Prospects of gravitational-wave follow-up through a wide-field ultraviolet satellite: A Dorado case study

The detection of gravitational waves from the binary neuron star merger GW170817 and electromagnetic counterparts GRB170817A and AT2017gfo kick-started the field of gravitational-wave multimessenger astronomy. The optically red to near-infrared emission ("red" component) of AT2017gfo was readily explained as produced by the decay of newly created nuclei produced by rapid neutron capture (a kilonova). However, the ultraviolet to optically blue emission ("blue" component) that was dominant at early times (up to 1.5 days) received no consensus regarding its driving physics. Among many explanations, two leading contenders are kilonova radiation from a lanthanide-poor ejecta component and shock interaction (cocoon emission). In this work, we simulate AT2017gfo-like light curves and perform a Bayesian analysis to study whether an ultraviolet satellite capable of rapid gravitational-wave follow-up, could distinguish between physical processes driving the early "blue" component. We find that ultraviolet data starting at 1.2 hr distinguishes the two early radiation models up to 160 Mpc, implying that an ultraviolet mission like Dorado would significantly contribute to insights into the driving emission physics of the postmerger system. While the same ultraviolet data and optical data starting at 12 hr have limited ability to constrain model parameters separately, the combination of the two unlocks tight constraints for all but one parameter of the kilonova model up to 160 Mpc. We further find that a Dorado-like ultraviolet satellite can distinguish the early radiation models up to at least 130 (60) Mpc if data collection starts within 3.2 (5.2) hr for AT2017gfo-like light curves

Analytic and Reidemeister torsion for representations in finite type Hilbert modules

For a closed Riemannian manifold we extend the definition of analytic and Reidemeister torsion associated to an orthogonal representation of fundamental group on a Hilbert module of finite type over a finite von Neumann algebra. If the representation is of determinant class we prove, generalizing the Cheeger-M\"uller theorem, that the analytic and Reidemeister torsion are equal. In particular, this proves the conjecture that for closed Riemannian manifolds with positive Novikov-Shubin invariants, the L2 analytic and Reidemeister torsions are equal.Comment: 78 pages, AMSTe

From mesoscale to nanoscale mechanics in single-wall carbon nanotubes

The experimental work was carried out in collaboration with W. Wenseleers and S. Cambré at the University of Antwerp, Belgium. The computational results presented have been achieved in part using the Vienna Scientific Cluster (VSC). DJD is grateful for support from the Region Rhône-Alpes through the programme “Accueil-PRO 2014” and from the iMUST Labex programme “Mobility in 2015”. ACTD, TFTC, WC, MALM, SB, DM and ASM acknowledge support from the French Agence Nationale de la Recherche through contract ANR-11-NANO-025 “TRI-CO”. ACTD acknowledges postdoctoral grant from Brazilian Ministry of Education (CAPES)

An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

A First Search for coincident Gravitational Waves and High Energy Neutrinos using LIGO, Virgo and ANTARES data from 2007

We present the results of the first search for gravitational wave bursts associated with high energy neutrinos. Together, these messengers could reveal new, hidden sources that are not observed by conventional photon astronomy, particularly at high energy. Our search uses neutrinos detected by the underwater neutrino telescope ANTARES in its 5 line configuration during the period January - September 2007, which coincided with the fifth and first science runs of LIGO and Virgo, respectively. The LIGO-Virgo data were analysed for candidate gravitational-wave signals coincident in time and direction with the neutrino events. No significant coincident events were observed. We place limits on the density of joint high energy neutrino - gravitational wave emission events in the local universe, and compare them with densities of merger and core-collapse events.Comment: 19 pages, 8 figures, science summary page at http://www.ligo.org/science/Publication-S5LV_ANTARES/index.php. Public access area to figures, tables at https://dcc.ligo.org/cgi-bin/DocDB/ShowDocument?docid=p120000

Study of the Process e+ e- --> pi0 pi0 gamma in c.m. Energy Range 600--970 MeV at CMD-2

The cross section of the process e+ e- --> pi0 pi0 gamma has been measured in the c.m. energy range 600--970 MeV with the CMD-2 detector. The following branching ratios have been determined: B(rho --> pi0 pi0 gamma) =(5.2^{+1.5}_{-1.3} +- 0.6)x10^{-5} and B(omega --> pi0 pi0 gamma) =(6.4^{+2.4}_{-2.0} +- 0.8)x10^{-5}. Evidence for the rho --> f0(600) gamma decay has been obtained: B(rho --> f0(600) gamma) = (6.0^{+3.3}_{-2.7}\pm 0.9)x10^{-5}. From a search for the process e+ e- --> eta pi0 gamma the following upper limit has been obtained: B(omega --> eta pi0 gamma) < 3.3 10^{-5} at 90% CL.Comment: 15 pages, 4 figure

Chronic obstructive pulmonary disease and related phenotypes: polygenic risk scores in population-based and case-control cohorts

Background Genetic factors influence chronic obstructive pulmonary disease (COPD) risk, but the individual variants that have been identified have small effects. We hypothesised that a polygenic risk score using additional variants would predict COPD and associated phenotypes. Methods We constructed a polygenic risk score using a genome-wide association study of lung function (FEV1 and FEV1/forced vital capacity [FVC]) from the UK Biobank and SpiroMeta. We tested this polygenic risk score in nine cohorts of multiple ethnicities for an association with moderate-to-severe COPD (defined as FEV1/FVC <0·7 and FEV1 <80% of predicted). Associations were tested using logistic regression models, adjusting for age, sex, height, smoking pack-years, and principal components of genetic ancestry. We assessed predictive performance of models by area under the curve. In a subset of studies, we also studied quantitative and qualitative CT imaging phenotypes that reflect parenchymal and airway pathology, and patterns of reduced lung growth. Findings The polygenic risk score was associated with COPD in European (odds ratio [OR] per SD 1·81 [95% CI 1·74–1·88] and non-European (1·42 [1·34–1·51]) populations. Compared with the first decile, the tenth decile of the polygenic risk score was associated with COPD, with an OR of 7·99 (6·56–9·72) in European ancestry and 4·83 (3·45–6·77) in non-European ancestry cohorts. The polygenic risk score was superior to previously described genetic risk scores and, when combined with clinical risk factors (ie, age, sex, and smoking pack-years), showed improved prediction for COPD compared with a model comprising clinical risk factors alone (AUC 0·80 [0·79–0·81] vs 0·76 [0·75–0·76]). The polygenic risk score was associated with CT imaging phenotypes, including wall area percent, quantitative and qualitative measures of emphysema, local histogram emphysema patterns, and destructive emphysema subtypes. The polygenic risk score was associated with a reduced lung growth pattern. Interpretation A risk score comprised of genetic variants can identify a small subset of individuals at markedly increased risk for moderate-to-severe COPD, emphysema subtyp