Supermassive Black Holes with High Accretion Rates in Active Galactic Nuclei. V. A New Size-Luminosity Scaling Relation for the Broad-Line Region

This paper reports results of the third-year campaign of monitoring super-Eddington accreting massive black holes (SEAMBHs) in active galactic nuclei (AGNs) between 2014-2015. Ten new targets were selected from quasar sample of Sloan Digital Sky Survey (SDSS), which are generally more luminous than the SEAMBH candidates in last two years. H$\beta$ lags ($\tau_{_{\rm H\beta}}$) in five of the 10 quasars have been successfully measured in this monitoring season. We find that the lags are generally shorter, by large factors, than those of objects with same optical luminosity, in light of the well-known $R_{_{\rm H\beta}}-L_{5100}$ relation. The five quasars have dimensionless accretion rates of $\dot{\mathscr{M}}=10-10^3$. Combining measurements of the previous SEAMBHs, we find that the reduction of H$\beta$ lags tightly depends on accretion rates, $\tau_{_{\rm H\beta}}/\tau_{_{R-L}}\propto\dot{\mathscr{M}}^{-0.42}$, where $\tau_{_{R-L}}$ is the H$\beta$ lag from the normal $R_{_{\rm H\beta}}-L_{5100}$ relation. Fitting 63 mapped AGNs, we present a new scaling relation for the broad-line region: $R_{_{\rm H\beta}}=\alpha_1\ell_{44}^{\beta_1}\,\min\left[1,\left(\dot{\mathscr{M}}/\dot{\mathscr{M}}_c\right)^{-\gamma_1}\right]$, where $\ell_{44}=L_{5100}/10^{44}\,\rm erg~s^{-1}$ is 5100 \AA\ continuum luminosity, and coefficients of $\alpha_1=(29.6_{-2.8}^{+2.7})$ lt-d, $\beta_1=0.56_{-0.03}^{+0.03}$, $\gamma_1=0.52_{-0.16}^{+0.33}$ and $\dot{\mathscr{M}}_c=11.19_{-6.22}^{+2.29}$. This relation is applicable to AGNs over a wide range of accretion rates, from $10^{-3}$ to $10^3$. Implications of this new relation are briefly discussed.Comment: 15 pages, 9 figures, 5 table, accepted for publication in The Astrophysical Journa

A Unified Approach to the Classical Statistical Analysis of Small Signals

We give a classical confidence belt construction which unifies the treatment of upper confidence limits for null results and two-sided confidence intervals for non-null results. The unified treatment solves a problem (apparently not previously recognized) that the choice of upper limit or two-sided intervals leads to intervals which are not confidence intervals if the choice is based on the data. We apply the construction to two related problems which have recently been a battle-ground between classical and Bayesian statistics: Poisson processes with background, and Gaussian errors with a bounded physical region. In contrast with the usual classical construction for upper limits, our construction avoids unphysical confidence intervals. In contrast with some popular Bayesian intervals, our intervals eliminate conservatism (frequentist coverage greater than the stated confidence) in the Gaussian case and reduce it to a level dictated by discreteness in the Poisson case. We generalize the method in order to apply it to analysis of experiments searching for neutrino oscillations. We show that this technique both gives correct coverage and is powerful, while other classical techniques that have been used by neutrino oscillation search experiments fail one or both of these criteria.Comment: 40 pages, 15 figures. Changes 15-Dec-99 to agree more closely with published version. A few small changes, plus the two substantive changes we made in proof back in 1998: 1) The definition of "sensitivity" in Sec. V(C). It was inconsistent with our actual definition in Sec. VI. 2) "Note added in proof" at end of the Conclusio

Evidence for e+e−→γχc1,2e^+e^-\to\gamma\chi_{c1, 2} at center-of-mass energies from 4.009 to 4.360 GeV

Using data samples collected at center-of-mass energies of $\sqrt{s}$ = 4.009, 4.230, 4.260, and 4.360 GeV with the BESIII detector operating at the BEPCII collider, we perform a search for the process $e^+e^-\to\gamma\chi_{cJ}$ $(J = 0, 1, 2)$ and find evidence for $e^+e^-\to\gamma\chi_{c1}$ and $e^+e^-\to\gamma\chi_{c2}$ with statistical significances of 3.0$\sigma$ and 3.4$\sigma$, respectively. The Born cross sections $\sigma^{B}(e^+e^-\to\gamma\chi_{cJ})$, as well as their upper limits at the 90% confidence level are determined at each center-of-mass energy.Comment: 8 pages, 7 figures, 3 table

Observation of χc1\chi_{c1} decays into vector meson pairs ϕϕ\phi\phi, ωω\omega\omega, and ωϕ\omega\phi

Decays of $\chi_{c1}$ to vector meson pairs $\phi\phi$, $\omega\omega$ and $\omega\phi$ are observed for the first time using $(106\pm4)\times 10^6$ \psip events accumulated at the BESIII detector at the BEPCII $e^+e^-$ collider. The branching fractions are measured to be $(4.4\pm 0.3\pm 0.5)\times 10^{-4}$, $(6.0\pm 0.3\pm 0.7)\times 10^{-4}$, and $(2.2\pm 0.6\pm 0.2)\times 10^{-5}$, for $\chi_{c1}\to \phi\phi$, $\omega\omega$, and $\omega\phi$, respectively. The observation of $\chi_{c1}$ decays into a pair of vector mesons $\phi\phi$, $\omega\omega$ and $\omega\phi$ indicates that the hadron helicity selection rule is significantly violated in $\chi_{cJ}$ decays. In addition, the measurement of $\chi_{cJ}\to \omega\phi$ gives the rate of doubly OZI-suppressed decay. Branching fractions for $\chi_{c0}$ and $\chi_{c2}$ decays into other vector meson pairs are also measured with improved precision.Comment: 4 pages, 2 figure

Genome-wide association study of endometrial cancer in E2C2

Endometrial cancer (EC), a neoplasm of the uterine epithelial lining, is the most common gynecological malignancy in developed countries and the fourth most common cancer among US women. Women with a family history of EC have an increased risk for the disease, suggesting that inherited genetic factors play a role. We conducted a two-stage genome-wide association study of Type I EC. Stage 1 included 5,472 women (2,695 cases and 2,777 controls) of European ancestry from seven studies. We selected independent single-nucleotide polymorphisms (SNPs) that displayed the most significant associations with EC in Stage 1 for replication among 17,948 women (4,382 cases and 13,566 controls) in a multiethnic population (African America, Asian, Latina, Hawaiian and European ancestry), from nine studies. Although no novel variants reached genome-wide significance, we replicated previously identified associations with genetic markers near the HNF1B locus. Our findings suggest that larger studies with specific tumor classification are necessary to identify novel genetic polymorphisms associated with EC susceptibility. Electronic supplementary material The online version of this article (doi:10.1007/s00439-013-1369-1) contains supplementary material, which is available to authorized users

Improved measurement of the absolute branching fraction of D+→Kˉ0μ+νμD^{+}\rightarrow \bar K^0 \mu^{+}\nu_{\mu}

By analyzing 2.93 fb$^{-1}$ of data collected at $\sqrt s=3.773$ GeV with the BESIII detector, we measure the absolute branching fraction ${\mathcal B}(D^{+}\rightarrow\bar K^0\mu^{+}\nu_{\mu})=(8.72 \pm 0.07_{\rm stat.} \pm 0.18_{\rm sys.})\%$, which is consistent with previous measurements within uncertainties but with significantly improved precision. Combining the Particle Data Group values of ${\mathcal B}(D^0\to K^-\mu^+\nu_\mu)$, ${\mathcal B}(D^{+}\rightarrow\bar K^0 e^{+}\nu_{e})$, and the lifetimes of the $D^0$ and $D^+$ mesons with the value of ${\mathcal B}(D^{+}\rightarrow\bar K^0 \mu^{+}\nu_{\mu})$ measured in this work, we determine the following ratios of partial widths: $\Gamma(D^0\to K^-\mu^+\nu_\mu)/\Gamma(D^{+}\rightarrow\bar K^0\mu^{+}\nu_{\mu})=0.963\pm0.044$ and $\Gamma(D^{+}\rightarrow\bar K^0 \mu^{+}\nu_{\mu})/\Gamma(D^{+}\rightarrow\bar K^0 e^{+}\nu_{e})=0.988\pm0.033$.Comment: 9 pages; 8 figure

Common variants at theCHEK2gene locus and risk of epithelial ovarian cancer

Genome-wide association studies have identified 20 genomic regions associated with risk of epithelial ovarian cancer (EOC), but many additional risk variants may exist. Here, we evaluated associations between common genetic variants [single nucleotide polymorphisms (SNPs) and indels] in DNA repair genes and EOC risk. We genotyped 2896 common variants at 143 gene loci in DNA samples from 15 397 patients with invasive EOC and controls. We found evidence of associations with EOC risk for variants at FANCA, EXO1, E2F4, E2F2, CREB5 and CHEK2 genes (P ≤ 0.001). The strongest risk association was for CHEK2 SNP rs17507066 with serous EOC (P = 4.74 x 10(-7)). Additional genotyping and imputation of genotypes from the 1000 genomes project identified a slightly more significant association for CHEK2 SNP rs6005807 (r (2) with rs17507066 = 0.84, odds ratio (OR) 1.17, 95% CI 1.11-1.24, P = 1.1×10(-7)). We identified 293 variants in the region with likelihood ratios of less than 1:100 for representing the causal variant. Functional annotation identified 25 candidate SNPs that alter transcription factor binding sites within regulatory elements active in EOC precursor tissues. In The Cancer Genome Atlas dataset, CHEK2 gene expression was significantly higher in primary EOCs compared to normal fallopian tube tissues (P = 3.72×10(-8)). We also identified an association between genotypes of the candidate causal SNP rs12166475 (r (2) = 0.99 with rs6005807) and CHEK2 expression (P = 2.70×10(-8)). These data suggest that common variants at 22q12.1 are associated with risk of serous EOC and CHEK2 as a plausible target susceptibility gene.Other Research Uni

Evidence that breast cancer risk at the 2q35 locus is mediated through IGFBP5 regulation.

GWAS have identified a breast cancer susceptibility locus on 2q35. Here we report the fine mapping of this locus using data from 101,943 subjects from 50 case-control studies. We genotype 276 SNPs using the 'iCOGS' genotyping array and impute genotypes for a further 1,284 using 1000 Genomes Project data. All but two, strongly correlated SNPs (rs4442975 G/T and rs6721996 G/A) are excluded as candidate causal variants at odds against >100:1. The best functional candidate, rs4442975, is associated with oestrogen receptor positive (ER+) disease with an odds ratio (OR) in Europeans of 0.85 (95% confidence interval=0.84-0.87; P=1.7 × 10(-43)) per t-allele. This SNP flanks a transcriptional enhancer that physically interacts with the promoter of IGFBP5 (encoding insulin-like growth factor-binding protein 5) and displays allele-specific gene expression, FOXA1 binding and chromatin looping. Evidence suggests that the g-allele confers increased breast cancer susceptibility through relative downregulation of IGFBP5, a gene with known roles in breast cell biology