Mcknightdaley4983

BACKGROUND Few studies have explored the underlying mechanism between physical frailty and cognitive function. The aim of this study is to explore the mediating role of psychological distress (PD) for the association between cognitive function and physical frailty among the elderly in rural China. METHODS A total of 3,242 rural older adults were included in the analysis. Logistic regression and Bootstrap analyses were employed to explore the association between cognitive function, PD and frailty, and the mediating role of PD. RESULTS This study found that the prevalence of frailty and cognitive impairment among the elderly in rural China was 18.0%, 22.4%. see more After adjusted for controlling variables, cognitive function was significantly associated with high level of PD, and elderly with higher level of PD had a higher probability of suffering from frailty. PD played a partially mediating effect in cognitive function and frailty and the mediating effect of PD can explain the 11.0% of the total effect of cognitive function on frailty. LIMITATIONS The data were cross-sectional, thus the causal relationship between variables could not be determined. The main variables in this study were measured by self-report information, which might result in recall bias. CONCLUSIONS This study provide evidence that the effect of cognitive function on physical frailty was partially mediated by PD among the elderly in rural China. Primary health care should strengthen the screening of PD characterized by depression and anxiety, and strive to improve the physical and psychological well-being of rural elderly in China. BACKGROUND The β2 subunit of the voltage-gated l-type calcium channel gene(CACNB2) rs11013860 polymorphism is a putative genetic susceptibility marker for bipolar disorder (BD). However, the neural effects of CACNB2 rs11013860 in BD are largely unknown. METHODS Forty-six bipolar patients with first-episode mania and eighty-three healthy controls (HC) were genotyped for CACNB2 rs11013860 and were scanned with a 3.0 Tesla structural magnetic resonance imaging system to measure cortical thickness of prefrontal cortex (PFC) components (superior frontal cortex, orbitofrontal cortex, middle and inferior frontal gyri). RESULTS Cortical thickness was thinner in patients on all PFC measurements compared to HC (p less then 0.050). Moreover, we found a significant interaction between CACNB2 genotype and diagnosis for the right superior frontal cortical thickness (F = 8.190, p = 0.040). Bonferroni corrected post-hoc tests revealed that, in CACNB2 A-allele carriers, patients displayed thinner superior frontal thickness compared to HC (p less then 0.001). In patients, CACNB2 A-allele carriers also exhibited reduced superior frontal thickness compared to CACNB2 CC-allele carriers (p = 0.016). LIMITATIONS Lithium treatment may influence our results, and the sample size in our study is relatively small. CONCLUSIONS Our results suggest that the CACNB2 rs11013860 might impact PFC thickness in patients with first-episode mania. These findings provide evidence to support CACNB2 rs11013860 involvement in the emotion-processing neural circuitry abnormality in the early stage of BD, which will ultimately contribute to revealing the link between the variation in calcium channel genes and the neuropathological mechanism of BD. V.BACKGROUND Our objective was to systematically review non-experimental studies of parental bipolar disorder (BD), current family environment, and offspring psychiatric disorders to identify characteristics of family environment associated with parental BD and risk for offspring psychiatric disorders. METHODS CINAHL, Embase, PsycINFO, and PubMed were searched using MeSH terms to identify studies on offspring of BD parents published through September 2017. We followed PRISMA guidelines and used the Risk of Bias Assessment Tool for Nonrandomized Studies (RoBANS). We calculated prevalence ratios and 95% confidence intervals to compare offspring psychiatric disorders within and across studies. RESULTS Of 10,454 unique documents retrieved, we included 13 studies. The most consistent finding was lower parent-reported cohesion in families with a BD parent versus no parental psychiatric disorders. Family environment did not differ between BD parents and parents with other disorders. Offspring of BD parents had higher prevalence of psychiatric disorders than offspring of parents without psychiatric disorders but did not differ from offspring of parents with other disorders. Families with a BD child had higher conflict than families without a BD child. LIMITATIONS Comparisons between studies were qualitative. A single reviewer conducted screening, data extraction, and bias assessment. CONCLUSIONS Family environment in families with a BD parent is heterogeneous. The pattern of findings across studies also suggests that family problems may be associated with parental psychiatric illness generally rather than parental BD in particular. Few studies included offspring-reported measures. Given the association of family conflict with offspring mood disorders, further study is merited on children's perceptions of the family environment in the BD high-risk context. Published by Elsevier B.V.OBJECTIVE Self-poisoning with non-opioid analgesics presents a growing challenge to health care providers. We aimed to assess the impact of an 18-year age restriction of OTC sales and a pack size restriction of non-opioid analgesics sold OTC in pharmacies on hospital-treated poisonings and poisoning severity measured using biomarkers. METHODS We applied a before and after design using interrupted time series analysis. Data on all poisonings recorded as hospital admissions were obtained during 2002-2015 and biochemical parameters from laboratory databases during 2011-2015, both covering the entire Danish population. RESULTS The age restriction was followed by a 17% level reduction in admissions for non-opioid analgesic poisoning among young people age 10-17 years (RR 0.830; 95% CI 0.697-0.988; p  less then  0.036). After the pack size restriction, an instant level reduction of 18.5% (RR 0.815; 95% CI 0.729-0.912; p  less then  0.001) was observed for the entire population. A 27% decrease in the number of poisonings with alanine transaminase levels (ALT) ≥ 210 U/L was observed (RR 0.