Branching Ratio and CP Asymmetry of Bs→π0η(′)B_s \to \pi^0 \eta^{(\prime)} Decays in the perturbative QCD Approach

We calculate the branching ratios and CP-violating asymmetries for $B_s^0 \to \pi^0 \eta^{(\prime)}$ decays in the perturbative QCD (pQCD) factorization approach here. We not only calculate the usual factorizable contributions, but also evaluate the non-factorizable and annihilation type contributions. The pQCD predictions for the CP-averaged branching ratios are $BR(B_s^0 \to \pi^0 \eta) \approx 0.86 \times 10^{-7}$ and $BR(B_s^0 \to \pi^0 \eta') \approx 1.86 \times 10^{-7}$. The pQCD predictions for the CP-violating asymmetries are $A_{CP}^{dir}(\pi^0 \eta)\sim -4.5$, $A_{CP}^{dir}(\pi^0 \eta')\sim -9.1$, $A_{CP}^{mix}(\pi^0 \eta)\sim -0.2$, and $A_{CP}^{mix}(\pi^0 \eta')\sim 27.0$ but with large errors. The above pQCD predictions can be tested in the near future LHC-b experiments at CERN and the BTeV experiments at Fermilab.Comment: 15 pages 3 eps figure

Robust filtering with stochastic nonlinearities and multiple missing measurements

This is the post print version of the article. The official published version can be obtained from the link - Copyright 2009 Elsevier LtdThis paper is concerned with the filtering problem for a class of discrete-time uncertain stochastic nonlinear time-delay systems with both the probabilistic missing measurements and external stochastic disturbances. The measurement missing phenomenon is assumed to occur in a random way, and the missing probability for each sensor is governed by an individual random variable satisfying a certain probabilistic distribution over the interval . Such a probabilistic distribution could be any commonly used discrete distribution over the interval . The multiplicative stochastic disturbances are in the form of a scalar Gaussian white noise with unit variance. The purpose of the addressed filtering problem is to design a filter such that, for the admissible random measurement missing, stochastic disturbances, norm-bounded uncertainties as well as stochastic nonlinearities, the error dynamics of the filtering process is exponentially mean-square stable. By using the linear matrix inequality (LMI) method, sufficient conditions are established that ensure the exponential mean-square stability of the filtering error, and then the filter parameters are characterized by the solution to a set of LMIs. Illustrative examples are exploited to show the effectiveness of the proposed design procedures.This work was supported in part by the Shanghai Natural Science Foundation under Grant 07ZR14002, the Engineering and Physical Sciences Research Council (EPSRC) of the UK under Grant GR/S27658/01, an International Joint Project sponsored by the Royal Society of the UK, the Nuffield Foundation of the UK under Grant NAL/00630/G and the Alexander von Humboldt Foundation of Germany

Robust-MSA: Understanding the Impact of Modality Noise on Multimodal Sentiment Analysis

Improving model robustness against potential modality noise, as an essential step for adapting multimodal models to real-world applications, has received increasing attention among researchers. For Multimodal Sentiment Analysis (MSA), there is also a debate on whether multimodal models are more effective against noisy features than unimodal ones. Stressing on intuitive illustration and in-depth analysis of these concerns, we present Robust-MSA, an interactive platform that visualizes the impact of modality noise as well as simple defence methods to help researchers know better about how their models perform with imperfect real-world data.Comment: Accept by AAAI 2023. Code is available at https://github.com/thuiar/Robust-MS

PKC-induced Sensitization of Ca2+-dependent Exocytosis Is Mediated by Reducing the Ca2+ Cooperativity in Pituitary Gonadotropes

The highly cooperative nature of Ca2+-dependent exocytosis is very important for the precise regulation of transmitter release. It is not known whether the number of binding sites on the Ca2+ sensor can be modulated or not. We have previously reported that protein kinase C (PKC) activation sensitizes the Ca2+ sensor for exocytosis in pituitary gonadotropes. To further unravel the underlying mechanism of how the Ca2+ sensor is modulated by protein phosphorylation, we have performed kinetic modeling of the exocytotic burst and investigated how the kinetic parameters of Ca2+-triggered fusion are affected by PKC activation. We propose that PKC sensitizes exocytosis by reducing the number of calcium binding sites on the Ca2+ sensor (from three to two) without significantly altering the Ca2+-binding kinetics. The reduction in the number of Ca2+-binding steps lowers the threshold for release and up-regulates release of fusion-competent vesicles distant from Ca2+ channels

