702 research outputs found

    Study of the Decays B0 --> D(*)+D(*)-

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    The decays B0 --> D*+D*-, B0 --> D*+D- and B0 --> D+D- are studied in 9.7 million Y(4S) --> BBbar decays accumulated with the CLEO detector. We determine Br(B0 --> D*+D*-) = (9.9+4.2-3.3+-1.2)e-4 and limit Br(B0 --> D*+D-) < 6.3e-4 and Br(B0 --> D+D-) < 9.4e-4 at 90% confidence level (CL). We also perform the first angular analysis of the B0 --> D*+D*- decay and determine that the CP-even fraction of the final state is greater than 0.11 at 90% CL. Future measurements of the time dependence of these decays may be useful for the investigation of CP violation in neutral B meson decays.Comment: 21 pages, 5 figures, submitted to Phys. Rev.

    Search for new phenomena in final states with an energetic jet and large missing transverse momentum in pp collisions at √ s = 8 TeV with the ATLAS detector

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    Results of a search for new phenomena in final states with an energetic jet and large missing transverse momentum are reported. The search uses 20.3 fb−1 of √ s = 8 TeV data collected in 2012 with the ATLAS detector at the LHC. Events are required to have at least one jet with pT > 120 GeV and no leptons. Nine signal regions are considered with increasing missing transverse momentum requirements between Emiss T > 150 GeV and Emiss T > 700 GeV. Good agreement is observed between the number of events in data and Standard Model expectations. The results are translated into exclusion limits on models with either large extra spatial dimensions, pair production of weakly interacting dark matter candidates, or production of very light gravitinos in a gauge-mediated supersymmetric model. In addition, limits on the production of an invisibly decaying Higgs-like boson leading to similar topologies in the final state are presente

    Observation of the Ωc0\Omega_{c}^{0} Charmed Baryon at CLEO

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    The CLEO experiment at the CESR collider has used 13.7 fb1^{-1} of data to search for the production of the Ωc0\Omega_c^0 (css-ground state) in e+ee^{+}e^{-} collisions at s10.6\sqrt{s} \simeq 10.6 {\rm GeV}. The modes used to study the Ωc0\Omega_c^0 are Ωπ+\Omega^- \pi^+, Ωπ+π0\Omega^- \pi^+ \pi^0, ΞKpi+π+\Xi^- K^- pi^+ \pi^+, Ξ0Kpi+\Xi^0 K^- pi^+, and Ωπ+ππ+\Omega^- \pi^+ \pi^- \pi^+. We observe a signal of 40.4±\pm9.0(stat) events at a mass of 2694.6±\pm2.6(stat)±\pm1.9(syst) {\rm MeV/c2c^2}, for all modes combined.Comment: 10 pages postscript, also available through http://w4.lns.cornell.edu/public/CLN

    Measurement of the Relative Branching Fraction of Υ(4S)\Upsilon(4S) to Charged and Neutral B-Meson Pairs

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    We analyze 9.7 x 10^6 B\bar{B}$ pairs recorded with the CLEO detector to determine the production ratio of charged to neutral B-meson pairs produced at the Y(4S) resonance. We measure the rates for B^0 -> J/psi K^{(*)0} and B^+ -> J/psi K^{(*)+} decays and use the world-average B-meson lifetime ratio to extract the relative widths f+-/f00 = Gamma(Y(4S) -> B+B-)/Gamma(Y(4S) -> B0\bar{B0}) = = 1.04 +/- 0.07(stat) +/- 0.04(syst). With the assumption that f+- + f00 = 1, we obtain f00 = 0.49 +/- 0.02(stat) +/- 0.01(syst) and f+- = 0.51 +/- 0.02(stat) +/- 0.01(syst). This production ratio and its uncertainty apply to all exclusive B-meson branching fractions measured at the Y(4S) resonance.Comment: 11 pages postscript, also available through http://w4.lns.cornell.edu/public/CLN

    Measurements of B --> D_s^{(*)+} D^{*(*)} Branching Fractions

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    This article describes improved measurements by CLEO of the B0Ds+DB^0 \to D_s^+ D^{*-} and B0Ds+DB^0 \to D_s^{*+} D^{*-} branching fractions, and first evidence for the decay B+Ds()+Dˉ0B^+ \to D_s^{(*)+} \bar{D}^{**0}, where Dˉ0\bar{D}^{**0} represents the sum of the Dˉ1(2420)0\bar{D}_1(2420)^0, Dˉ2(2460)0\bar{D}_2^*(2460)^0, and Dˉ1(j=1/2)0\bar{D}_1(j=1/2)^0 L=1 charm meson states. Also reported is the first measurement of the Ds+D_s^{*+} polarization in the decay B0Ds+DB^0 \to D_s^{*+} D^{*-}. A partial reconstruction technique, employing only the fully reconstructed Ds+D_s^+ and slow pion πs\pi_s^- from the DDˉ0πsD^{*-} \to \bar{D}^0 \pi^-_s decay, enhances sensitivity. The observed branching fractions are B(B0Ds+D)=(1.10±0.18±0.10±0.28){\mathcal B} (B^0 \to D_s^+ D^{*-}) = (1.10 \pm 0.18 \pm 0.10 \pm 0.28)%, B(B0Ds+D)=(1.82±0.37±0.24±0.46){\mathcal B} (B^0 \to D_s^{*+} D^{*-}) = (1.82 \pm 0.37 \pm 0.24 \pm 0.46)%, and B(B+Ds()+Dˉ0)=(2.73±0.78±0.48±0.68){\mathcal B} (B^+ \to D_s^{(*)+} \bar{D}^{**0}) = (2.73 \pm 0.78 \pm 0.48 \pm 0.68)%, where the first error is statistical, the second systematic, and the third is due to the uncertainty in the Ds+ϕπ+D_s^+ \to \phi \pi^+ branching fraction. The measured Ds+D_s^{*+} longitudinal polarization, ΓL/Γ=(50.6±13.9±3.6)\Gamma_L/\Gamma = (50.6 \pm 13.9 \pm 3.6)%, is consistent with the factorization prediction of 54%.Comment: 26 pages (LaTeX), 15 figures. To be submitted to PR

