Bounds on the width, mass difference and other properties of X(3872) --> pi+pi-J/psi decays

We present results from a study of X(3872) --> pi+pi- J/psi decays produced via exclusive B--> K X(3872) decays. We determine the mass to be M_X(3872)= (3871.84\pm 0.27 (stat)\pm 0.19 (syst)) MeV, a 90% CL upper limit on the natural width of Gamma_X(3872) K+X(3872))xBf(X(3872)-->pi+pi-J/psi)=(8.61 \pm 0.82(stat) \pm 0.52 (syst)) x10^{-6}, and a ratio of branching fractions Bf(B0--> K0 X(3872))/BF(B+--> K+ X(3872))=0.50\pm 0.14(stat)\pm0.04(syst). The difference in mass between the X(3872)-->pi+pi-J/psi signals in B+ and B0 decays is Delta M_{X(3872)= (-0.69 \pm 0.97 (stat)} \pm 0.19 (syst)) MeV. A search for a charged partner of the X(3872) in the decays Bbar0-->K- X+ or B+-->K0X+, X+-->pi+pi0 J/psi resulted in upper limits on the product branching fractions for these processes that are well below expectations for the case that the X(3872) is the neutral member of an isospin triplet. In addition, we examine possible J^{PC} quantum number assignments for the X(3872) based on comparisons of angular correlations between final state particles in X(3872)-->pi+pi-J/psi decays with simulated data for J^{PC} values of 1^{++} and 2^{-+}. We examine the influence of rho-omega interference in the M(pi+pi-) spectrum. The analysis is based on a 711fb^{-1} data sample that contains 772 million BBbar meson pairs collected at the Upsilon(4S) resonance in the Belle detector at the KEKB e+e- collider.Comment: 15 pages, 10 figures and 6 tables. Submitted to Physical Review

Search for CP Violation in the Decay D+→KS0K+D^+\rightarrow K^0_S K^+

We search for CP violation in the decay $D^+\rightarrow K^0_S K^+$ using a data sample with an integrated luminosity of 977 fb$^{-1}$ collected with the Belle detector at the KEKB $e^+e^-$ asymmetric-energy collider. No CP violation has been observed and the CP asymmetry in $D^+\rightarrow K^0_S K^+$ decay is measured to be $(-0.25\pm0.28\pm0.14)$, which is the most sensitive measurement to date. After subtracting CP violation due to $K^0-\bar{K}^0$ mixing, the CP asymmetry in $D^+\rightarrow\bar{K}^0 K^+$ decay is found to be $(+0.08\pm0.28\pm0.14)$.Comment: 15 pages, 4 figures, 1 table. Published in JHE

Precision measurement of charged pion and kaon differential cross sections in electron-positron annihilation at Q = 10.52 GeV

Measurements of inclusive differential cross sections for charged pion and kaon production in electron-positron annihilation have been carried out at a center-of-mass energy of Q = 10.52 GeV. The measurements were performed with the Belle detector at the KEKB electron-positron collider using a data sample containing 113 million e+e- -> qqbar events, where q={u,d,s,c}. We present charge-integrated differential cross sections d\sigma_h+-/dz for h+- = pi+-, K+- as a function of the relative hadron energy z = 2*E_h / sqrt{s} from 0.2 to 0.98. The combined statistical and systematic uncertainties for pi+- (K+-) are 4% (4%) at z ~ 0.6 and 15% (24%) at z ~ 0.9. The cross sections are the first measurements of the z-dependence of pion and kaon production for z > 0.7 as well as the first precision cross section measurements at a center-of-mass energy far below the Z^0 resonance used by the experiments at LEP and SLC.Comment: 7 pages, 3 figures. Ancillary file including all cross section and uncertainty values with 10 pages, 5 figure

Evidence of Υ(1S)→J/ψ+χc1\Upsilon(1S) \to J/\psi+\chi_{c1} and search for double-charmonium production in Υ(1S)\Upsilon(1S) and Υ(2S)\Upsilon(2S) decays

Using data samples of $102\times10^6$ $\Upsilon(1S)$ and $158\times10^6$ $\Upsilon(2S)$ events collected with the Belle detector, a first experimental search has been made for double-charmonium production in the exclusive decays $\Upsilon(1S,2S)\rightarrow J/\psi(\psi')+X$, where $X=\eta_c$, $\chi_{cJ} (J=~0,~1,~2)$, $\eta_c(2S)$, $X(3940)$, and $X(4160)$. No significant signal is observed in the spectra of the mass recoiling against the reconstructed $J/\psi$ or $\psi'$ except for the evidence of $\chi_{c1}$ production with a significance of $4.6\sigma$ for $\Upsilon(1S)\rightarrow J/\psi+\chi_{c1}$. The measured branching fraction \BR(\Upsilon(1S)\rightarrow J/\psi+\chi_{c1}) is $(3.90\pm1.21(\rm stat.)\pm0.23 (\rm syst.))\times10^{-6}$. The $90\%$ confidence level upper limits on the branching fractions of the other modes having a significance of less than $3\sigma$ are determined. These results are consistent with theoretical calculations using the nonrelativistic QCD factorization approach.Comment: 12 pages, 4 figures, 1 table. The fit range was extended to include X(4160) signal according to referee's suggestions. Other results unchanged. Paper was accepted for publication as a regular article in Physical Review

