Evidence for Isospin Violation and Measurement of C P Asymmetries in B → K ∗ ( 892 ) γ

We report the first evidence for isospin violation in B→K∗γ and the first measurement of the difference of CP asymmetries between B+→K*+γ and B0→K*0γ. This analysis is based on the data sample containing 772×106B¯B pairs that was collected with the Belle detector at the KEKB energy-asymmetric e+e− collider. We find evidence for the isospin violation with a significance of 3.1σ, Δ0+=[+6.2±1.5(stat)±0.6(syst)±1.2(f+−/f00)]%, where the third uncertainty is due to the uncertainty on the fraction of B+B− to B0¯B0 production in Υ(4S) decays. The measured value is consistent with predictions of the standard model. The result for the difference of CP asymmetries is ΔACP=[+2.4±2.8(stat)±0.5(syst)]%, consistent with zero. The measured branching fractions and CP asymmetries for charged and neutral B meson decays are the most precise to date. We also calculate the ratio of branching fractions of B0→K*0γ to B0s→ϕγ

Caffeic Acid Phenethyl Ester Causes p21Cip1 Induction, Akt Signaling Reduction, and Growth Inhibition in PC-3 Human Prostate Cancer Cells

Caffeic acid phenethyl ester (CAPE) treatment suppressed proliferation, colony formation, and cell cycle progression in PC-3 human prostate cancer cells. CAPE decreased protein expression of cyclin D1, cyclin E, SKP2, c-Myc, Akt1, Akt2, Akt3, total Akt, mTOR, Bcl-2, Rb, as well as phosphorylation of Rb, ERK1/2, Akt, mTOR, GSK3α, GSK3β, PDK1; but increased protein expression of KLF6 and p21Cip1. Microarray analysis indicated that pathways involved in cellular movement, cell death, proliferation, and cell cycle were affected by CAPE. Co-treatment of CAPE with chemotherapeutic drugs vinblastine, paclitaxol, and estramustine indicated synergistic suppression effect. CAPE administration may serve as a potential adjuvant therapy for prostate cancer