Examination of the Resonance Contributions to Dileptonic Rare B-Decays

We analyse the long-distance contribution to $B\to X_s\ell^+\ell^-$ differential decay rate when the momentum dependence of $\psi$ and $\psi'$-$\gamma$ conversion strength is taken into account. The results indicate that the resonance to nonresonance interference in the dilepton invariant mass distribution is substantially reduced.Comment: 10 pages, Latex, one figure (included

Causality in real-time dynamic substructure testing

Causality, in the bond graph sense, is shown to provide a conceptual framework for the design of real-time dynamic substructure testing experiments. In particular, known stability problems with split-inertia substructured systems are reinterpreted as causality issues within the new conceptual framework. As an example, causality analysis is used to provide a practical solution to a split-inertia substructuring problem and the solution is experimentally verified

Mitochondria-derived reactive oxygen species drive GANT61-induced mesothelioma cell apoptosis

Gli transcription factors of the Hedgehog (Hh) pathway have been reported to be drivers of malignant mesothelioma (MMe) cell survival. The Gli inhibitor GANT61 induces apoptosis in various cancer cell models, and has been associated directly with Gli inhibition. However various chemotherapeutics can induce cell death through generation of reactive oxygen species (ROS) but whether ROS mediates GANT61-induced apoptosis is unknown. In this study human MMe cells were treated with GANT61 and the mechanisms regulating cell death investigated. Exposure of MMe cells to GANT61 led to G1 phase arrest and apoptosis, which involved ROS but not its purported targets, GLI1 or GLI2. GANT61 triggered ROS generation and quenching of ROS protected MMe cells from GANT61-induced apoptosis. Furthermore, we demonstrated that mitochondria are important in mediating GANT61 effects: (1) ROS production and apoptosis were blocked by mitochondrial inhibitor rotenone; (2) GANT61 promoted superoxide formation in mitochondria; and (3) mitochondrial DNA-deficient LO68 cells failed to induce superoxide, and were more resistant to apoptosis induced by GANT61 than wild-type cells. Our data demonstrate for the first time that GANT61 induces apoptosis by promoting mitochondrial superoxide generation independent of Gli inhibition, and highlights the therapeutic potential of mitochondrial ROS-mediated anticancer drugs in MMe

Electron transport in gated InGaAs and InAsP quantum well wires in selectively-grown InP ridge structures

The purpose of this work is to fabricate ribbon-like InGaAs and InAsP wires embedded in InP ridge structures and investigate their transport properties. The InP ridge structures that contain the wires are selectively grown by chemical beam epitaxy (CBE) on pre-patterned InP substrates. To optimize the growth and micro-fabrication processes for electronic transport, we explore the Ohmic contact resistance, the electron density, and the mobility as a function of the wire width using standard transport and Shubnikov-de Haas measurements. At low temperatures the ridge structures reveal reproducible mesoscopic conductance fluctuations. We also fabricate ridge structures with submicron gate electrodes that exhibit non-leaky gating and good pinch-off characteristics acceptable for device operation. Using such wrap gate electrodes, we demonstrate that the wires can be split to form quantum dots evidenced by Coulomb blockade oscillations in transport measurements.Comment: 5 pages, 4 figures, additional references and improved Fig. 4c, MSS-14 conference, submitted to Physica

Mutational Analysis of Hedgehog Signaling Pathway Genes in Human Malignant Mesothelioma

Background The Hedgehog (HH) signaling pathway is critical for embryonic development and adult homeostasis. Recent studies have identified regulatory roles for this pathway in certain cancers with mutations in the HH pathway genes. The extent to which mutations of the HH pathway genes are involved in the pathogenesis of malignant mesothelioma (MMe) is unknown. Methodology/Principal Findings Real-time PCR analysis of HH pathway genes PTCH1, GLI1 and GLI2 were performed on 7 human MMe cell lines. Exon sequencing of 13 HH pathway genes was also performed in cell lines and human MMe tumors. In silico programs were used to predict the likelihood that an amino-acid substitution would have a functional effect. GLI1, GLI2 and PTCH1 were highly expressed in MMe cells, indicative of active HH signaling. PTCH1, SMO and SUFU mutations were found in 2 of 11 MMe cell lines examined. A non-synonymous missense SUFU mutation (p.T411M) was identified in LO68 cells. In silico characterization of the SUFU mutant suggested that the p.T411M mutation might alter protein function. However, we were unable to demonstrate any functional effect of this mutation on Gli activity. Deletion of exons of the PTCH1 gene was found in JU77 cells, resulting in loss of one of two extracellular loops implicated in HH ligand binding and the intracellular C-terminal domain. A 3-bp insertion (69_70insCTG) in SMO, predicting an additional leucine residue in the signal peptide segment of SMO protein was also identified in LO68 cells and a MMe tumour. Conclusions/Significance We identified the first novel mutations in PTCH1, SUFU and SMO associated with MMe. Although HH pathway mutations are relatively rare in MMe, these data suggest a possible role for dysfunctional HH pathway in the pathogenesis of a subgroup of MMe and help rationalize the exploration of HH pathway inhibitors for MMe therapy

Observing b→s μ+μ−b \rightarrow s \, \mu^+ \mu^- Decays at Hadron Colliders

We examine the prospects for observing weak flavour-changing neutral current (FCNC) decays of \B\ mesons at hadron colliders, including effects of anomalous $WWZ$~vertices. Since it is very difficult to measure the inclusive rate B \rightarrow X_s \, \lp \lm one should consider exclusive modes such as \BKsmumu\ and \BKmumu. Even though this requires one to compute hadronic matrix elements, we show that experimentally observable quantities (ratios of decay rates) are not strongly parametrisation dependent. Some possibilities for reducing the theoretical uncertainties from other experimental data are discussed.Comment: 17 pages, uses LaTeX, epsf and uufiles. UCLA/93/TEP/2

Lepton Polarization and Forward-Backward Asymmetries in b -> s tau+ tau-

We study the spin polarizations of both tau leptons in the decay b -> s tau+ tau-. In addition to the polarization asymmetries involving a single tau, we construct asymmetries for the case where both polarizations are simultaneously measured. We also study forward-backward asymmetries with polarized tau's. We find that a large number of asymmetries are predicted to be large, >~ 10%. This permits the measurement of all Wilson coefficients and the b-quark mass, thus allowing the standard model (SM) to be exhaustively tested. Furthermore, there are many unique signals for the presence of new physics. For example, asymmetries involving triple-product correlations are predicted to be tiny within the SM, O(10^{-2}). Their observation would be a clear signal of new physics.Comment: 21 pages, LaTeX, 4 figures (included). Paper somewhat reorganized, references greatly expanded, conclusions unchange

Possible Supersymmetric Effects on Angular Distributions in B→K∗(→Kπ)ℓ+ℓ−B \to K^* (\to K \pi) \ell^+ \ell^- Decays

We investigate the angular distributions of the rare B decay, $B \to K^* (\to K \pi) \ell^+ \ell^-$, in general supersymmetric extensions of the standard model. We consider the new physics contributions from the operators $O_{7,8,9,10}$ in small invariant mass region of lepton pair. We show that the azimuthal angle distribution of the decay can tell us the new physics effects clearly from the behavior of the distribution, even if new physics does not change the decay rate substantially from the standard model prediction

A Systematic Analysis of the Lepton Polarization Asymmetries in the Rare B Decay, B -> X_s\tau^+\tau^-

The most general model-independent analysis of the lepton polarization asymmetries in the rare B decay, \Bstt, is presented. We present the longitudinal, normal and transverse polarization asymmetries for the $\tau^+$ and $\tau^-$, and combinations of them, as functions of the Wilson coefficients of twelve independent four-Fermi interactions, ten of them local and two nonlocal. These procedures will tell us which type of operators contributes to the process. And it will be very useful to pin down new physics systematically, once we have the experimental data with high statistics and a deviation from the Standard Model is found.Comment: 24 pages, 8 figures, LaTe