We report observations of the Cabibbo suppressed decays B-->D((*))K- using a 10.4 fb(-1) data sample accumulated at the Upsilon(4S) resonance with the Belle detector at the KEKB e(+)e(-) storage ring. We find that the ratios of Cabibbo suppressed to Cabibbo favored branching fractions are B(B--->D0K-)/B(B--->D0pi(-)) = 0.079+/-0.009+/-0.006, B(B(0)-->D+K-)/B(B(0)-->D+pi(-)) = 0.068+/-0.015+/-0.007, B(B--->D(*0)K-)/B(B--->D(*0)pi(-)) = 0.078+/-0.019+/-0.009, and B(B(0)-->D(*+)K-)/B(B(0)-->D(*+)pi(-)) = 0.074+/-0.015+/-0.006. These are the first observations of the B-->D+K-, D(*0)K-, and D(*+)K- decay processes.

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We present a measurement of the standard model CP violation parameter sin2 phi(1) based on a 29.1 fb(-1) data sample collected at the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric-energy e(+)e(-) collider. One neutral B meson is fully reconstructed as a J/psi K(S), psi(2S)K(S), chi(c1)K(S), eta(c)K(S), J/psi K(L), or J/psi K(*0) decay and the flavor of the accompanying B meson is identified from its decay products. From the asymmetry in the distribution of the time intervals between the two B meson decay points, we determine sin2 phi(1) = 0.99+/-0.14(stat)+/-0.06(syst). We conclude that we have observed CP violation in the neutral B meson system.

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A new proinflammatory cytokine interleukin-32 (IL-32) has six isoforms. Although IL-32 can be detected in sera from patients suffering from Crohn's disease and rheumatoid arthritis, it is unclear which isoforms are involved. To this end, we investigated the functions of the most abundant IL-32b by generating K562-IL-32b stable cell lines. This report confirms, using IL-32 small interfering RNA, that IL-32b induces an anti-inflammatory cytokine IL-10 in K562-IL-32b cells and U937 promonocytic cells, which express endogenous IL-32b upon phorbol 12-myristate 13-acetate (PMA) treatment, and monocyte-derived dendritic cells (DC) upon lipopolysaccharide (LPS) treatment. Interleukin-32b was induced in monocyte-derived macrophages by LPS and in monocyte-derived DC by LPS, poly(I:C), or anti-CD40 antibody, but was not induced by PMA. We showed that IL-32b expression was increased in a time-dependent manner in monocyte-derived DC upon LPS treatment and peaked at 24 hr. Production of IL-10 was exactly coincident with IL-32b expression, but IL-1b and tumour necrosis factor-a production peaked at 6 hr after LPS treatment, then steeply declined. Interleukin-12 p40 was induced at 9 hr and gradually increased until 48 hr, at which time IL-32b and IL-10 were no longer increased. Knock-down of IL-32b by IL-32 small interfering RNA led to the decrease of IL-10, but the increase of IL-12 in monocytederived DC, which means that IL-32b promotes IL-10 production, but limits IL-12 production. We also showed that IL-10 neutralization increases IL-12, IL-1b and tumour necrosis factor-a production, which implies that IL-10 suppresses such proinflammatory cytokines. Taken together, our results suggest that IL-32b upregulates the production of an anti-inflammatory cytokine IL-10, and then IL-10 suppresses proinflammatory cytokines.Keywords: cytokine; dendritic cell; inflammation; interleukin-10; interleukin-32Please cite this article in press as: Kang J.-W. et al. A proinflammatory cytokine interleukin-32b promotes the production of an anti-inflammatory cytokine interleukin-10, Immunology (2009)

We report the observation of prompt J/psi via double cc; production from the e+e- continuum. In this process one cc; pair fragments into a J/psi meson while the remaining pair either produces a charmonium state or fragments into open charm. Both cases have been experimentally observed. We find cross sections of sigma[e+e- -->J/psieta(c)(gamma)]xB(eta(c)-->>or=4 charged)=(0.033(+0.007)(-0.006)+/-0.009) pb and sigma(e+e- -->J/psiD(*+)X)=(0.53(+0.19)(-0.15)+/-0.14) pb and infer sigma(e+e- -->J/psicc;)/sigma(e+e- -->J/psiX)=0.59(+0.15)(-0.13)+/-0.12. These results are obtained from a 46.2 fb(-1) data sample collected near the Upsilon(4S) resonance, with the Belle detector at the KEKB collider.

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