Finite-precision measurement does not nullify the Kochen-Specker theorem

It is proven that any hidden variable theory of the type proposed by Meyer [Phys. Rev. Lett. {\bf 83}, 3751 (1999)], Kent [{\em ibid.} {\bf 83}, 3755 (1999)], and Clifton and Kent [Proc. R. Soc. London, Ser. A {\bf 456}, 2101 (2000)] leads to experimentally testable predictions that are in contradiction with those of quantum mechanics. Therefore, it is argued that the existence of dense Kochen-Specker-colorable sets must not be interpreted as a nullification of the physical impact of the Kochen-Specker theorem once the finite precision of real measurements is taken into account.Comment: REVTeX4, 5 page

Insights into Nuclear Clusters in 28^{28}Si via Resonant Radiative Capture Measurements

International audienceThe heavyion radiative capture reaction 12C(16O,$\gamma$)28Si has been studied at three energies on( ELab = 20.0 and 21.2 MeV) and off( ELab = 20.7 MeV) resonance at Triumf (Vancouver) using the stateoftheart Dragon 0° spectrometer and its very efficient associated BGO $\gamma$ array. Intermediate states around Ex = 11.5 MeV, carrying a large part of the resonant flux have been observed for the first time in this system. The nature of those doorway states is discussed in terms of recently calculated cluster bands in 28Si. The results are compared to a recent similar investigation of the 12C(12C,$\gamma$)24Mg reaction

Decay Modes of Narrow Molecular Resonances

présenté par Sandrine Courtin (DRS-IPHC)The heavy-ion radiative capture reactions $^{12}C(^{12}C,\gamma)^{24}Mg$ and $^{12}C(^{16}O,\gamma)^{28}Si$ have been performed on and off resonance at TRIUMF using the Dragon separator and its associated BGO array. The decay of the studied narrow resonances has been shown to proceed predominantly through quasi-bound doorway states which cluster and deformed configurations would have a large overlap with the entry resonance states

Isospin symmetry in the odd-odd mirror nuclei 44V/44Sc

Excited states in the N=Z-2 nucleus 44V have been observed for the first time. The states have been identified through particle-γ-γ coincidence relationships and comparison with analog states in the mirror nucleus 44Sc. Mirror energy differences have been extracted and compared to state-of-the-art shell-model calculations which include charge-symmetry-breaking forces. Observed decay pattern asymmetries between the mirror pair are discussed in terms of core excitations, electromagnetic spin-orbit effects and isospin mixing

Drug-gene interactions of antihypertensive medications and risk of incident cardiovascular disease: A pharmacogenomics study from the CHARGE consortium

Background Hypertension is a major risk factor for a spectrum of cardiovascular diseases (CVD), including myocardial infarction, sudden death, and stroke. In the US, over 65 million people have high blood pressure and a large proportion of these individuals are prescribed antihypertensive medications. Although large long-term clinical trials conducted in the last several decades have identified a number of effective antihypertensive treatments that reduce the risk of future clinical complications, responses to therapy and protection from cardiovascular events vary among individuals. Methods Using a genome-wide association study among 21,267 participants with pharmaceutically treated hypertension, we explored the hypothesis that genetic variants might influence or modify the effectiveness of common antihypertensive therapies on the risk ofmajor cardiovascular outcomes. The classes of drug treatments included angiotensin-converting enzyme inhibitors, beta-blockers, calcium channel blockers, and diuretics. In the setting of the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium, each study performed array-based genome-wide genotyping, imputed to HapMap Phase II reference panels, and used additive genetic models in proportional hazards or logistic regressionmodels to evaluate drug-gene interactions for each of four therapeutic drug classes. We used meta-analysis to combine study-specific interaction estimates for approximately 2 million single nucleotide polymorphisms (SNPs) in a discovery analysis among 15,375 European Ancestry participants (3,527 CVD cases) with targeted follow-up in a case-only study of 1,751 European Ancestry GenHAT participants as well as among 4,141 African-Americans (1,267 CVD cases). Results Although drug-SNP interactions were biologically plausible, exposures and outcomes were well measured, and power was sufficient to detect modest interactions, we did not identify any statistically significant interactions from the four antihypertensive therapy meta-analyses (Pinteraction > 5.0×10-8). Similarly, findings were null for meta-analyses restricted to 66 SNPs with significant main effects on coronary artery disease or blood pressure from large published genom

Genetic Interactions with Age, Sex, Body Mass Index, and Hypertension in Relation to Atrial Fibrillation: The AFGen Consortium

It is unclear whether genetic markers interact with risk factors to influence atrial fibrillation (AF) risk. We performed genome-wide interaction analyses between genetic variants and age, sex, hypertension, and body mass index in the AFGen Consortium. Study-specific results were combined using meta-analysis (88,383 individuals of European descent, including 7,292 with AF). Variants with nominal interaction associations in the discovery analysis were tested for association in four independent studies (131,441 individuals, including 5,722 with AF). In the discovery analysis, the AF risk associated with the minor rs6817105 allele (at the PITX2 locus) was greater among subjects ≤ 65 years of age than among those > 65 years (interaction p-value = 4.0 × 10-5). The interaction p-value exceeded genome-wide significance in combined discovery and replication analyses (interaction p-value = 1.7 × 10-8). We observed one genome-wide significant interaction with body mass index and several suggestive interactions with age, sex, and body mass index in the discovery analysis. However, none was replicated in the independent sample. Our findings suggest that the pathogenesis of AF may differ according to age in individuals of European descent, but we did not observe evidence of statistically significant genetic interactions with sex, body mass index, or hypertension on AF risk

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies