Low to moderate alcohol consumption in women increases the risk of certain cancers. For every additional drink regularly consumed per day, the increase in incidence up to age 75 years per 1000 for women in developed countries is estimated to be about 11 for breast cancer, 1 for cancers of the oral cavity and pharynx, 1 for cancer of the rectum, and 0.7 each for cancers of the esophagus, larynx and liver, giving a total excess of about 15 cancers per 1000 women up to age 75.

We introduce QuEST, the Quantum Exact Simulation Toolkit, and compare it to ProjectQ, qHipster and a recent distributed implementation of Quantum++. QuEST is the first open source, hybrid multithreaded and distributed, GPU accelerated simulator of universal quantum circuits. Embodied as a C library, it is designed so that a user’s code can be deployed seamlessly to any platform from a laptop to a supercomputer. QuEST is capable of simulating generic quantum circuits of general one and two-qubit gates and multi-qubit controlled gates, on pure and mixed states, represented as state-vectors and density matrices, and under the presence of decoherence. Using the ARCUS and ARCHER supercomputers, we benchmark QuEST’s simulation of random circuits of up to 38 qubits, distributed over up to 2048 compute nodes, each with up to 24 cores. We directly compare QuEST’s performance to ProjectQ’s on single machines, and discuss the differences in distribution strategies of QuEST, qHipster and Quantum++. QuEST shows excellent scaling, both strong and weak, on multicore and distributed architectures.

Phenotype-driven genetics can be used to create mouse models of human disease and birth defects. However, the utility of these mutant models is limited without identification of the causal gene. To facilitate genetic mapping, we developed a fixed single nucleotide polymorphism (SNP) panel of 394 SNPs as an alternative to analyses using simple sequence length polymorphism (SSLP) marker mapping. With the SNP panel, chromosomal locations for 22 monogenic mutants were identified. The average number of affected progeny genotyped for mapped monogenic mutations is nine. Map locations for several mutants have been obtained with as few as four affected progeny. The average size of genetic intervals obtained for these mutants is 43 Mb, with a range of 17-83 Mb. Thus, our SNP panel allows for identification of moderate resolution map position with small numbers of mice in a high-throughput manner. Importantly, the panel is suitable for mapping crosses from many inbred and wild-derived inbred strain combinations. The chromosomal localizations obtained with the SNP panel allow one to quickly distinguish between potentially novel loci or remutations in known genes, and facilitates fine mapping and positional cloning. By using this approach, we identified DNA sequence changes in two ethylnitrosourea-induced mutants.[Supplemental material is available online at www.genome.org.]Until recently, genetic mapping in the mouse was performed most efficiently by analysis of simple sequence length polymorphism (SSLP) markers both for initial identification of chromosomal (Chr.) localization and for high-resolution mapping (Dietrich et al. 1994). A typical SSLP-based genome scan of 80-100 markers allowed identification of genetic intervals at low to moderate resolution. Chromosomal localization can be obtained with fewer markers and small numbers of mice if techniques such as haplotype analysis are employed (Neuhaus and Beier 1998). Although SSLP-based genotyping has been used successfully for the genetic mapping of hundreds of mutations, it is labor intensive and any single SSLP panel is generally not fully informative for crosses using a variety of strain combinations.Advances in genome sequencing have led to the discovery of thousands of single nucleotide polymorphisms (SNPs) in the mouse genome (Lindblad-Toh et al. 2000;Wiltshire et al. 2003;Pletcher et al. 2004). Recently, several groups have demonstrated the utility of SNPs for examining the haplotype structure of the mouse genome (Wade et al. 2002;Fraser et al. 2004;Liao et al. 2004); for investigating relationships between inbred strains (Petkov et al. 2004;Pletcher et al. 2004); and for developing computational methods for mapping qualitative and quantitative trait loci (QTL) in the mouse (Grupe et al. 2001;Liao et al. 2004;Pletcher et al. 2004). On a smaller scale, a strain-specific, lowdensity, genome-wide SNP panel was used to identify genetic modifiers (Owens et al. 2005).We sought to utilize SNP genotyping as an alternative to microsatellite marker analysis for mapping muta...

BackgroundElectronic linkage of UK cohorts to routinely collected National Health Service (NHS) records provides virtually complete follow-up for cause-specific hospital admissions and deaths. The reliability of dementia diagnoses recorded in NHS hospital data is not well documented.MethodsFor a sample of Million Women Study participants in England we compared dementia recorded in routinely collected NHS hospital data (Hospital Episode Statistics: HES) with dementia recorded in two separate sources of primary care information: a primary care database [Clinical Practice Research Datalink (CPRD), n = 340] and a survey of study participants’ General Practitioners (GPs, n = 244).ResultsDementia recorded in HES fully agreed both with CPRD and with GP survey data for 85% of women; it did not agree for 1 and 4%, respectively. Agreement was uncertain for the remaining 14 and 11%, respectively; and among those classified as having uncertain agreement in CPRD, non-specific terms compatible with dementia, such as ‘memory loss’, were recorded in the CPRD database for 79% of the women. Agreement was significantly better (p < 0.05 for all comparisons) for women with HES diagnoses for Alzheimer’s disease (95 and 94% agreement with any dementia for CPRD and GP survey, respectively) and for vascular dementia (88 and 88%, respectively) than for women with a record only of dementia not otherwise specified (70 and 72%, respectively). Dementia in the same woman was first mentioned an average 1.6 (SD 2.6) years earlier in primary care (CPRD) than in hospital (HES) data. Age-specific rates for dementia based on the hospital admission data were lower than the rates based on the primary care data, but were similar if the delay in recording in HES was taken into account.ConclusionsDementia recorded in routinely collected NHS hospital admission data for women in England agrees well with primary care records of dementia assessed separately from two different sources, and is sufficiently reliable for epidemiological research.Electronic supplementary materialThe online version of this article (doi:10.1186/s12982-016-0053-z) contains supplementary material, which is available to authorized users.

Hormonal and reproductive factors affect the risk of hip and knee replacement, more so for the knee than the hip. The reasons for this are unclear.