12 research outputs found
The type II-plateau supernova 2017eaw in NGC 6946 and its red supergiant progenitor
We present extensive optical photometric and spectroscopic observations, from 4 to 482 days after explosion, of the Type II-plateau (II-P) supernova (SN) 2017eaw in NGC 6946. SN 2017eaw is a normal SN II-P intermediate in properties between, for example, SN 1999em and SN 2012aw and the more luminous SN 2004et, also in NGC 6946. We have determined that the extinction to SN 2017eaw is primarily due to the Galactic foreground and that the SN site metallicity is likely subsolar. We have also independently confirmed a tip-of-the-red-giant-branch (TRGB) distance to NGC 6946 of 7.73 ± 0.78 Mpc. The distances to the SN that we have also estimated via both the standardized candle method and expanding photosphere method corroborate the TRGB distance. We confirm the SN progenitor identity in pre-explosion archival Hubble Space Telescope (HST) and Spitzer Space Telescope images, via imaging of the SN through our HST Target of Opportunity program. Detailed modeling of the progenitor's spectral energy distribution indicates that the star was a dusty, luminous red supergiant consistent with an initial mass of ~15 M ⊙
Genome-Wide Association Study in BRCA1 Mutation Carriers Identifies Novel Loci Associated with Breast and Ovarian Cancer Risk
BRCA1-associated breast and ovarian cancer risks can be modified by common genetic variants. To identify further cancer risk-modifying loci, we performed a multi-stage GWAS of 11,705 BRCA1 carriers (of whom 5,920 were diagnosed with breast and 1,839 were diagnosed with ovarian cancer), with a further replication in an additional sample of 2,646 BRCA1 carriers. We identified a novel breast cancer risk modifier locus at 1q32 for BRCA1 carriers (rs2290854, P = 2.7Ă—10-8, HR = 1.14, 95% CI: 1.09-1.20). In addition, we identified two novel ovarian cancer risk modifier loci: 17q21.31 (rs17631303, P = 1.4Ă—10-8, HR = 1.27, 95% CI: 1.17-1.38) and 4q32.3 (rs4691139, P = 3.4Ă—10-8, HR = 1.20, 95% CI: 1.17-1.38). The 4q32.3 locus was not associated with ovarian cancer risk in the general population or BRCA2 carriers, suggesting a BRCA1-specific associat
Eimeria tenella: Relative Survival of Drug-Resistant and Drug-Sensitive Populations in Floor Pen Chickens
Consultative Group on International Agricultural Research (CGIAR) research-for-development agenda on mycotoxins for enhanced food safety and trade
Characterization of cellular furin content as a potential factor determining the susceptibility of cultured human and animal cells to coronavirus infectious bronchitis virus infection
Telecom-grade fiber laser-based difference-frequency generation and ppb-level detection of benzene vapor in air around 3 ÎĽm
Activation of Cdc42, Rac, PAK, and Rho-Kinase in Response to Hepatocyte Growth Factor Differentially Regulates Epithelial Cell Colony Spreading and Dissociation
Common variants of the <i>BRCA1</i> wild-type allele modify the risk of breast cancer in <i>BRCA1</i> mutation carriers
Mutations in the <i>BRCA1</i> gene substantially increase a woman's lifetime risk of breast cancer. However, there is great variation in this increase in risk with several genetic and non-genetic modifiers identified. The <i>BRCA1</i> protein plays a central role in DNA repair, a mechanism that is particularly instrumental in safeguarding cells against tumorigenesis. We hypothesized that polymorphisms that alter the expression and/or function of <i>BRCA1</i> carried on the wild-type (non-mutated) copy of the <i>BRCA1</i> gene would modify the risk of breast cancer in carriers of <i>BRCA1</i> mutations. A total of 9874 <i>BRCA1</i> mutation carriers were available in the Consortium of Investigators of Modifiers of <i>BRCA1/2</i> (CIMBA) for haplotype analyses of <i>BRCA1</i>. Women carrying the rare allele of single nucleotide polymorphism rs16942 on the wild-type copy of <i>BRCA1</i> were at decreased risk of breast cancer (hazard ratio 0.86, 95% confidence interval 0.77–0.95, <i>P</i> = 0.003). Promoter <i>in vitro</i> assays of the major <i>BRCA1</i> haplotypes showed that common polymorphisms in the regulatory region alter its activity and that this effect may be attributed to the differential binding affinity of nuclear proteins. In conclusion, variants on the wild-type copy of <i>BRCA1</i> modify risk of breast cancer among carriers of <i>BRCA1</i> mutations, possibly by altering the efficiency of <i>BRCA1</i> transcription