Measurement of the electron transmission rate of the gating foil for the TPC of the ILC experiment

We have developed a gating foil for the time projection chamber envisaged as a central tracker for the international linear collider experiment. It has a structure similar to the Gas Electron Multiplier (GEM) with a higher optical aperture ratio and functions as an ion gate without gas amplification. The transmission rate for electrons was measured in a counting mode for a wide range of the voltages applied across the foil using an $^{55}$Fe source and a laser in the absence of a magnetic field. The blocking power of the foil against positive ions was estimated from the electron transmissions.Comment: 25 pages containing 14 figures and 1 tabl

Study of Excited Ξc\Xi_c States Decaying into Ξc0\Xi_c^0 and Ξc+\Xi_c^+ Baryons

Using a data sample of 980 ${\rm fb}^{-1}$ of $e^+e^-$ annihilation data taken with the Belle detector operating at the KEKB asymmetric-energy $e^+e^-$ collider, we report the results of a study of excited $\Xi_c$ states that decay, via the emission of photons and/or charged pions, into $\Xi_c^0$ or $\Xi_c^+$ ground state charmed-strange baryons. We present new measurements of the masses of all members of the $\Xi_c^{\prime}$, $\Xi_c(2645)$, $\Xi_c(2790)$, $\Xi_c(2815)$, and $\Xi_c(2980)$ isodoublets, measurements of the intrinsic widths of those that decay strongly, and evidence of previously unknown transitions.Comment: Submitted to PR

Search for a massive invisible particle X0X^0 in B+→e+X0B^{+}\to e^{+}X^{0} and B+→μ+X0B^{+}\to \mu^{+}X^{0} decays

We present a search for a non-Standard-Model invisible particle $X^0$ in the mass range $0.1\textrm{-}1.8 \,{\rm GeV}/{c^2}$ in $B^{+}\to e^{+} X^{0}$ and $B^{+}\to \mu^{+} X^{0}$ decays. The results are obtained from a $711~{\rm fb}^{-1}$ data sample that corresponds to $772 \times 10^{6} B\bar{B}$ pairs, collected at the $\Upsilon(4S)$ resonance with the Belle detector at the KEKB $e^+ e^-$ collider. One $B$ meson is fully reconstructed in a hadronic mode to determine the momentum of the lepton of the signal decay in the rest frame of the recoiling partner $B$ meson. We find no evidence of a signal and set upper limits on the order of $10^{-6}$.Comment: 8 pages, 4 figures, 3 table

First Observation of Doubly Cabibbo-Suppressed Decay of a Charmed Baryon: Λc+→pK+π−\Lambda^{+}_{c} \rightarrow p K^{+} \pi^{-}

We report the first observation of the decay $\Lambda^{+}_{c} \rightarrow p K^{+} \pi^{-}$ using a 980 $\mathrm{fb^{-1}}$ data sample collected by the Belle detector at the KEKB asymmetric-energy $e^{+}e^{-}$ collider. This is the first doubly Cabibbo-suppressed decay of a charmed baryon to be observed. We measure the branching ratio of this decay with respect to its Cabibbo-favored counterpart to be $\mathcal{B}(\Lambda^{+}_{c} \rightarrow p K^{+} \pi^{-})/\mathcal{B}(\Lambda^{+}_{c} \rightarrow p K^{-} \pi^{+})=(2.35\pm0.27\pm0.21)\times10^{-3}$, where the uncertainties are statistical and systematic, respectively.Comment: 6 pages, 3 figure

Co-ordinated Role of TLR3, RIG-I and MDA5 in the Innate Response to Rhinovirus in Bronchial Epithelium

The relative roles of the endosomal TLR3/7/8 versus the intracellular RNA helicases RIG-I and MDA5 in viral infection is much debated. We investigated the roles of each pattern recognition receptor in rhinovirus infection using primary bronchial epithelial cells. TLR3 was constitutively expressed; however, RIG-I and MDA5 were inducible by 8–12 h following rhinovirus infection. Bronchial epithelial tissue from normal volunteers challenged with rhinovirus in vivo exhibited low levels of RIG-I and MDA5 that were increased at day 4 post infection. Inhibition of TLR3, RIG-I and MDA5 by siRNA reduced innate cytokine mRNA, and increased rhinovirus replication. Inhibition of TLR3 and TRIF using siRNA reduced rhinovirus induced RNA helicases. Furthermore, IFNAR1 deficient mice exhibited RIG-I and MDA5 induction early during RV1B infection in an interferon independent manner. Hence anti-viral defense within bronchial epithelium requires co-ordinated recognition of rhinovirus infection, initially via TLR3/TRIF and later via inducible RNA helicases

Angular analysis of B0→K∗(892)0ℓ+ℓ−B^0 \to K^\ast(892)^0 \ell^+ \ell^-

We present a measurement of angular observables, $P_4'$, $P_5'$, $P_6'$, $P_8'$, in the decay $B^0 \to K^\ast(892)^0 \ell^+ \ell^-$, where $\ell^+\ell^-$ is either $e^+e^-$ or $\mu^+\mu^-$. The analysis is performed on a data sample corresponding to an integrated luminosity of $711~\mathrm{fb}^{-1}$ containing $772\times 10^{6}$ $B\bar B$ pairs, collected at the $\Upsilon(4S)$ resonance with the Belle detector at the asymmetric-energy $e^+e^-$ collider KEKB. Four angular observables, $P_{4,5,6,8}'$ are extracted in five bins of the invariant mass squared of the lepton system, $q^2$. We compare our results for $P_{4,5,6,8}'$ with Standard Model predictions including the $q^2$ region in which the LHCb collaboration reported the so-called $P_5'$ anomaly.Comment: Conference paper for LHC Ski 2016. SM prediction for $P_{6}'$ corrected and reference for arXiv:1207.2753 adde

Shared and Distinct Functions of the Transcription Factors IRF4 and IRF8 in Myeloid Cell Development

Interferon regulatory factor (IRF) 8 and IRF4 are structurally-related, hematopoietic cell-specific transcription factors that cooperatively regulate the differentiation of dendritic cells and B cells. Whilst in myeloid cells IRF8 is known to modulate growth and differentiation, the role of IRF4 is poorly understood. In this study, we show that IRF4 has activities similar to IRF8 in regulating myeloid cell development. The ectopic expression of IRF4 in myeloid progenitor cells in vitro inhibits cell growth, promotes macrophages, but hinders granulocytic cell differentiation. We also show that IRF4 binds to and activates transcription through the IRF-Ets composite sequence (IECS). Furthermore, we demonstrate that Irf8-/-Irf4-/- mice exhibit a more severe chronic myeloid leukemia (CML)-like disease than Irf8-/- mice, involving a disproportionate expansion of granulocytes at the expense of monocytes/macrophages. Irf4-/- mice, however, display no obvious abnormality in myeloid cell development, presumably because IRF4 is expressed at a much lower level than IRF8 in granulocyte-macrophage progenitors. Our results also suggest that IRF8 and IRF4 have not only common but also specific activities in myeloid cells. Since the expression of both the IRF8 and IRF4 genes is downregulated in CML patients, these results may add to our understanding of CML pathogenesis