IgG from AQP4 Ab-positive NMO patients but not in mice transferred with IgG from AQP4 Ab-negative NMO patients or healthy subjects; but there was no loss of glial fibrillary acidic protein immunoreactivity in all mice. Markedly increased proliferation of astrocytic processes suggestive of astrocytic activation was observed in mice transferred with IgG from AQP4 Ab-positive patients. CONCLUSION: AQP4 Ab cause asymptomatic AQP4 loss and astrocytic activation but not myelitis, demyelination or astrocytic cytotoxicity in spinal cord of mouse in the absence of complement activation.