Type 2 diabetes (T2D) has been shown to increase dementia risk, but few studies evaluated the relationship between antidiabetic treatment and dementia. We followed up 67,731 participants who were nondemented, nondiabetic, aged 65 or over at baseline from January 2004 to December 2009, to observe the onset of T2D (median follow-up 2.4 years), and to compare the risk of the development of dementia associated with particular types of antidiabetic medication among participants with T2D who had solely one type of antidiabetic agents throughout the follow-up period (median follow-up for participants with T2D 3.1 years). The hazard ratio for dementia diagnosis in the new-onset T2D participants compared with the non-T2D participants was 1.56 (95%CI: 1.39–2.18). The relative rate of dementia was 5.31 (95% CI: 1.89–14.96) for participants taking thiazolidinediones (n = 28) and 1.22 (95% CI: 0.78–1.91) for those taking sulfonylureas (n = 796) compared to those taking metformin (n = 1,033). The risk of dementia was higher in ever (n = 841) versus never users (n = 4,579) of thiazolidinediones: 1.44 (95% CI: 1.12–1.86). Diabetes is associated with an increased risk of dementia. The risk effect becomes weaker provided that participants take sulfonylureas or metformin rather than thiazolidinediones for a longer period.

Although many epidemiologic studies have shown that both short and long nighttime sleep durations are associated with increased mortality in the general population, limited data have been reported for older persons, especially those taking afternoon nap. Data from a prospective cohort study of the elderly in Taiwan were used to examine the relationship among nighttime sleep, Chinese afternoon nap, and mortality. Prospective cohort study General population A nationally representative sample of 3079 Taiwanese community residents aged 64 and over was studied, using reported sleep related information collected in 1993 and subsequent 10-year mortality data. None Cox proportional hazards models, separated by sex, were computed to estimate mortality hazard ratios in relation to nighttime sleep duration and afternoon nap duration, adjusting for potential confounders. Compared to older adults sleeping 7~7.9 hours at night, those with longer sleeping time (≥ 10 hours in males and ≥ 8 hours in females) had a significantly higher risk of total mortality. Afternoon nap alone was not associated with total mortality. When nighttime sleep duration and afternoon nap duration were considered together by adding the interaction term in the model or stratifying sleep hours and nap duration, the effect of afternoon nap on mortality risk remained insignificant. Longer nighttime sleep duration increases mortality risk in older adults. Chinese afternoon nap is not an independent predictor of mortality. There is no significant benefit or harm of practicing afternoon nap in addition to the regular night sleep on elderly mortality.

Chronic schizophrenic patients have been reported as having higher osteoporosis prevalence. Survey the bone mass among schizophrenic patients and compare with that of the local community population and reported data of the same country to figure out the distribution of bone mass among schizophrenic patients.

Significance: Using network analysis of resting-state functional MRI data, we demonstrate that significant randomization of global network metrics, and greater resilience to targeted attack on network hubs, was replicably demonstrable in Chinese patients with schizophrenia, and was also demonstrated for the first time in their nonpsychotic first-degree relatives. These results support the hypothesis that functional networks are abnormally randomized and resilient in schizophrenia and indicate that network randomization/resilience may be an endophenotype, or marker of familial risk, for schizophrenia. We suggest that the greater randomization of the brain network endophenotype of schizophrenia may confer advantages in terms of greater resilience to pathological attack that may explain the selection and persistence of risk genes for schizophrenia in the general population.

The purpose of this study was to assess 65 pedigrees ascertained through a Bipolar I (BPI) proband for evidence of linkage, using nonparametric methods in a genome-wide scan and for possible parent of origin effect using several analytical methods. We identified 15 loci with nominally significant evidence for increased allele sharing among affected relative pairs. Eight of these regions, at 8q24, 18q22, 4q32, 13q12, 4q35, 10q26, 2p12, and 12q24, directly overlap with previously reported evidence of linkage to bipolar disorder. Five regions at 20p13, 2p22, 14q23, 9p13, and 1q41 are within several Mb of previously reported regions. We report our findings in rank order and the top five markers had an NPL>2.5. The peak finding in these regions were D8S256 at 8q24, NPL 3.13; D18S878 at 18q22, NPL 2.90; D4S1629 at 4q32, NPL 2.80; D2S99 at 2p12, NPL 2.54; and D13S1493 at 13q12, NPL 2.53. No locus produced statistically significant evidence for linkage at the genome-wide level. The parent of origin effect was studied and consistent with our previous findings, evidence for a locus on 18q22 was predominantly from families wherein the father or paternal lineage was affected. There was evidence consistent with paternal imprinting at the loci on 13q12 and 1q41.