Incidence rate of schizophrenia after the Tangshan earthquake in China: a 44-year retrospective birth cohort study.

Preliminary evidence indicates that natural disasters are associated with an increased risk for schizophrenia. With few longitudinal studies on earthquakes, this retrospective cohort study examined exposure to the 1976 Tangshan earthquake and the subsequent risk of schizophrenia. Population counts and visits to all nine psychiatric hospitals in Tangshan city were collected. We created three cohort groups by earthquake exposure: infant (August 1972 to July 1976 births), fetal (August 1976 to May 1977 births), and unexposed (June 1977 to May 1981 births). The cumulative incidence of schizophrenia in each cohort was calculated by dividing the number of schizophrenia patients by total births in the corresponding period. Altogether, 6424 schizophrenia patients were identified, with 2786 in the infant group, 663 in the fetal group, and 2975 in the unexposed group. The crude cumulative incidence of schizophrenia in the infant, fetal and unexposed groups were 7.64 (95% confidence interval [CI] = 7.36-7.92), 9.07 (95% CI = 8.38-9.76), and 7.40 (95% CI = 7.13-7.66) per thousand population respectively. Adjusted for mortality, the corresponding figures were 7.73 (95% CI = 7.44-8.01), 9.30 (95% CI = 8.60-10.01) and 7.44 (95% CI = 7.18-7.71) per thousand population respectively. The mortality-adjusted risk ratio (aRR) was 1.25 (95% CI = 1.15-1.36) between fetal and unexposed groups (χ2 = 27.31, P < 0.001). Males exposed as infants did not differ from the unexposed in cumulative schizophrenia incidence. People with fetal exposure to the 1976 earthquake had 25% higher risk of developing schizophrenia compared to unexposed counterparts.

High glucose suppresses ABCG1 expression by increasing oxidative stress and inducing nuclear factor-kappaB activation in vascular smooth muscle cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the role of high glucose in the expression of ATP-binding cassette (ABC) transporters A1 (ABCA1) and G1 (ABCG1) in human vascular smooth muscle cells (VSMCs) and its possible mechanisms.</p><p><b>METHODS</b>VSMCs were incubated in the presence of glucose at the concentrations ranging from 5 to 30 mmol/L for 1 to 7 days, and real-time PCR and Western blotting were used to measure the mRNA and protein expressions of ABCA1 and ABCG1. The effects of cells pretreatment with antioxidant NAC (10 mmol/L) and nuclear factor-kappaB (NF-kappaB) inhibitors BAY 11-7085 (10 micromol/L) and TPCK (10 micromol/L) were also tested on ABCA1 and ABCG1 expressions.</p><p><b>RESULTS</b>High glucose suppressed, in a time- and dose-dependent manner, ABCG1 expression in incubated human VSMCs, and this effect was abolished by pretreatment with the antioxidant and nuclear factor-kappaB (NF-kappaB) inhibitors, but ABCA1 expression was not significantly decreased in the presence of high glucose.</p><p><b>CONCLUSION</b>High glucose suppresses ABCG1 expression in human VSMCs possibly due to increased oxidative stress and NF-kappaB activation induced by high glucose.</p>