We study the B s → π + π − and B d → K + K − decays in the standard model and the family-non-universal Z model. Since none of the quarks in the final states is the same as the initial quark, these decay modes can occur only via power-suppressed annihilation diagrams. Despite the consistency of the standard model prediction with the available data, room remains for a light Z boson. Taking into account the Z contribution, we find that theoretical results for the branching fractions can better accommodate the data. With the relevant data, we also derive a constraint on the parameter space for the Z . Moreover, for B d → K + K − , both the direct and the mixing-induced CP asymmetry are sensitive to the couplings between Z and fermions in the parameter spaces constrained by the data. The measurements at future experimental facilities, including the LHCb, Belle-II, and the proposed high energy e + e − collider, will provide us useful hints for direct searching for the light Z boson.

Glaucoma is a leading cause of irreversible blindness. Injury of retinal ganglion cells (RGCs) accounts for visual impairment of glaucoma. Here, we report rapamycin protects RGCs from death in experimental glaucoma model and the underlying mechanisms. Our results showed that treatment with rapamycin dramatically promote RGCs survival in a rat chronic ocular hypertension model. This protective action appears to be attributable to inhibition of neurotoxic mediators release and/or direct suppression of RGC apoptosis. In support of this mechanism, in vitro, rapamycin significantly inhibits the production of NO, TNF-α in BV2 microglials by modulating NF-κB signaling. In experimental animals, treatment with rapamycin also dramatically inhibited the activation of microglials. In primary RGCs, rapamycin was capable of direct suppression the apoptosis of primary RGCs induced by glutamate. Mechanistically, rapamycin-mediated suppression of RGCs apoptosis is by sparing phosphorylation of Akt at a site critical for maintenance of its survival-promoting activity in cell and animal model. These results demonstrate that rapamycin is neuroprotective in experimental glaucoma, possibly via decreasing neurotoxic releasing and suppressing directly apoptosis of RGCs.

A systematic analysis shows that the main uncertainties in the form factors are due to the twist-3 wave functions of the light mesons in the light-cone QCD sum rules. We propose an improved approach, in which the twist-3 wave functions do not make any contribution and therefore the possible pollution by them can be avoided, to reexamine B→ semileptonic form factors. Also, a comparison between previous results and our results from the light-cone QCD sum rules is made. Our method will be beneficial to the precise extraction of ͉V ub ͉ from the experimental data on the processes B→l l .

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