Single-particle nonlocality and entanglement with the vacuum

We propose a single-particle experiment that is equivalent to the conventional two-particle experiment used to demonstrate a violation of Bell's inequalities. Hence, we argue that quantum mechanical nonlocality can be demonstrated by single-particle states. The validity of such a claim has been discussed in the literature, but without reaching a clear consensus. We show that the disagreement can be traced to what part of the total state of the experiment one assigns to the (macroscopic) measurement apparatus. However, with a conventional and legitimate interpretation of the measurement process one is led to the conclusion that even a single particle can show nonlocal properties.Comment: 6 pages, 5 figure

Вітання Президента України В.Ф. Януковича з нагоди 50-річчя обрання академіка Б.Є. Патона президентом Національної академії наук України

Phthalates which are widely used, are ubiquitous in the environment and in some human tissues. It is generally accepted that phthalates exert their toxic action by inhibiting Leydig cell synthesis of testosterone, but in vitro studies have also shown anti-androgenic effects at the receptor level. Some cross-sectional studies have shown inverse associations between urinary levels of phthalates and reproductive hormones, but results are conflicting and the evidence base is limited. The aim of this study was to investigate if levels of di-2-ethylhexyl phthalate (DEHP) and diisononyl phthalate (DiNP) metabolites in serum are associated with serum concentrations of male reproductive hormones and semen quality. A secondary aim was to investigate metabolic pathways of DEHP and DiNP on semen quality and reproductive hormones. A cross-sectional sample of 589 spouses of pregnant women from Greenland, Poland and Ukraine were enrolled between 2002 and 2004. The men gave semen and blood samples and were interviewed. Six phthalate metabolites of DEHP and DiNP were measured by liquid chromatography tandem mass spectrometry in serum. The metabolites were summed according to their molar weight. We observed significant inverse associations between serum levels of the metabolites, the proxies and serum testosterone. Negative associations were also discovered between some metabolites and sex hormone-binding globulin, semen volume and total sperm count Findings are compatible with a weak anti-androgenic action of DEHP metabolites, but less so for DiNP metabolites. Metabolic pathways differed significantly between the three study sites, but without major effect on semen quality or reproductive hormones. (C) 2014 Elsevier Ltd. All rights reserved

Predictors of Societal Costs of Older Care-Dependent Adults Living in the Community in 11 European Countries

BACKGROUND: The objective was to identify predictors of societal costs covering formal and informal care utilization by older home care clients in 11 European countries. METHODS : Societal costs of 1907 older clients receiving home care for 12 months from the Aged in Home care (AdHoc) study were estimated using the InterRAI Minimum Data Set for Home Care's (MDS-HC) resource use items. Predictors (medical, functional, and psychosocial domains) of societal costs were identified by performing univariate and multivariate generalized linear model analyses. RESULTS : Mean societal costs per participant were (sic)36 442, ranging from (sic)14 865 in Denmark to (sic)78 836 in the United Kingdom. In the final multivariate model, country, being married, activities of daily living (ADL) dependency, cognitive impairment, limitations of going out, oral conditions, number of medications, arthritis, and cerebro vascular accident (CVA) were significantly associated with societal costs. CONCLUSIONS: Of the predictors, ADL dependency and limitations of going out may be modifiable. Developing interventions targeted at improving these conditions may create opportunities to curtail societal costs.Peer reviewe

Six pelagic seabird species of the North Atlantic engage in a fly-and-forage strategy during their migratory movements

Bird migration is commonly defined as a seasonal movement between breeding and non-breeding grounds. It generally involves relatively straight and directed large-scale movements, with a latitudinal change, and specific daily activity patterns comprising less or no foraging and more traveling time. Our main objective was to describe how this general definition applies to seabirds. We investigated migration characteristics of 6 pelagic seabird species (little auk Alle alle, Atlantic puffin Fratercula arctica, common guillemot Uria aalge, Brünnich’s guillemot U. lomvia, black-legged kittiwake Rissa tridactyla and northern fulmars Fulmarus glacialis). We analysed an extensive geolocator positional and saltwater immersion dataset from 29 colonies in the North-East Atlantic and across several years (2008-2019). We used a novel method to identify active migration periods based on segmentation of time series of track characteristics (latitude, longitude, net-squared displacement). Additionally, we used the saltwater immersion data of geolocators to infer bird activity. We found that the 6 species had, on average, 3 to 4 migration periods and 2 to 3 distinct stationary areas during the non-breeding season. On average, seabirds spent the winter at lower latitudes than their breeding colonies and followed specific migration routes rather than non-directionally dispersing from their colonies. Differences in daily activity patterns were small between migratory and stationary periods, suggesting that all species continued to forage and rest while migrating, engaging in a ‘fly-and-forage’ migratory strategy. We thereby demonstrate the importance of habitats visited during seabird migrations as those that are not just flown over, but which may be important for re-fuelling.publishedVersio