    Programmable in situ amplification for multiplexed imaging of mRNA expression

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    In situ hybridization methods enable the mapping of mRNA expression within intact biological samples. With current approaches, it is challenging to simultaneously map multiple target mRNAs within whole-mount vertebrate embryos, representing a significant limitation in attempting to study interacting regulatory elements in systems most relevant to human development and disease. Here, we report a multiplexed fluorescent in situ hybridization method based on orthogonal amplification with hybridization chain reactions (HCR). With this approach, RNA probes complementary to mRNA targets trigger chain reactions in which fluorophore-labeled RNA hairpins self-assemble into tethered fluorescent amplification polymers. The programmability and sequence specificity of these amplification cascades enable multiple HCR amplifiers to operate orthogonally at the same time in the same sample. Robust performance is achieved when imaging five target mRNAs simultaneously in fixed whole-mount and sectioned zebrafish embryos. HCR amplifiers exhibit deep sample penetration, high signal-to-background ratios and sharp signal localization

    NEDD9 Stabilizes Focal Adhesions, Increases Binding to the Extra-Cellular Matrix and Differentially Effects 2D versus 3D Cell Migration

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    The speed of cell migration on 2-dimensional (2D) surfaces is determined by the rate of assembly and disassembly of clustered integrin receptors known as focal adhesions. Different modes of cell migration that have been described in 3D environments are distinguished by their dependence on integrin-mediated interactions with the extra-cellular matrix. In particular, the mesenchymal invasion mode is the most dependent on focal adhesion dynamics. The focal adhesion protein NEDD9 is a key signalling intermediary in mesenchymal cell migration, however whether NEDD9 plays a role in regulating focal adhesion dynamics has not previously been reported. As NEDD9 effects on 2D migration speed appear to depend on the cell type examined, in the present study we have used mouse embryo fibroblasts (MEFs) from mice in which the NEDD9 gene has been depleted (NEDD9 −/− MEFs). This allows comparison with effects of other focal adhesion proteins that have previously been demonstrated using MEFs. We show that focal adhesion disassembly rates are increased in the absence of NEDD9 expression and this is correlated with increased paxillin phosphorylation at focal adhesions. NEDD9−/− MEFs have increased rates of migration on 2D surfaces, but conversely, migration of these cells is significantly reduced in 3D collagen gels. Importantly we show that myosin light chain kinase is activated in 3D in the absence of NEDD9 and is conversely inhibited in 2D cultures. Measurement of adhesion strength reveals that NEDD9−/− MEFs have decreased adhesion to fibronectin, despite upregulated α5β1 fibronectin receptor expression. We find that β1 integrin activation is significantly suppressed in the NEDD9−/−, suggesting that in the absence of NEDD9 there is decreased integrin receptor activation. Collectively our data suggest that NEDD9 may promote 3D cell migration by slowing focal adhesion disassembly, promoting integrin receptor activation and increasing adhesion force to the ECM.NHMRC Project Grants 512551 and 63251

    NEDD9 Stabilizes Focal Adhesions, Increases Binding to the Extra-Cellular Matrix and Differentially Effects 2D versus 3D Cell Migration

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    The speed of cell migration on 2-dimensional (2D) surfaces is determined by the rate of assembly and disassembly of clustered integrin receptors known as focal adhesions. Different modes of cell migration that have been described in 3D environments are distinguished by their dependence on integrin-mediated interactions with the extra-cellular matrix. In particular, the mesenchymal invasion mode is the most dependent on focal adhesion dynamics. The focal adhesion protein NEDD9 is a key signalling intermediary in mesenchymal cell migration, however whether NEDD9 plays a role in regulating focal adhesion dynamics has not previously been reported. As NEDD9 effects on 2D migration speed appear to depend on the cell type examined, in the present study we have used mouse embryo fibroblasts (MEFs) from mice in which the NEDD9 gene has been depleted (NEDD9 −/− MEFs). This allows comparison with effects of other focal adhesion proteins that have previously been demonstrated using MEFs. We show that focal adhesion disassembly rates are increased in the absence of NEDD9 expression and this is correlated with increased paxillin phosphorylation at focal adhesions. NEDD9−/− MEFs have increased rates of migration on 2D surfaces, but conversely, migration of these cells is significantly reduced in 3D collagen gels. Importantly we show that myosin light chain kinase is activated in 3D in the absence of NEDD9 and is conversely inhibited in 2D cultures. Measurement of adhesion strength reveals that NEDD9−/− MEFs have decreased adhesion to fibronectin, despite upregulated α5β1 fibronectin receptor expression. We find that β1 integrin activation is significantly suppressed in the NEDD9−/−, suggesting that in the absence of NEDD9 there is decreased integrin receptor activation. Collectively our data suggest that NEDD9 may promote 3D cell migration by slowing focal adhesion disassembly, promoting integrin receptor activation and increasing adhesion force to the ECM.NHMRC Project Grants 512551 and 63251
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