215 research outputs found

    A review of wildland fire spread modelling, 1990-present 3: Mathematical analogues and simulation models

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    In recent years, advances in computational power and spatial data analysis (GIS, remote sensing, etc) have led to an increase in attempts to model the spread and behvaiour of wildland fires across the landscape. This series of review papers endeavours to critically and comprehensively review all types of surface fire spread models developed since 1990. This paper reviews models of a simulation or mathematical analogue nature. Most simulation models are implementations of existing empirical or quasi-empirical models and their primary function is to convert these generally one dimensional models to two dimensions and then propagate a fire perimeter across a modelled landscape. Mathematical analogue models are those that are based on some mathematical conceit (rather than a physical representation of fire spread) that coincidentally simulates the spread of fire. Other papers in the series review models of an physical or quasi-physical nature and empirical or quasi-empirical nature. Many models are extensions or refinements of models developed before 1990. Where this is the case, these models are also discussed but much less comprehensively.Comment: 20 pages + 9 pages references + 1 page figures. Submitted to the International Journal of Wildland Fir

    Prediction of individual genetic risk to prostate cancer using a polygenic score

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    BACKGROUND Polygenic risk scores comprising established susceptibility variants have shown to be informative classifiers for several complex diseases including prostate cancer. For prostate cancer it is unknown if inclusion of genetic markers that have so far not been associated with prostate cancer risk at a genome-wide significant level will improve disease prediction. METHODS We built polygenic risk scores in a large training set comprising over 25,000 individuals. Initially 65 established prostate cancer susceptibility variants were selected. After LD pruning additional variants were prioritized based on their association with prostate cancer. Six-fold cross validation was performed to assess genetic risk scores and optimize the number of additional variants to be included. The final model was evaluated in an independent study population including 1,370 cases and 1,239 controls. RESULTS The polygenic risk score with 65 established susceptibility variants provided an area under the curve (AUC) of 0.67. Adding an additional 68 novel variants significantly increased the AUC to 0.68 (P-=-0.0012) and the net reclassification index with 0.21 (P-=-8.5E-08). All novel variants were located in genomic regions established as associated with prostate cancer risk. CONCLUSIONS Inclusion of additional genetic variants from established prostate cancer susceptibility regions improves disease prediction

    Perfectionism, burnout and engagement in youth sport: The mediating role of basic psychological needs

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    © 2016 Elsevier Ltd. Recent research indicates perfectionistic concerns and perfectionistic strivings share divergent associations with athlete burnout and athlete engagement. Guided by self-determination theory, the present study examined whether these associations were explained by basic psychological needs. Youth athletes (n = 222, M age = 16.01, SD = 2.68) completed measures of multidimensional perfectionism, athlete burnout, athlete engagement, basic psychological need satisfaction and thwarting. Structural equation modelling revealed that basic psychological need satisfaction and thwarting mediated the perfectionism-engagement and perfectionism-burnout relationships. Perfectionistic concerns shared a negative relationship (via need satisfaction) with athlete engagement and a positive relationship (via need satisfaction and thwarting) with athlete burnout. In contrast, perfectionistic strivings shared a positive relationship (via need satisfaction) with athlete engagement and a negative relationship (via need satisfaction and thwarting) with athlete burnout. The findings highlight the role of basic psychological needs in explaining the differential associations that perfectionistic concerns and strivings share with athlete burnout and engagement

    Reconstructing the basal angiosperm phylogeny: evaluating information content of mitochondrial genes

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    Three mitochondrial (atp1, matR, nad5), four chloroplast (atpB, matK, rbcL, rpoC2), and one nuclear (18S) genes from 162 seed plants, representing all major lineages of gymnosperms and angiosperms, were analyzed together in a supermatrix or in various partitions using likelihood and parsimony methods. The results show that Amborella + Nymphaeales together constitute the first diverging lineage of angiosperms, and that the topology of Amborella alone being sister to all other angiosperms likely represents a local long branch attraction artifact. The monophyly of magnoliids, as well as sister relationships between Magnoliales and Laurales, and between Canellales and Piperales, are all strongly supported. The sister relationship to eudicots of Ceratophyllum is not strongly supported by this study; instead a placement of the genus with Chloranthaceae receives moderate support in the mitochondrial gene analyses. Relationships among magnoliids, monocots, and eudicots remain unresolved. Direct comparisons of analytic results from several data partitions with or without RNA editing sites show that in multigene analyses, RNA editing has no effect on well supported relationships, but minor effect on weakly supported ones. Finally, comparisons of results from separate analyses of mitochondrial and chloroplast genes demonstrate that mitochondrial genes, with overall slower rates of substitution than chloroplast genes, are informative phylogenetic markers, and are particularly suitable for resolving deep relationships.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/147147/1/tax25065680.pd

    Fast and efficient QTL mapper for thousands of molecular phenotypes

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    In order to discover quantitative trait loci, multi-dimensional genomic datasets combining DNA-seq and ChiP-/RNA-seq require methods that rapidly correlate tens of thousands of molecular phenotypes with millions of genetic variants while appropriately controlling for multiple testing

    Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction.

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    Prostate cancer is a highly heritable disease with large disparities in incidence rates across ancestry populations. We conducted a multiancestry meta-analysis of prostate cancer genome-wide association studies (107,247 cases and 127,006 controls) and identified 86 new genetic risk variants independently associated with prostate cancer risk, bringing the total to 269 known risk variants. The top genetic risk score (GRS) decile was associated with odds ratios that ranged from 5.06 (95% confidence interval (CI), 4.84-5.29) for men of European ancestry to 3.74 (95% CI, 3.36-4.17) for men of African ancestry. Men of African ancestry were estimated to have a mean GRS that was 2.18-times higher (95% CI, 2.14-2.22), and men of East Asian ancestry 0.73-times lower (95% CI, 0.71-0.76), than men of European ancestry. These findings support the role of germline variation contributing to population differences in prostate cancer risk, with the GRS offering an approach for personalized risk prediction

    Формирование эмоциональной культуры как компонента инновационной культуры студентов

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    Homozygosity has long been associated with rare, often devastating, Mendelian disorders1 and Darwin was one of the first to recognise that inbreeding reduces evolutionary fitness2. However, the effect of the more distant parental relatedness common in modern human populations is less well understood. Genomic data now allow us to investigate the effects of homozygosity on traits of public health importance by observing contiguous homozygous segments (runs of homozygosity, ROH), which are inferred to be homozygous along their complete length. Given the low levels of genome-wide homozygosity prevalent in most human populations, information is required on very large numbers of people to provide sufficient power3,4. Here we use ROH to study 16 health-related quantitative traits in 354,224 individuals from 102 cohorts and find statistically significant associations between summed runs of homozygosity (SROH) and four complex traits: height, forced expiratory lung volume in 1 second (FEV1), general cognitive ability (g) and educational attainment (nominal p<1 × 10−300, 2.1 × 10−6, 2.5 × 10−10, 1.8 × 10−10). In each case increased homozygosity was associated with decreased trait value, equivalent to the offspring of first cousins being 1.2 cm shorter and having 10 months less education. Similar effect sizes were found across four continental groups and populations with different degrees of genome-wide homozygosity, providing convincing evidence for the first time that homozygosity, rather than confounding, directly contributes to phenotypic variance. Contrary to earlier reports in substantially smaller samples5,6, no evidence was seen of an influence of genome-wide homozygosity on blood pressure and low density lipoprotein (LDL) cholesterol, or ten other cardio-metabolic traits. Since directional dominance is predicted for traits under directional evolutionary selection7, this study provides evidence that increased stature and cognitive function have been positively selected in human evolution, whereas many important risk factors for late-onset complex diseases may not have been

    Germline variation at 8q24 and prostate cancer risk in men of European ancestry

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    Chromosome 8q24 is a susceptibility locus for multiple cancers, including prostate cancer. Here we combine genetic data across the 8q24 susceptibility region from 71,535 prostate cancer cases and 52,935 controls of European ancestry to define the overall contribution of germline variation at 8q24 to prostate cancer risk. We identify 12 independent risk signals for prostate cancer (p < 4.28 × 10−15), including three risk variants that have yet to be reported. From a polygenic risk score (PRS) model, derived to assess the cumulative effect of risk variants at 8q24, men in the top 1% of the PRS have a 4-fold (95%CI = 3.62–4.40) greater risk compared to the population average. These 12 variants account for ~25% of what can be currently explained of the familial risk of prostate cancer by known genetic risk factors. These findings highlight the overwhelming contribution of germline variation at 8q24 on prostate cancer risk which has implications for population risk stratification

    Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants

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    Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Peer reviewe
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