Branching Ratio and CP Asymmetry of B→ρη(′)B \to \rho \eta^{(\prime)} Decays in the Perturbative QCD Approach

In this paper,we calculate the branching ratios and CP-violating asymmetries for $B^0 \to \rho^0 \eta^{(\prime)}$ and B^+\to \rho^+ \etap decays in the perturbative QCD factorization approach. In this approach, we not only calculate the usual factorizable contributions, but also evaluate the non-factorizable and annihilation type contributions. Besides the current-current operators, the contributions from the QCD and electroweak penguin operators are also taken into account. The theoretical predictions for the branching ratios are $Br(B^+ \to \rho^+ \eta^{(\prime)}) \approx 9 \times 10^{-6}$ and $Br(B^0 \to \rho^0 \eta^{(\prime)}) \approx 5 \times 10^{-8}$, which agree well with the measured values and currently available experimental upper limits. We also predict large CP-violating asymmetries in these decays: $A_{CP}^{dir}(\rho^\pm \eta)\approx -13$, $A_{CP}^{dir}(\rho^\pm \eta^\prime)\approx -18$, $A_{CP}^{dir}(\rho^0 \eta)\approx -41$, $A_{CP}^{dir}(\rho^0 \eta^\prime)\approx -27$, $A_{CP}^{mix}(\rho^0 \eta)\approx +25$, and $A_{CP}^{mix}(\rho^0 \eta^\prime) \approx +11$, which can be tested by the current or future B factory experiments.Comment: 29 pages, 9 ps figures, more phenomenological discussions added, scale dependence of computed observables are considered, typos corrected, the figures and conclusions remain unchange

Robust stability for stochastic Hopfield neural networks with time delays

This is the post print version of the article. The official published version can be obtained from the link below - Copyright 2006 Elsevier Ltd.In this paper, the asymptotic stability analysis problem is considered for a class of uncertain stochastic neural networks with time delays and parameter uncertainties. The delays are time-invariant, and the uncertainties are norm-bounded that enter into all the network parameters. The aim of this paper is to establish easily verifiable conditions under which the delayed neural network is robustly asymptotically stable in the mean square for all admissible parameter uncertainties. By employing a Lyapunov–Krasovskii functional and conducting the stochastic analysis, a linear matrix inequality (LMI) approach is developed to derive the stability criteria. The proposed criteria can be checked readily by using some standard numerical packages, and no tuning of parameters is required. Examples are provided to demonstrate the effectiveness and applicability of the proposed criteria.This work was supported in part by the Engineering and Physical Sciences Research Council (EPSRC) of the UK under Grant GR/S27658/01, the Nuffield Foundation of the UK under Grant NAL/00630/G, and the Alexander von Humboldt Foundation of German

Cytotoxicity of Botulinum Neurotoxins Reveals a Direct Role of Syntaxin 1 and SNAP-25 in Neuron Survival

Botulinum neurotoxins (BoNT/A-G) are well-known to act by blocking synaptic vesicle exocytosis. Whether BoNTs disrupt additional neuronal functions has not been addressed. Here we report that cleavage of syntaxin 1 (Syx 1) by BoNT/C and cleavage of SNAP-25 by BoNT/E both induce degeneration of cultured rodent and human neurons. Furthermore, although SNAP-25 cleaved by BoNT/A can still support neuron survival, it has reduced capacity to tolerate additional mutations and also fails to pair with syntaxin isoforms other than Syx 1. Syx 1 and SNAP-25 are well-known for mediating synaptic vesicle exocytosis, but we found that neuronal death is due to blockage of plasma membrane recycling processes that share Syx 1/SNAP-25 for exocytosis, independent of blockage of synaptic vesicle exocytosis. These findings reveal neuronal cytotoxicity for a subset of BoNTs and directly link Syx 1/SNAP-25 to neuron survival as the prevalent SNARE proteins mediating multiple fusion events on neuronal plasma membranes