Antimicrobial resistance among migrants in Europe: a systematic review and meta-analysis

BACKGROUND: Rates of antimicrobial resistance (AMR) are rising globally and there is concern that increased migration is contributing to the burden of antibiotic resistance in Europe. However, the effect of migration on the burden of AMR in Europe has not yet been comprehensively examined. Therefore, we did a systematic review and meta-analysis to identify and synthesise data for AMR carriage or infection in migrants to Europe to examine differences in patterns of AMR across migrant groups and in different settings. METHODS: For this systematic review and meta-analysis, we searched MEDLINE, Embase, PubMed, and Scopus with no language restrictions from Jan 1, 2000, to Jan 18, 2017, for primary data from observational studies reporting antibacterial resistance in common bacterial pathogens among migrants to 21 European Union-15 and European Economic Area countries. To be eligible for inclusion, studies had to report data on carriage or infection with laboratory-confirmed antibiotic-resistant organisms in migrant populations. We extracted data from eligible studies and assessed quality using piloted, standardised forms. We did not examine drug resistance in tuberculosis and excluded articles solely reporting on this parameter. We also excluded articles in which migrant status was determined by ethnicity, country of birth of participants' parents, or was not defined, and articles in which data were not disaggregated by migrant status. Outcomes were carriage of or infection with antibiotic-resistant organisms. We used random-effects models to calculate the pooled prevalence of each outcome. The study protocol is registered with PROSPERO, number CRD42016043681. FINDINGS: We identified 2274 articles, of which 23 observational studies reporting on antibiotic resistance in 2319 migrants were included. The pooled prevalence of any AMR carriage or AMR infection in migrants was 25·4% (95% CI 19·1-31·8; I2 =98%), including meticillin-resistant Staphylococcus aureus (7·8%, 4·8-10·7; I2 =92%) and antibiotic-resistant Gram-negative bacteria (27·2%, 17·6-36·8; I2 =94%). The pooled prevalence of any AMR carriage or infection was higher in refugees and asylum seekers (33·0%, 18·3-47·6; I2 =98%) than in other migrant groups (6·6%, 1·8-11·3; I2 =92%). The pooled prevalence of antibiotic-resistant organisms was slightly higher in high-migrant community settings (33·1%, 11·1-55·1; I2 =96%) than in migrants in hospitals (24·3%, 16·1-32·6; I2 =98%). We did not find evidence of high rates of transmission of AMR from migrant to host populations. INTERPRETATION: Migrants are exposed to conditions favouring the emergence of drug resistance during transit and in host countries in Europe. Increased antibiotic resistance among refugees and asylum seekers and in high-migrant community settings (such as refugee camps and detention facilities) highlights the need for improved living conditions, access to health care, and initiatives to facilitate detection of and appropriate high-quality treatment for antibiotic-resistant infections during transit and in host countries. Protocols for the prevention and control of infection and for antibiotic surveillance need to be integrated in all aspects of health care, which should be accessible for all migrant groups, and should target determinants of AMR before, during, and after migration. FUNDING: UK National Institute for Health Research Imperial Biomedical Research Centre, Imperial College Healthcare Charity, the Wellcome Trust, and UK National Institute for Health Research Health Protection Research Unit in Healthcare-associated Infections and Antimictobial Resistance at Imperial College London

Multiple Recurrent De Novo CNVs, Including Duplications of the 7q11.23 Williams Syndrome Region, Are Strongly Associated with Autism

SummaryWe have undertaken a genome-wide analysis of rare copy-number variation (CNV) in 1124 autism spectrum disorder (ASD) families, each comprised of a single proband, unaffected parents, and, in most kindreds, an unaffected sibling. We find significant association of ASD with de novo duplications of 7q11.23, where the reciprocal deletion causes Williams-Beuren syndrome, characterized by a highly social personality. We identify rare recurrent de novo CNVs at five additional regions, including 16p13.2 (encompassing genes USP7 and C16orf72) and Cadherin 13, and implement a rigorous approach to evaluating the statistical significance of these observations. Overall, large de novo CNVs, particularly those encompassing multiple genes, confer substantial risks (OR = 5.6; CI = 2.6–12.0, p = 2.4 × 10-7). We estimate there are 130–234 ASD-related CNV regions in the human genome and present compelling evidence, based on cumulative data, for association of rare de novo events at 7q11.23, 15q11.2-13.1, 16p11.2, and Neurexin 1