Catheter Colonization and Abscess Formation Due to Staphylococcus epidermidis with Normal and Small-Colony-Variant Phenotype Is Mouse Strain Dependent

Coagulase-negative staphylococci (CoNS) form a thick, multilayered biofilm on foreign bodies and are a major cause of nosocomial implant-associated infections. Although foreign body infection models are well-established, limited in vivo data are available for CoNS with small-colony-variant (SCV) phenotype described as causative agents in implant-associated infections. Therefore, we investigated the impact of the Staphylococcus epidermidis phenotype on colonization of implanted PVC catheters and abscess formation in three different mouse strains. Following introduction of a catheter subcutaneously in each flank of 8- to 12-week-old inbred C57BL/6JCrl (B6J), outbred Crl:CD1(ICR) (CD-1), and inbred BALB/cAnNCrl (BALB/c) male mice, doses of S. epidermidis O-47 wild type, its hemB mutant with stable SCV phenotype, or its complemented mutant at concentrations of 106 to 109 colony forming units (CFUs) were gently spread onto each catheter. On day 7, mice were sacrificed and the size of the abscesses as well as bacterial colonization was determined. A total of 11,500 CFUs of the complemented mutant adhered to the catheter in BALB/c followed by 9,960 CFUs and 9,900 CFUs from S. epidermidis wild type in BALB/c and CD-1, respectively. SCV colonization was highest in CD-1 with 9,500 CFUs, whereas SCVs were not detected in B6J. The minimum dose that led to colonization or abscess formation in all mouse strains was 107 or 108 CFUs of the normal phenotype, respectively. A minimum dose of 108 or 109 CFU of the hemB mutant with stable SCV phenotype led to colonization only or abscess formation, respectively. The largest abscesses were detected in BALB/c inoculated with wild type bacteria or SCV (64 mm2 vs. 28 mm2). Our results indicate that colonization and abscess formation by different phenotypes of S. epidermidis in a foreign body infection model is most effective in inbred BALB/c followed by outbred CD-1 and inbred B6J mice

A sequence variant at 4p16.3 confers susceptibility to urinary bladder cancer

To access publisher full text version of this article. Please click on the hyperlink in Additional Links fieldPreviously, we reported germline DNA variants associated with risk of urinary bladder cancer (UBC) in Dutch and Icelandic subjects. Here we expanded the Icelandic sample set and tested the top 20 markers from the combined analysis in several European case-control sample sets, with a total of 4,739 cases and 45,549 controls. The T allele of rs798766 on 4p16.3 was found to associate with UBC (odds ratio = 1.24, P = 9.9 x 10(-12)). rs798766 is located in an intron of TACC3, 70 kb from FGFR3, which often harbors activating somatic mutations in low-grade, noninvasive UBC. Notably, rs798766[T] shows stronger association with low-grade and low-stage UBC than with more aggressive forms of the disease and is associated with higher risk of recurrence in low-grade stage Ta tumors. The frequency of rs798766[T] is higher in Ta tumors that carry an activating mutation in FGFR3 than in Ta tumors with wild-type FGFR3. Our results show a link between germline variants, somatic mutations of FGFR3 and risk of UBC.info:eu-repo/grantAgreement/EC/FP7/21807

Genetic fine mapping and genomic annotation defines causal mechanisms at type 2 diabetes susceptibility loci.

We performed fine mapping of 39 established type 2 diabetes (T2D) loci in 27,206 cases and 57,574 controls of European ancestry. We identified 49 distinct association signals at these loci, including five mapping in or near KCNQ1. 'Credible sets' of the variants most likely to drive each distinct signal mapped predominantly to noncoding sequence, implying that association with T2D is mediated through gene regulation. Credible set variants were enriched for overlap with FOXA2 chromatin immunoprecipitation binding sites in human islet and liver cells, including at MTNR1B, where fine mapping implicated rs10830963 as driving T2D association. We confirmed that the T2D risk allele for this SNP increases FOXA2-bound enhancer activity in islet- and liver-derived cells. We observed allele-specific differences in NEUROD1 binding in islet-derived cells, consistent with evidence that the T2D risk allele increases islet MTNR1B expression. Our study demonstrates how integration of genetic and genomic information can define molecular mechanisms through which variants underlying association signals exert their effects on disease

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe