299 research outputs found

    Observation of D0ρ0γD^0\to \rho^0\gamma and search for CPCP violation in radiative charm decays

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    We report the first observation of the radiative charm decay D0ρ0γD^0 \to \rho^0 \gamma and the first search for CPCP violation in decays D0ρ0γD^0 \to \rho^0 \gamma, ϕγ\phi\gamma, and K0γ\overline{K}{}^{*0} \gamma, using a data sample of 943 fb1^{-1} collected with the Belle detector at the KEKB asymmetric-energy e+ee^+e^- collider. The branching fraction is measured to be B(D0ρ0γ)=(1.77±0.30±0.07)×105\mathcal{B}(D^0 \to \rho^0 \gamma)=(1.77 \pm 0.30 \pm 0.07) \times 10^{-5}, where the first uncertainty is statistical and the second is systematic. The obtained CPCP asymmetries, ACP(D0ρ0γ)=+0.056±0.152±0.006\mathcal{A}_{CP}(D^0 \to \rho^0 \gamma)=+0.056 \pm 0.152 \pm 0.006, ACP(D0ϕγ)=0.094±0.066±0.001\mathcal{A}_{CP}(D^0 \to \phi \gamma)=-0.094 \pm 0.066 \pm 0.001, and ACP(D0K0γ)=0.003±0.020±0.000\mathcal{A}_{CP}(D^0 \to \overline{K}{}^{*0} \gamma)=-0.003 \pm 0.020 \pm 0.000, are consistent with no CPCP violation. We also present an improved measurement of the branching fractions B(D0ϕγ)=(2.76±0.19±0.10)×105\mathcal{B}(D^0 \to \phi \gamma)=(2.76 \pm 0.19 \pm 0.10) \times 10^{-5} and B(D0K0γ)=(4.66±0.21±0.21)×104\mathcal{B}(D^0 \to \overline{K}{}^{*0} \gamma)=(4.66 \pm 0.21 \pm 0.21) \times 10^{-4}

    Search for CPCP violation in the D+π+π0D^{+}\to\pi^{+}\pi^{0} decay at Belle

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    We search for CPCP violation in the charged charm meson decay D+π+π0D^{+}\to\pi^{+}\pi^{0}, based on a data sample corresponding to an integrated luminosity of 921 fb1\rm 921~fb^{-1} collected by the Belle experiment at the KEKB e+ee^{+}e^{-} asymmetric-energy collider. The measured CPCP violating asymmetry is [+2.31±1.24(stat)±0.23(syst)]%[+2.31\pm1.24({\rm stat})\pm0.23({\rm syst})]\%, which is consistent with the standard model prediction and has a significantly improved precision compared to previous results.Comment: 8 pages, 3 figure

    Evidence for Isospin Violation and Measurement of CPCP Asymmetries in BK(892)γB \to K^{\ast}(892) \gamma

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    We report the first evidence for isospin violation in BKγB \to K^* \gamma and the first measurement of difference of CPCP asymmetries between B+K+γB^+ \to K^{*+} \gamma and B0K0γB^0 \to K^{*0} \gamma. This analysis is based on the data sample containing 772×106BBˉ772 \times 10^6 B\bar{B} pairs that was collected with the Belle detector at the KEKB energy-asymmetric e+ee^+ e^- collider. We find evidence for the isospin violation with a significance of 3.1σ\sigma, Δ0+=(+6.2±1.5(stat.)±0.6(syst.)±1.2(f+/f00))\Delta_{0+} = (+6.2 \pm 1.5 ({\rm stat.}) \pm 0.6 ({\rm syst.}) \pm 1.2 (f_{+-}/f_{00}))\%, where the third uncertainty is due to the uncertainty on the fraction of B+BB^+B^- to B0Bˉ0B^0\bar{B}^0 production in Υ(4S)\Upsilon(4S) decays. The measured value is consistent with predictions of the SM. The result for the difference of CPCP asymmetries is ΔACP=(+2.4±2.8(stat.)±0.5(syst.))\Delta A_{CP} = (+2.4 \pm 2.8({\rm stat.}) \pm 0.5({\rm syst.}))\%, consistent with zero. The measured branching fractions and CPCP asymmetries for charged and neutral BB meson decays are the most precise to date. We also calculate the ratio of branching fractions of B0K0γB^0 \to K^{*0} \gamma to Bs0ϕγB_s^0 \to \phi \gamma.Comment: 11 pages, 7 figures. shown at FPCP2017. accepted by PR

    Measurement of the τ\tau lepton polarization and R(D)R(D^*) in the decay BˉDτνˉτ\bar{B} \to D^* \tau^- \bar{\nu}_\tau

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    We report the first measurement of the τ\tau lepton polarization Pτ(D)P_\tau(D^*) in the decay BˉDτνˉτ\bar{B} \rightarrow D^* \tau^- \bar{\nu}_\tau as well as a new measurement of the ratio of the branching fractions R(D)=B(BˉDτνˉτ)/B(BˉDνˉ)R(D^{*}) = \mathcal{B}(\bar {B} \rightarrow D^* \tau^- \bar{\nu}_\tau) / \mathcal{B}(\bar{B} \rightarrow D^* \ell^- \bar{\nu}_\ell), where \ell^- denotes an electron or a muon, and the τ\tau is reconstructed in the modes τπντ\tau^- \rightarrow \pi^- \nu_\tau and τρντ\tau^- \rightarrow \rho^- \nu_\tau. We use the full data sample of 772×106772 \times 10^6 BBˉB{\bar B} pairs recorded with the Belle detector at the KEKB electron-positron collider. Our results, Pτ(D)=0.38±0.51(stat.)0.16+0.21(syst.)P_\tau(D^*) = -0.38 \pm 0.51 {\rm (stat.)} ^{+0.21}_{-0.16} {\rm (syst.)} and R(D)=0.270±0.035(stat.)0.025+0.028(syst.)R(D^*) = 0.270 \pm 0.035{\rm (stat.)} ^{+0.028}_{-0.025}{\rm (syst.)}, are consistent with the theoretical predictions of the Standard Model.Comment: 7 pages, 2 figures, submitted to Physical Review Letters; one figure was removed from the first versio

    Search for CPCP Violation and Measurement of the Branching Fraction in the Decay D0KS0KS0D^{0} \to K^0_S K^0_S

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    We report a study of the decay D0KS0KS0D^0 \to K^0_S K^0_S using 921~fb1^{-1} of data collected at or near the Υ(4S)\Upsilon(4S) and Υ(5S)\Upsilon(5S) resonances with the Belle detector at the KEKB asymmetric energy e+ee^+e^- collider. The measured time-integrated CPCP asymmetry is ACP(D0KS0KS0)=(0.02±1.53±0.02±0.17)% A_{CP}(D^0 \to K^0_S K^0_S) = (-0.02 \pm 1.53 \pm 0.02 \pm 0.17) \%, and the branching fraction is B(D0KS0KS0)\mathcal{B} (D^{0}\rightarrow K_{S}^{0}K_{S}^{0}) = (1.321 ±\pm 0.023 ±\pm 0.036 ±\pm 0.044) ×\times 104^{-4}, where the first uncertainty is statistical, the second is systematic, and the third is due to the normalization mode (D0KS0π0D^0 \to K_S^0 \pi^0). These results are significantly more precise than previous measurements available for this mode. The ACPA_{CP} measurement is consistent with the standard model expectation.Comment: 7 pages,1 figure, Submitted to PR

    Angular analysis of B0K(892)0+B^0 \to K^\ast(892)^0 \ell^+ \ell^-

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    We present a measurement of angular observables, P4P_4', P5P_5', P6P_6', P8P_8', in the decay B0K(892)0+B^0 \to K^\ast(892)^0 \ell^+ \ell^-, where +\ell^+\ell^- is either e+ee^+e^- or μ+μ\mu^+\mu^-. The analysis is performed on a data sample corresponding to an integrated luminosity of 711 fb1711~\mathrm{fb}^{-1} containing 772×106772\times 10^{6} BBˉB\bar B pairs, collected at the Υ(4S)\Upsilon(4S) resonance with the Belle detector at the asymmetric-energy e+ee^+e^- collider KEKB. Four angular observables, P4,5,6,8P_{4,5,6,8}' are extracted in five bins of the invariant mass squared of the lepton system, q2q^2. We compare our results for P4,5,6,8P_{4,5,6,8}' with Standard Model predictions including the q2q^2 region in which the LHCb collaboration reported the so-called P5P_5' anomaly.Comment: Conference paper for LHC Ski 2016. SM prediction for P6P_{6}' corrected and reference for arXiv:1207.2753 adde

    Expression profiles for six zebrafish genes during gonadal sex differentiation

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    <p>Abstract</p> <p>Background</p> <p>The mechanism of sex determination in zebrafish is largely unknown and neither sex chromosomes nor a sex-determining gene have been identified. This indicates that sex determination in zebrafish is mediated by genetic signals from autosomal genes. The aim of this study was to determine the precise timing of expression of six genes previously suggested to be associated with sex differentiation in zebrafish. The current study investigates the expression of all six genes in the same individual fish with extensive sampling dates during sex determination and -differentiation.</p> <p>Results</p> <p>In the present study, we have used quantitative real-time PCR to investigate the expression of ar, sox9a, dmrt1, fig alpha, cyp19a1a and cyp19a1b during the expected sex determination and gonadal sex differentiation period. The expression of the genes expected to be high in males (ar, sox9a and dmrt1a) and high in females (fig alpha and cyp19a1a) was segregated in two groups with more than 10 times difference in expression levels. All of the investigated genes showed peaks in expression levels during the time of sex determination and gonadal sex differentiation. Expression of all genes was investigated on cDNA from the same fish allowing comparison of the high and low expressers of genes that are expected to be highest expressed in either males or females. There were 78% high or low expressers of all three "male" genes (ar, sox9a and dmrt1) in the investigated period and 81% were high or low expressers of both "female" genes (fig alpha and cyp19a1a). When comparing all five genes with expected sex related expression 56% show expression expected for either male or female. Furthermore, the expression of all genes was investigated in different tissue of adult male and female zebrafish.</p> <p>Conclusion</p> <p>In zebrafish, the first significant peak in gene expression during the investigated period (2–40 dph) was dmrt1 at 10 dph which indicates involvement of this gene in the early gonadal sex differentiation of males.</p

    Identification of Widespread Ultra-Edited Human RNAs

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    Adenosine-to-inosine modification of RNA molecules (A-to-I RNA editing) is an important mechanism that increases transciptome diversity. It occurs when a genomically encoded adenosine (A) is converted to an inosine (I) by ADAR proteins. Sequencing reactions read inosine as guanosine (G); therefore, current methods to detect A-to-I editing sites align RNA sequences to their corresponding DNA regions and identify A-to-G mismatches. However, such methods perform poorly on RNAs that underwent extensive editing (“ultra”-editing), as the large number of mismatches obscures the genomic origin of these RNAs. Therefore, only a few anecdotal ultra-edited RNAs have been discovered so far. Here we introduce and apply a novel computational method to identify ultra-edited RNAs. We detected 760 ESTs containing 15,646 editing sites (more than 20 sites per EST, on average), of which 13,668 are novel. Ultra-edited RNAs exhibit the known sequence motif of ADARs and tend to localize in sense strand Alu elements. Compared to sites of mild editing, ultra-editing occurs primarily in Alu-rich regions, where potential base pairing with neighboring, inverted Alus creates particularly long double-stranded RNA structures. Ultra-editing sites are underrepresented in old Alu subfamilies, tend to be non-conserved, and avoid exons, suggesting that ultra-editing is usually deleterious. A possible biological function of ultra-editing could be mediated by non-canonical splicing and cleavage of the RNA near the editing sites
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