Observation of e+e−→π+π−π0χbJe^+e^- \to \pi^+ \pi^- \pi^0 \chi_{bJ} and search for Xb→ωΥ(1S)X_b \to \omega \Upsilon(1S) at s∼10.867\sqrt{s}\sim 10.867 GeV

The $e^+e^- \to \pi^+ \pi^- \pi^0 \chi_{bJ}$ ($J=0,~1,~2$) processes are studied using a 118~fb$^{-1}$ data sample collected at a center-of-mass energy of 10.867 GeV, in the $\Upsilon(10860)$ energy range, with the Belle detector. The $\pi^+ \pi^- \pi^0 \chi_{b1}$, $\pi^+\pi^-\pi^0\chi_{b2}$, $\omega\chi_{b1}$ signals and the evidence of $\omega\chi_{b2}$ are observed for the first time and the cross sections are measured. No significant $\pi^+\pi^-\pi^0\chi_{b0}$ or $\omega\chi_{b0}$ signal is observed and 90\% confidence level upper limits on the cross sections for these two processes are obtained. In the $\pi^+\pi^-\pi^0$ invariant mass spectrum, significant non-$\omega$ signals are also observed. We search for the $X(3872)$-like state with a hidden $b\bar{b}$ component (named $X_b$) decaying into $\omega \Upsilon(1S)$; no significant signal is observed with a mass between $10.55$ and $10.65$ GeV/$c^2$.Comment: 7 pages, 3 figures, accepted for publication as a Letter in Physical Review Letter

The degree of segmental aneuploidy measured by total copy number abnormalities predicts survival and recurrence in superficial gastroesophageal adenocarcinoma

Background: Prognostic biomarkers are needed for superficial gastroesophageal adenocarcinoma (EAC) to predict clinical outcomes and select therapy. Although recurrent mutations have been characterized in EAC, little is known about their clinical and prognostic significance. Aneuploidy is predictive of clinical outcome in many malignancies but has not been evaluated in superficial EAC. Methods: We quantified copy number changes in 41 superficial EAC using Affymetrix SNP 6.0 arrays. We identified recurrent chromosomal gains and losses and calculated the total copy number abnormality (CNA) count for each tumor as a measure of aneuploidy. We correlated CNA count with overall survival and time to first recurrence in univariate and multivariate analyses. Results: Recurrent segmental gains and losses involved multiple genes, including: HER2, EGFR, MET, CDK6, KRAS (recurrent gains); and FHIT, WWOX, CDKN2A/B, SMAD4, RUNX1 (recurrent losses). There was a 40-fold variation in CNA count across all cases. Tumors with the lowest and highest quartile CNA count had significantly better overall survival (p = 0.032) and time to first recurrence (p = 0.010) compared to those with intermediate CNA counts. These associations persisted when controlling for other prognostic variables. Significance: SNP arrays facilitate the assessment of recurrent chromosomal gain and loss and allow high resolution, quantitative assessment of segmental aneuploidy (total CNA count). The non-monotonic association of segmental aneuploidy with survival has been described in other tumors. The degree of aneuploidy is a promising prognostic biomarker in a potentially curable form of EAC. © 2014 Davison et al

Meta-Analysis of Genome-Wide Association Studies and Network Analysis-Based Integration with Gene Expression Data Identify New Suggestive Loci and Unravel a Wnt-Centric Network Associated with Dupuytren’s Disease

Dupuytren´s disease, a fibromatosis of the connective tissue in the palm, is a common complex disease with a strong genetic component. Up to date nine genetic loci have been found to be associated with the disease. Six of these loci contain genes that code for Wnt signalling proteins. In spite of this striking first insight into the genetic factors in Dupuytren´s disease, much of the inherited risk in Dupuytren´s disease still needs to be discovered. The already identified loci jointly explain ~1% of the heritability in this disease. To further elucidate the genetic basis of Dupuytren´s disease, we performed a genome-wide meta-analysis combining three genome-wide association study (GWAS) data sets, comprising 1,580 cases and 4,480 controls. We corroborated all nine previously identified loci, six of these with genome-wide significance (p-value < 5x10-8). In addition, we identified 14 new suggestive loci (p-value < 10−5). Intriguingly, several of these new loci contain genes associated with Wnt signalling and therefore represent excellent candidates for replication. Next, we compared whole-transcriptome data between patient- and control-derived tissue samples and found the Wnt/β-catenin pathway to be the top deregulated pathway in patient samples. We then conducted network and pathway analyses in order to identify protein networks that are enriched for genes highlighted in the GWAS meta-analysis and expression data sets. We found further evidence that the Wnt signalling pathways in conjunction with other pathways may play a critical role in Dupuytren´s disease