1,304 research outputs found
Application of quasi-Monte Carlo methods to PDEs with random coefficients -- an overview and tutorial
This article provides a high-level overview of some recent works on the
application of quasi-Monte Carlo (QMC) methods to PDEs with random
coefficients. It is based on an in-depth survey of a similar title by the same
authors, with an accompanying software package which is also briefly discussed
here. Embedded in this article is a step-by-step tutorial of the required
analysis for the setting known as the uniform case with first order QMC rules.
The aim of this article is to provide an easy entry point for QMC experts
wanting to start research in this direction and for PDE analysts and
practitioners wanting to tap into contemporary QMC theory and methods.Comment: arXiv admin note: text overlap with arXiv:1606.0661
Measuring nickel masses in Type Ia supernovae using cobalt emission in nebular phase spectra
The light curves of Type Ia supernovae (SNe Ia) are powered by the
radioactive decay of Ni to Co at early times, and the decay of
Co to Fe from ~60 days after explosion. We examine the evolution
of the [Co III] 5892 A emission complex during the nebular phase for SNe Ia
with multiple nebular spectra and show that the line flux follows the square of
the mass of Co as a function of time. This result indicates both
efficient local energy deposition from positrons produced in Co decay,
and long-term stability of the ionization state of the nebula. We compile 77
nebular spectra of 25 SN Ia from the literature and present 17 new nebular
spectra of 7 SNe Ia, including SN2014J. From these we measure the flux in the
[Co III] 5892 A line and remove its well-behaved time dependence to infer the
initial mass of Ni () produced in the explosion. We then examine
Ni yields for different SN Ia ejected masses ( - calculated
using the relation between light curve width and ejected mass) and find the
Ni masses of SNe Ia fall into two regimes: for narrow light curves (low
stretch s~0.7-0.9), is clustered near ~ 0.4 and
shows a shallow increase as increases from ~1-1.4; at high
stretch, clusters at the Chandrasekhar mass (1.4) while
spans a broad range from 0.6-1.2. This could constitute
evidence for two distinct SN Ia explosion mechanisms.Comment: 16 pages, 12 figures (main text), plus data tables in appendix.
Spectra released on WISeREP. Submitted to MNRAS, comments welcom
Fine-mapping of the HNF1B multicancer locus identifies candidate variants that mediate endometrial cancer risk.
Common variants in the hepatocyte nuclear factor 1 homeobox B (HNF1B) gene are associated with the risk of Type II diabetes and multiple cancers. Evidence to date indicates that cancer risk may be mediated via genetic or epigenetic effects on HNF1B gene expression. We previously found single-nucleotide polymorphisms (SNPs) at the HNF1B locus to be associated with endometrial cancer, and now report extensive fine-mapping and in silico and laboratory analyses of this locus. Analysis of 1184 genotyped and imputed SNPs in 6608 Caucasian cases and 37 925 controls, and 895 Asian cases and 1968 controls, revealed the best signal of association for SNP rs11263763 (P = 8.4 × 10(-14), odds ratio = 0.86, 95% confidence interval = 0.82-0.89), located within HNF1B intron 1. Haplotype analysis and conditional analyses provide no evidence of further independent endometrial cancer risk variants at this locus. SNP rs11263763 genotype was associated with HNF1B mRNA expression but not with HNF1B methylation in endometrial tumor samples from The Cancer Genome Atlas. Genetic analyses prioritized rs11263763 and four other SNPs in high-to-moderate linkage disequilibrium as the most likely causal SNPs. Three of these SNPs map to the extended HNF1B promoter based on chromatin marks extending from the minimal promoter region. Reporter assays demonstrated that this extended region reduces activity in combination with the minimal HNF1B promoter, and that the minor alleles of rs11263763 or rs8064454 are associated with decreased HNF1B promoter activity. Our findings provide evidence for a single signal associated with endometrial cancer risk at the HNF1B locus, and that risk is likely mediated via altered HNF1B gene expression
Dark sectors 2016 Workshop: community report
This report, based on the Dark Sectors workshop at SLAC in April 2016,
summarizes the scientific importance of searches for dark sector dark matter
and forces at masses beneath the weak-scale, the status of this broad
international field, the important milestones motivating future exploration,
and promising experimental opportunities to reach these milestones over the
next 5-10 years
Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.
Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 × 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and γ-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition
BRCA2 polymorphic stop codon K3326X and the risk of breast, prostate, and ovarian cancers
Background: The K3326X variant in BRCA2 (BRCA2*c.9976A>T; p.Lys3326*; rs11571833) has been found to be associated with small increased risks of breast cancer. However, it is not clear to what extent linkage disequilibrium with fully pathogenic mutations might account for this association. There is scant information about the effect of K3326X in other hormone-related cancers.
Methods: Using weighted logistic regression, we analyzed data from the large iCOGS study including 76 637 cancer case patients and 83 796 control patients to estimate odds ratios (ORw) and 95% confidence intervals (CIs) for K3326X variant carriers in relation to breast, ovarian, and prostate cancer risks, with weights defined as probability of not having a pathogenic BRCA2 variant. Using Cox proportional hazards modeling, we also examined the associations of K3326X with breast and ovarian cancer risks among 7183 BRCA1 variant carriers. All statistical tests were two-sided.
Results: The K3326X variant was associated with breast (ORw = 1.28, 95% CI = 1.17 to 1.40, P = 5.9x10- 6) and invasive ovarian cancer (ORw = 1.26, 95% CI = 1.10 to 1.43, P = 3.8x10-3). These associations were stronger for serous ovarian cancer and for estrogen receptor–negative breast cancer (ORw = 1.46, 95% CI = 1.2 to 1.70, P = 3.4x10-5 and ORw = 1.50, 95% CI = 1.28 to 1.76, P = 4.1x10-5, respectively). For BRCA1 mutation carriers, there was a statistically significant inverse association of the K3326X variant with risk of ovarian cancer (HR = 0.43, 95% CI = 0.22 to 0.84, P = .013) but no association with breast cancer. No association with prostate cancer was observed.
Conclusions: Our study provides evidence that the K3326X variant is associated with risk of developing breast and ovarian cancers independent of other pathogenic variants in BRCA2. Further studies are needed to determine the biological mechanism of action responsible for these associations
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