Measurement of CP asymmetry in Cabibbo suppressed D0 decays

We measure the CP-violating asymmetries in decays to the D0 -> K+K- and D0 -> pi+pi- CP eigenstates using 540 fb^{-1} of data collected with the Belle detector at or near the Upsilon(4S) resonance. Cabibbo-favored D0 -> K-pi+ decays are used to correct for systematic detector effects. The results, A_{CP}^{KK} = (-0.43 +- 0.30 +- 0.11)% and A_{CP}^{pipi} = (+0.43 +- 0.52 +- 0.12)%, are consistent with no CP violation.Comment: Submitted to Phys. Lett.

Measurement of the Decay B_s^0 -> D_s^- pi^+ and Evidence for B_s^0 -> D_s^{+/-} K^{-/+} in e+e- Annihilation at sqrt(s)~10.87 GeV

We have studied Bs0 -> Ds- pi+ and Bs0 -> Ds^(-/+) K^(+/-) decays using 23.6 /fb of data collected at the Upsilon(5S) resonance with the Belle detector at the KEKB e+e- collider. This highly pure Bs0 -> Ds- pi+ sample is used to measure the branching fraction, BR(Bs0 -> Ds- pi+)=[3.67 +0.35,-0.33}(stat.) +0.43,-0.42(syst.) +-0.49(f_s)] x 10^{-3} (f_s=N(Bs(*) Bs(*)bar)/N(b\bar b)) and the fractions of Bs0 event types at the Upsilon(5S) energy, {in particular N(Bs* Bs*bar}/N(N(Bs(*) Bs(*)bar)=(90.1 +3.8,-4.0 +-0.2)%. We also determine the masses M(Bs0)=(5364.4 +-1.3 +-0.7) MeV/c^2 and M(Bs*)=(5416.4 +-0.4 +-0.5) MeV/c^2. In addition, we observe Bs0 -> Ds^(-/+) K^(+/-) decays with a significance of 3.5\sigma and measure BR(Bs0 -> Ds^(-/+) K^(+/-))=[2.4 +1.2,-1.0(stat.) +-0.3(syst.) +-0.3(f_s)] x 10^{-4}.Comment: 5 pages, 4 figures, accepted by PR

Search for B0→J/ψϕB^0 \to J/\psi \phi

We report a search for the decay $B^0 \to J/\psi \phi$, using a sample of 657 $\times 10^6$ $B\bar{B}$ pairs collected with the Belle detector at the $\Upsilon(4S)$ resonance. No statistically significant signal is found and an upper limit for the branching fraction is determined to be $\mathcal{B}(B^0 \to J/\psi \phi) < 9.4 \times 10^{-7}$ at 90% confidence level.Comment: 5 pages, 2 figures, 3 tables, submitted to PRD(RC

Evidence for Neutral B Meson Decays to wK*0

We present the results of a study of the charmless vector-vector decay B0->wK*0 with 657x10^6 BB(bar) pairs collected with the Belle detector at the KEKB e+e- collider. We measure the branching fraction to be B(B0->wK*0)=[1.8+/-0.7(stat)+/-0.3(syst)]x10^-6 with 3.0sigma significance. We also perform a helicity analysis of the w and K*0 vector mesons, and obtain the longitudinal polarization fraction fL(B0->wK*0)=0.56+/-0.29(stat)+0.18-0.08(syst). Finally, we measure a large non-resonant branching fraction B[B->wK+pi-; M(Kpi)\in(0.755,1.250) GeV/c^2]=[5.1+/-0.7(stat)+/-0.7(syst)]x10^-6 with a significance of 9.5sigma.Comment: 6 pages, 3 figures (7 figure files

Evidence-based efficacy of Kampo formulas in a model of non alcoholic fatty liver

Data on the efficacy of herbal compounds are often burdened by the lack of appropriate controls or a limited statistical power. Treatments to prevent the progression of non alcoholic fatty liver disease (NAFLD) to steatohepatitis (NASH) remain unsatisfactory. A total of 56 rabbits were arrayed into 7 groups fed with standard rabbit chow (SRC), SRC with 1% cholesterol, or each of the five experimental treatments (Kampo formulas 1% keishibukuryogan [KBG], 1% orengedokuto [OGT], and 1% shosaikoto [SST]; vitamin E [VE]; or pioglitazone [PG]) in a 1% cholesterol SRC. We analyzed changes after 12 weeks in plasma and liver lipid profiles, glucose metabolism, adipocytokines, oxidative stress, and liver fibrosis. Data demonstrated that all five treatments were associated with significant amelioration of lipid profiles, oxidative stress, and liver fibrosis compared to no supplementation. KBG was superior to VE and PG in the reduction of liver total cholesterol (P < 0.01) and lipid peroxidase levels (P < 0.05), urinary 8-hydroxy-2'-deoxyguanosine (P < 0.05), hepatic alpha-smooth muscle actin positive areas (P < 0.01) and activated stellate cells (P < 0.01). In conclusion, there was a statistically significant benefit of Kampo formulas (KBG in particular) on a dietary model of NAFLD/NASH. Future studies need to be directed at the mechanisms in the treatment of NAS