Use of SMS texts for facilitating access to online alcohol interventions: a feasibility study

A41 Use of SMS texts for facilitating access to online alcohol interventions: a feasibility study In: Addiction Science & Clinical Practice 2017, 12(Suppl 1): A4

Study of the lineshape of the chi(c1) (3872) state

A study of the lineshape of the chi(c1) (3872) state is made using a data sample corresponding to an integrated luminosity of 3 fb(-1) collected in pp collisions at center-of-mass energies of 7 and 8 TeV with the LHCb detector. Candidate chi(c1)(3872) and psi(2S) mesons from b-hadron decays are selected in the J/psi pi(+)pi(-) decay mode. Describing the lineshape with a Breit-Wigner function, the mass splitting between the chi(c1 )(3872) and psi(2S) states, Delta m, and the width of the chi(c1 )(3872) state, Gamma(Bw), are determined to be (Delta m=185.598 +/- 0.067 +/- 0.068 Mev,)(Gamma BW=1.39 +/- 0.24 +/- 0.10 Mev,) where the first uncertainty is statistical and the second systematic. Using a Flatte-inspired model, the mode and full width at half maximum of the lineshape are determined to be (mode=3871.69+0.00+0.05 MeV.)(FWHM=0.22-0.04+0.13+0.07+0.11-0.06-0.13 MeV, ) An investigation of the analytic structure of the Flatte amplitude reveals a pole structure, which is compatible with a quasibound D-0(D) over bar*(0) state but a quasivirtual state is still allowed at the level of 2 standard deviations

Measurement of the CKM angle γγ in B±→DK±B^\pm\to D K^\pm and B±→Dπ±B^\pm \to D π^\pm decays with D→KS0h+h−D \to K_\mathrm S^0 h^+ h^-

A measurement of $CP$-violating observables is performed using the decays $B^\pm\to D K^\pm$ and $B^\pm\to D \pi^\pm$, where the $D$ meson is reconstructed in one of the self-conjugate three-body final states $K_{\mathrm S}\pi^+\pi^-$ and $K_{\mathrm S}K^+K^-$ (commonly denoted $K_{\mathrm S} h^+h^-$). The decays are analysed in bins of the $D$-decay phase space, leading to a measurement that is independent of the modelling of the $D$-decay amplitude. The observables are interpreted in terms of the CKM angle $\gamma$. Using a data sample corresponding to an integrated luminosity of $9\,\text{fb}^{-1}$ collected in proton-proton collisions at centre-of-mass energies of $7$, $8$, and $13\,\text{TeV}$ with the LHCb experiment, $\gamma$ is measured to be $\left(68.7^{+5.2}_{-5.1}\right)^\circ$. The hadronic parameters $r_B^{DK}$, $r_B^{D\pi}$, $\delta_B^{DK}$, and $\delta_B^{D\pi}$, which are the ratios and strong-phase differences of the suppressed and favoured $B^\pm$ decays, are also reported

Loss of functional OPA1 unbalances redox state: implications in dominant optic atrophy pathogenesis

OBJECTIVE: OPA1 mutations cause protein haploinsufficiency leading to dominant optic atrophy (DOA), an incurable retinopathy with variable severity. Up to 20% of patients also develop extraocular neurological complications. The mechanisms that cause this optic atrophy or its syndromic forms are still unknown. After identifying oxidative stress in a mouse model of the pathology, we sought to determine the consequences of OPA1 dysfunction on redox homeostasis. METHODS: Mitochondrial respiration, reactive oxygen species levels, antioxidant defenses, and cell death were characterized by biochemical and in situ approaches in both in vitro and in vivo models of OPA1 haploinsufficiency. RESULTS: A decrease in aconitase activity suggesting an increase in reactive oxygene species and an induction of antioxidant defenses was observed in cortices of a murine model as well as in OPA1 downregulated cortical neurons. This increase is associated with a decline in mitochondrial respiration in vitro. Upon exogenous oxidative stress, OPA1-depleted neurons did not further exhibit upregulated antioxidant defenses but were more sensitive to cell death. Finally, low levels of antioxidant enzymes were found in fibroblasts from patients supporting their role as modifier factors. INTERPRETATION: Our study suggests that the pro-oxidative state induced by OPA1 loss may contribute to DOA pathogenesis and that differences in antioxidant defenses can explain the variability in expressivity. Furthermore, antioxidants may be used as therapy as they could prevent or delay DOA symptoms in patients

Rediscovery of B0→J/ψKL0B^0 \rightarrow J/\psi K^0_L at Belle II

We present preliminary results on the reconstruction of the $B^0\to J\mskip 1mu / \psi\mskip 2mu K^0_{\scriptscriptstyle L}$ decay, where $J\mskip 1mu / \psi\mskip 2mu\to\mu^+\mu^-$ or $e^+e^-$. Using a dataset corresponding to a luminosity of 62.8\pm0.6\mbox{fb}^{-1} collected by the Belle II experiment at the SuperKEKB asymmetric energy $e^+e^-$ collider, we measure a total of $267\pm21$ candidates with $J\mskip 1mu / \psi\mskip 2mu\to\mu^+\mu^-$ and $226\pm20$ with with $J\mskip 1mu / \psi\mskip 2mu\to e^+e^-$. The quoted errors are statistical only

Measurement of the branching fraction for B0→π0π0B^{0} \rightarrow \pi^{0} \pi^{0} decays reconstructed in 2019-2020 Belle II data

International audienceWe report the first reconstruction of the $B^{0} \to \pi^{0} \pi^{0}$ decay mode at Belle II using samples of 2019 and 2020 data that correspond to 62.8 fb$^{-1}$ of integrated luminosity. We find $14.0^{+6.8}_{-5.6}$ signal decays, corresponding to a significance of 3.4 standard deviations and determine a branching ratio of $\mathcal{B}(B^{0} \rightarrow \pi^{0} \pi^{0}) = [0.98^{+0.48}_{-0.39} \pm 0.27] \times 10^{-6}$. The results agree with previous determinations and contribute important information to an early assessment of detector performance and Belle II's potential for future determinations of $\alpha/\phi_2$ using $B \rightarrow \pi \pi$ modes