Analysis of Neutral Higgs-Boson Contributions to the Decays B_s -> l^+l^- and B -> K l^+l^-

We report on a calculation of Higgs-boson contributions to the decays B_s -> l^+l^- and B -> K l^+l^- (l=e, mu) which are governed by the effective Hamiltonian describing b -> s l^+ l^-. Compact formulae for the Wilson coefficients are provided in the context of the type-II two-Higgs-doublet model (2HDM) and supersymmetry (SUSY) with minimal flavour violation, focusing on the case of large tan(beta). We derive, in a model-independent way, constraints on Higgs-boson-mediated interactions, using present experimental results on rare B decays including b -> s gamma, B_s -> mu^+ mu^-, and B -> K^(*) mu^+ mu^-. In particular, we assess the impact of possible scalar and pseudoscalar interactions transcending the standard model (SM) on the branching ratio of B_s -> mu^+ mu^- and the forward-backward (FB) asymmetry of mu^- in B -> K mu^+ mu^- decay. We find that the average FB asymmetry, which is unobservably small within the SM, and therefore a potentially valuable tool to search for new physics, is predicted to be no greater than 4% for a nominal branching ratio of about 6x10^{-7}. Moreover, striking effects on the decay spectrum of B -> K mu^+ mu^- are already ruled out by experimental data on the B_s -> mu^+ mu^- branching fraction. In addition, we study the constraints on the parameter space of the 2HDM and SUSY with minimal flavour violation. While the type-II 2HDM does not give any sizable contributions to the above decay modes, we find that SUSY contributions obeying the constraint on b -> s gamma can affect significantly the branching ratio of B_s -> mu^+ mu^-. We also comment on previous calculations contained in the literature.Comment: 29 pages, REVTeX, 8 figures. Minor corrections in Eqs. (5.4), (5.11) and (6.3) of the published versio

β-Catenin Signaling Increases during Melanoma Progression and Promotes Tumor Cell Survival and Chemoresistance

Beta-catenin plays an important role in embryogenesis and carcinogenesis by controlling either cadherin-mediated cell adhesion or transcriptional activation of target gene expression. In many types of cancers nuclear translocation of beta-catenin has been observed. Our data indicate that during melanoma progression an increased dependency on the transcriptional function of beta-catenin takes place. Blockade of beta-catenin in metastatic melanoma cell lines efficiently induces apoptosis, inhibits proliferation, migration and invasion in monolayer and 3-dimensional skin reconstructs and decreases chemoresistance. In addition, subcutaneous melanoma growth in SCID mice was almost completely inhibited by an inducible beta-catenin knockdown. In contrast, the survival of benign melanocytes and primary melanoma cell lines was less affected by beta-catenin depletion. However, enhanced expression of beta-catenin in primary melanoma cell lines increased invasive capacity in vitro and tumor growth in the SCID mouse model. These data suggest that beta-catenin is an essential survival factor for metastatic melanoma cells, whereas it is dispensable for the survival of benign melanocytes and primary, non-invasive melanoma cells. Furthermore, beta-catenin increases tumorigenicity of primary melanoma cell lines. The differential requirements for beta-catenin signaling in aggressive melanoma versus benign melanocytic cells make beta-catenin a possible new target in melanoma therapy

The Physics of the B Factories

This work is on the Physics of the B Factories. Part A of this book contains a brief description of the SLAC and KEK B Factories as well as their detectors, BaBar and Belle, and data taking related issues. Part B discusses tools and methods used by the experiments in order to obtain results. The results themselves can be found in Part C

LILE2019: 8th International Workshop on Learning and Education with Web Data

Contains fulltext : 207819.pdf (Publisher’s version ) (Open Access)WebSci '19 Companion Publication of the 10th ACM Conference on Web Science, Boston, Massachusetts, USA — June 30 - July 03, 201