Full-Folding Optical Potentials for Elastic Nucleon-Nucleus Scattering based on Realistic Densities

Optical model potentials for elastic nucleon nucleus scattering are calculated for a number of target nuclides from a full-folding integral of two different realistic target density matrices together with full off-shell nucleon-nucleon t-matrices derived from two different Bonn meson exchange models. Elastic proton and neutron scattering observables calculated from these full-folding optical potentials are compared to those obtained from `optimum factorized' approximations in the energy regime between 65 and 400 MeV projectile energy. The optimum factorized form is found to provide a good approximation to elastic scattering observables obtained from the full-folding optical potentials, although the potentials differ somewhat in the structure of their nonlocality.Comment: 21 pages, LaTeX, 17 postscript figure

Improved Measurements of Partial Rate Asymmetry in B -> h h Decays

We report improved measurements of the partial rate asymmetry (Acp) in B -> h h decays with 140fb^-1 of data collected with the Belle detector at the KEKB e+e- collider. Here h stands for a charged or neutral pion or kaon and in total five decay modes are included: K-+ pi+-, K0s pi-+, K-+ pi0, pi-+ pi0 and K0s pi0. The flavor of the last decay mode is determined from the accompanying B meson. Using a data sample 4.7 times larger than that of our previous measurement, we find Acp(K-+ pi+-) -0.088+-0.035+-0.013, 2.4 sigma from zero. Results for other decay modes are also presented.Comment: 9 pages, 1 figur

Study of the decays B->D_s1(2536)+ anti-D(*)

We report a study of the decays B -> D_s1(2536)+ anti-D(*), where anti-D(*) is anti-D0, D- or D*-, using a sample of 657 x 10^6 B anti-B pairs collected at the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric-energy e+e- collider. The branching fractions of the decays B+ -> D_s1(2536)+ anti-D0, B0 -> D_s1(2536)+ D- and B0 -> D_s1(2536)+ D*- multiplied by that of D_s1(2536)+ -> (D*0K+ + D*+K0) are found to be (3.97+-0.85+-0.56) x 10^-4, (2.75+-0.62+-0.36) x 10^-4 and (5.01+-1.21+-0.70) x 10^-4, respectively.Comment: 6 pages, 2 figues, submitted to PRD (RC

Evidence for B- -> tau- nu_bar with a Semileptonic Tagging Method

We present a measurement of the decay B- -> tau- nu_bar using a data sample containing 657 million BB_bar pairs collected at the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric-energy e+e- collider. A sample of BB_bar pairs are tagged by reconstructing one B meson decaying semileptonically. We detect the B- -> tau- nu_bar candidate in the recoil. We obtain a signal with a significance of 3.6 standard deviations including systematic uncertainties, and measure the branching fraction to be Br(B- -> tau- nu_bar) = [1.54+0.38-0.37(stat)+0.29-0.31(syst)]*10^-4. This result confirms the evidence for B- -> tau- nu_bar obtained in a previous Belle measurement that used a hadronic B tagging method.Comment: 7 pages, 3 figures, corrected references, to appear in PRD-R

Search for CP violation in the decay B0->D*+-D-+

We report a search for CP-violating asymmetry in B0 -> D*+- D-+ decays. The analysis employs two methods of B0 reconstruction: full and partial. In the full reconstruction method all daughter particles of the B0 are required to be detected; the partial reconstruction technique requires a fully reconstructed D- and only a slow pion from the D*+ -> D0 pi_slow+ decay. From a fit to the distribution of the time interval corresponding to the distance between two B meson decay points we calculate the CP-violating parameters and find the significance of nonzero CP asymmetry to be 2.7 standard deviations.Comment: 4 pages, 3 figure

Belle II Technical Design Report

The Belle detector at the KEKB electron-positron collider has collected almost 1 billion Y(4S) events in its decade of operation. Super-KEKB, an upgrade of KEKB is under construction, to increase the luminosity by two orders of magnitude during a three-year shutdown, with an ultimate goal of 8E35 /cm^2 /s luminosity. To exploit the increased luminosity, an upgrade of the Belle detector has been proposed. A new international collaboration Belle-II, is being formed. The Technical Design Report presents physics motivation, basic methods of the accelerator upgrade, as well as key improvements of the detector.Comment: Edited by: Z. Dole\v{z}al and S. Un

In Vitro and In Vivo Anti-Inflammatory Activity of 17-O-Acetylacuminolide through the Inhibition of Cytokines, NF-κB Translocation and IKKβ Activity

BACKGROUND AND PURPOSE: 17-O-acetylacuminolide (AA), a diterpenoid labdane, was isolated for the first time from the plant species Neouvaria foetida. The anti-inflammatory effects of this compound were studied both in vitro and in vivo. EXPERIMENTAL APPROACH: Plant extracts were initially tested against LPS-stimulated release of tumor necrosis factor alpha (TNF-α) from murine macrophages (RAW264.7 cells). Based on bioassay-guided fractionation, the active compound was identified as AA. AA was tested for its ability to reduce nitric oxide (NO) production, and the inducible nitric oxide synthase (iNOS) expression. The inhibition of a panel of inflammatory cytokines (TNF, IL-1β, IL-6, KC, and GM-CSF) by AA was assessed at the expression and the mRNA levels. Moreover, the effect of AA on the translocation of the transcription factor nuclear factor kappa B (NF-κB) was evaluated in LPS-stimulated RAW264.7 cells and in TNF-stimulated L929 cells. Subsequently, AA was tested in the inhibitor of NF-κB kinase beta (IKKβ) activity assay. Lastly, the anti-inflammatory activity of AA in vivo was evaluated by testing TNF production in LPS-stimulated Balb/c mice. KEY RESULTS: AA effectively inhibited TNF-α release with an IC(50) of 2.7 µg/mL. Moreover, AA significantly inhibited both NO production and iNOS expression. It significantly and dose-dependently inhibited TNF and IL-1β proteins and mRNA expression; as well as IL-6 and KC proteins. Additionally, AA prevented the translocation of NF-κB in both cell lines; suggesting that it is acting at a post receptor level. This was confirmed by AA's ability to inhibit IKKβ activity, a kinase responsible for activating NF-κB, hence providing an insight on AA's mechanism of action. Finally, AA significantly reduced TNF production in vivo. CONCLUSIONS AND IMPLICATIONS: This study presents the potential utilization of this compound, as a lead for the development of an anti-inflammatory drug