Entropy and Wigner Functions

The properties of an alternative definition of quantum entropy, based on Wigner functions, are discussed. Such definition emerges naturally from the Wigner representation of quantum mechanics, and can easily quantify the amount of entanglement of a quantum state. It is shown that smoothing of the Wigner function induces an increase in entropy. This fact is used to derive some simple rules to construct positive definite probability distributions which are also admissible Wigner functionsComment: 18 page

Syntheses, structures and redox properties of tris(pyrazolyl)borate-capped ruthenium vinyl complexes.

Reaction of RuHCl(CO)(PPh3)3 with aryl alkynes HCCC6H4R-4 [1: R = N(C6H4Me-4)2 (a), OMe (b), Me (c), CO2Me (d), NO2 (e)] gives the five-coordinate vinyl complexes Ru(CHCHC6H4R-4)Cl(CO)(PPh3)2 (2a–e). Reaction of 2a with excess PMe3 gives crystallographically characterised Ru{CHCHC6H4N(C6H4Me-4)2-4}Cl(CO)(PMe3)3 (3a), whilst reaction of 2a–e with KTp affords Ru(CHCHC6H4R-4)(CO)(PPh3)Tp (4a–e) bearing the facially capping Tp− ligand. Electrochemical and spectroelectochemical properties of 4a–e are consistent with substantial redox activity associated with the vinyl ligand, and these properties have been satisfactorily modelled by DFT based calculations of electronic structure

Broken seniority symmetry in the semimagic proton mid-shell nucleus ⁹⁵Rh

Lifetime measurements of low-lying excited states in the semimagic ( N = 50 ) nucleus 95Rh have been performed by means of the fast-timing technique. The experiment was carried out using γ -ray detector arrays consisting of LaBr3(Ce) scintillators and germanium detectors integrated into the DESPEC experimental setup commissioned for the Facility for Antiproton and Ion Research (FAIR) Phase-0, Darmstadt, Germany. The excited states in 95Rh were populated primarily via the β decays of 95Pd nuclei, produced in the projectile fragmentation of a 850 MeV/nucleon 124Xe beam impinging on a 4 g / cm2 9Be target. The deduced electromagnetic E2 transition strengths for the γ -ray cascade within the multiplet structure depopulating from the isomeric Iπ = 21 / 2+ state are found to exhibit strong deviations from predictions of standard shell model calculations which feature approximately conserved seniority symmetry. In particular, the observation of a strongly suppressed E2 strength for the 13 / 2+ → 9 / 2+ ground state transition cannot be explained by calculations employing standard interactions. This remarkable result may require revision of the nucleon-nucleon interactions employed in state-of-the-art theoretical model calculations, and might also point to the need for including three-body forces in the Hamiltonian

Genome-wide association analyses identify 143 risk variants and putative regulatory mechanisms for type 2 diabetes

Type 2 diabetes (T2D) is a very common disease in humans. Here we conduct a meta-analysis of genome-wide association studies (GWAS) with ~16 million genetic variants in 62,892 T2D cases and 596,424 controls of European ancestry. We identify 139 common and 4 rare variants associated with T2D, 42 of which (39 common and 3 rare variants) are independent of the known variants. Integration of the gene expression data from blood (n = 14,115 and 2765) with the GWAS results identifies 33 putative functional genes for T2D, 3 of which were targeted by approved drugs. A further integration of DNA methylation (n = 1980) and epigenomic annotation data highlight 3 genes (CAMK1D, TP53INP1, and ATP5G1) with plausible regulatory mechanisms, whereby a genetic variant exerts an effect on T2D through epigenetic regulation of gene expression. Our study uncovers additional loci, proposes putative genetic regulatory mechanisms for T2D, and provides evidence of purifying selection for T2D-associated variants

RANTES/CCL5 and risk for coronary events: Results from the MONICA/KORA Augsburg case-cohort, Athero-express and CARDIoGRAM studies

Background: The chemokine RANTES (regulated on activation, normal T-cell expressed and secreted)/CCL5 is involved in the pathogenesis of cardiovascular disease in mice, whereas less is known in humans. We hypothesised that its relevance for atherosclerosis should be reflected by associations between CCL5 gene variants, RANTES serum concentrations and protein levels in atherosclerotic plaques and risk for coronary events. Methods and Findings: We conducted a case-cohort study within the population-based MONICA/KORA Augsburg studies. Baseline RANTES serum levels were measured in 363 individuals with incident coronary events and 1,908 non-cases (mean follow-up: 10.2±

Epstein-Barr virus: clinical and epidemiological revisits and genetic basis of oncogenesis

Epstein-Barr virus (EBV) is classified as a member in the order herpesvirales, family herpesviridae, subfamily gammaherpesvirinae and the genus lymphocytovirus. The virus is an exclusively human pathogen and thus also termed as human herpesvirus 4 (HHV4). It was the first oncogenic virus recognized and has been incriminated in the causation of tumors of both lymphatic and epithelial nature. It was reported in some previous studies that 95% of the population worldwide are serologically positive to the virus. Clinically, EBV primary infection is almost silent, persisting as a life-long asymptomatic latent infection in B cells although it may be responsible for a transient clinical syndrome called infectious mononucleosis. Following reactivation of the virus from latency due to immunocompromised status, EBV was found to be associated with several tumors. EBV linked to oncogenesis as detected in lymphoid tumors such as Burkitt's lymphoma (BL), Hodgkin's disease (HD), post-transplant lymphoproliferative disorders (PTLD) and T-cell lymphomas (e.g. Peripheral T-cell lymphomas; PTCL and Anaplastic large cell lymphomas; ALCL). It is also linked to epithelial tumors such as nasopharyngeal carcinoma (NPC), gastric carcinomas and oral hairy leukoplakia (OHL). In vitro, EBV many studies have demonstrated its ability to transform B cells into lymphoblastoid cell lines (LCLs). Despite these malignancies showing different clinical and epidemiological patterns when studied, genetic studies have suggested that these EBV- associated transformations were characterized generally by low level of virus gene expression with only the latent virus proteins (LVPs) upregulated in both tumors and LCLs. In this review, we summarize some clinical and epidemiological features of EBV- associated tumors. We also discuss how EBV latent genes may lead to oncogenesis in the different clinical malignancie

Novel genetic loci associated with hippocampal volume

The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer's disease (rg =-0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness