Exercise mediates the association between positive affect and 5-year mortality in patients with ischemic heart disease

Background Positive affect has been associated with better prognosis in patients with ischemic heart disease, but the underlying mechanisms remain unclear. We examined whether positive affect predicted time to first cardiac-related hospitalization and all-cause mortality, and whether exercise mediated this relationship in patients with established ischemic heart disease. Methods and Results The sample comprised 607 patients with ischemic heart disease from Holbæk Hospital, Denmark. In 2005, patients completed the Global Mood Scale (GMS) to assess positive affect and a purpose-designed question on exercise. Data on mortality and hospitalization were collected from Danish national registers for the period 2006–2010. Adjusted Cox and logistic regression were used to analyze the mediation model. Because no significant association between positive affect and cardiac-related hospitalization was found, we constructed no mediation model for hospitalization. Importantly, patients with high positive affect had a significantly reduced risk of all-cause mortality (hazard ratio, 0.58; 95% confidence interval, 0.37–0.92; unadjusted analysis) and were more likely to exercise (odds ratio, 1.99; 95% confidence interval, 1.44–2.76; unadjusted analysis; odds ratio, 1.48; 95% confidence interval, 1.03–2.13; adjusted analysis). When controlling for positive affect and other relevant variables, patients engaged in exercise were less likely to die during follow-up (hazard ratio, 0.50; 95% confidence interval, 0.31–0.80; P=0.004). Importantly, exercise acted as a mediator in the relationship between positive affect and mortality. Conclusions Patients with higher levels of positive affect were more likely to exercise and had a lower risk of dying during 5-year follow-up, with exercise mediating the relationship between positive affect and mortality. Interventions aimed at increasing both positive affect and exercise may have better results with respect to patients’ prognosis and psychological well-being than interventions focusing on 1 of these factors alone

A Methodology and Tool for Rapid Prototyping of Data Warehouses using Data Mining: Application to Birds Biodiversity

International audienceData Warehouses (DWs) are large repositories of data aimed at supporting the decision-making process by enabling flexible and interactive analyses via OLAP systems. Rapid prototyping of DWs is necessary when OLAP applications are complex. Some work about the integration of Data Mining and OLAP systems has been done to enhance OLAP operators with mined indicators, and/or to define the DW schema. However, to best of our knowledge, prototyping methods for DWs do not support this kind of integration. Then, in this paper we present a new prototyping methodology for DWs, extending [3], where DM methods are used to define the DW schema. We validate our approach on a real data set concerning bird biodiversity

Transparent code authentication at the processor level

The authors present a lightweight authentication mechanism that verifies the authenticity of code and thereby addresses the virus and malicious code problems at the hardware level eliminating the need for trusted extensions in the operating system. The technique proposed tightly integrates the authentication mechanism into the processor core. The authentication latency is hidden behind the memory access latency, thereby allowing seamless on-the-fly authentication of instructions. In addition, the proposed authentication method supports seamless encryption of code (and static data). Consequently, while providing the software users with assurance for authenticity of programs executing on their hardware, the proposed technique also protects the software manufacturers’ intellectual property through encryption. The performance analysis shows that, under mild assumptions, the presented technique introduces negligible overhead for even moderate cache sizes

Influence of microwave fields on the electron transport through a quantum dot in the presence of a direct tunneling between leads

We consider the time-dependent electron transport through a quantum dot coupled to two leads in the presence of the additional over-dot (bridge) tunneling channel. By using the evolution operator method together with the wide-band limit approximation we derived the analytical formulaes for the quantum dot charge and current flowing in the system. The influence of the external microwave field on the time-average quantum dot charge, the current and the derivatives of the average current with respect to the gate and source-drain voltages has been investigated for a wide range of parameters.Comment: 28 Pages, 11 Postscript figure

Identification of common genetic risk variants for autism spectrum disorder

Autism spectrum disorder (ASD) is a highly heritable and heterogeneous group of neurodevelopmental phenotypes diagnosed in more than 1% of children. Common genetic variants contribute substantially to ASD susceptibility, but to date no individual variants have been robustly associated with ASD. With a marked sample-size increase from a unique Danish population resource, we report a genome-wide association meta-analysis of 18,381 individuals with ASD and 27,969 controls that identified five genome-wide-significant loci. Leveraging GWAS results from three phenotypes with significantly overlapping genetic architectures (schizophrenia, major depression, and educational attainment), we identified seven additional loci shared with other traits at equally strict significance levels. Dissecting the polygenic architecture, we found both quantitative and qualitative polygenic heterogeneity across ASD subtypes. These results highlight biological insights, particularly relating to neuronal function and corticogenesis, and establish that GWAS performed at scale will be much more productive in the near term in ASD.Peer reviewe

Physical activity attenuates the influence of FTO variants on obesity risk: A meta-analysis of 218,166 adults and 19,268 children

Background: The FTO gene harbors the strongest known susceptibility locus for obesity. While many individual studies have suggested that physical activity (PA) may attenuate the effect of FTO on obesity risk, other studies have not been able to confirm this interaction. To confirm or refute unambiguously whether PA attenuates the association of FTO with obesity risk, we meta-analyzed data from 45 studies of adults (n = 218,166) and nine studies of children and adolescents (n = 19,268). Methods and Findings: All studies identified to have data on the FTO rs9939609 variant (or any proxy [r2>0.8]) and PA were invited to participate, regardless of ethnicity or age of the participants. PA was standardized by categorizing it into a dichotomous variable (physically inactive versus active) in each study. Overall, 25% of adults and 13% of children were categorized as inactive. Interaction analyses were performed within each study by including the FTO×PA interaction term in an additive model, adjusting for age and sex. Subsequently, random effects meta-analysis was used to pool the interaction terms. In adults, the minor (A-) allele of rs9939609 increased the odds of obesity by 1.23-fold/allele (95% CI 1.20-1.26), but PA attenuated this effect (pinteraction= 0.001). More specifically, the minor allele of rs9939609 increased the odds of obesity less in the physically active group (odds ratio = 1.22/allele, 95% CI 1.19-1.25) than in the inactive group (odds ratio = 1.30/allele, 95% CI 1.24-1.36). No such interaction was found in children and adolescents. Concl

Genome-wide meta-analysis uncovers novel loci influencing circulating leptin levels.

Leptin is an adipocyte-secreted hormone, the circulating levels of which correlate closely with overall adiposity. Although rare mutations in the leptin (LEP) gene are well known to cause leptin deficiency and severe obesity, no common loci regulating circulating leptin levels have been uncovered. Therefore, we performed a genome-wide association study (GWAS) of circulating leptin levels from 32,161 individuals and followed up loci reaching P<10(-6) in 19,979 additional individuals. We identify five loci robustly associated (P<5 × 10(-8)) with leptin levels in/near LEP, SLC32A1, GCKR, CCNL1 and FTO. Although the association of the FTO obesity locus with leptin levels is abolished by adjustment for BMI, associations of the four other loci are independent of adiposity. The GCKR locus was found associated with multiple metabolic traits in previous GWAS and the CCNL1 locus with birth weight. Knockdown experiments in mouse adipose tissue explants show convincing evidence for adipogenin, a regulator of adipocyte differentiation, as the novel causal gene in the SLC32A1 locus influencing leptin levels. Our findings provide novel insights into the regulation of leptin production by adipose tissue and open new avenues for examining the influence of variation in leptin levels on adiposity and metabolic health