Semileptonic BB Meson Decays Into A Highly Excited Charmed Meson Doublet

We study the heavy quark effective theory prediction for semileptonic $B$ decays into an orbital excited $F$-wave charmed doublet, the ($2^{+}$, $3^{+}$) states ($D^{*'}_{2}$, $D_{3}$), at the leading order of heavy quark expansion. The corresponding universal form factor is estimated by using the QCD sum rule method. The decay rates we predict are $\Gamma_{B\to D^{*'}_{2}\ell\overline{\nu}}=1.85\times10^{-19} {GeV}$ and $\Gamma_{B\to D_{3}\ell\overline{\nu}}=1.78\times10^{-19} {GeV}$. The branching ratios are $\mathcal {B}(B\to D_{2}^{*'}\ell\overline{\nu})=4.6\times10^{-7}$ and $\mathcal {B}(B\to D_{3}\ell\overline{\nu})=4.4\times10^{-7}$, respectively.Comment: 6 pages,2 figure

On the Inducibility of Stackelberg Equilibrium for Security Games

Strong Stackelberg equilibrium (SSE) is the standard solution concept of Stackelberg security games. As opposed to the weak Stackelberg equilibrium (WSE), the SSE assumes that the follower breaks ties in favor of the leader and this is widely acknowledged and justified by the assertion that the defender can often induce the attacker to choose a preferred action by making an infinitesimal adjustment to her strategy. Unfortunately, in security games with resource assignment constraints, the assertion might not be valid; it is possible that the defender cannot induce the desired outcome. As a result, many results claimed in the literature may be overly optimistic. To remedy, we first formally define the utility guarantee of a defender strategy and provide examples to show that the utility of SSE can be higher than its utility guarantee. Second, inspired by the analysis of leader's payoff by Von Stengel and Zamir (2004), we provide the solution concept called the inducible Stackelberg equilibrium (ISE), which owns the highest utility guarantee and always exists. Third, we show the conditions when ISE coincides with SSE and the fact that in general case, SSE can be extremely worse with respect to utility guarantee. Moreover, introducing the ISE does not invalidate existing algorithmic results as the problem of computing an ISE polynomially reduces to that of computing an SSE. We also provide an algorithmic implementation for computing ISE, with which our experiments unveil the empirical advantage of the ISE over the SSE.Comment: The Thirty-Third AAAI Conference on Artificial Intelligenc

The exclusive rare decay b->s gamma of heavy b-Baryons

We present an analysis on the exclusive rare radiative decay modes Sigma_b->Sigma gamma and Xi_b->Xi gamma. The transition form factors which parameterize these processes are calculated using QCD light-cone sum rules. The decay widths we predict are Gamma(Sigma_b->Sigma gamma)=(7.21\pm0.04)\times10^{-18}GeV} and Gamma(Xi_b->Xi gamma)=(1.34\pm0.07)\times10^{-16}GeV. The Branching ratio of Xi_b->Xi gamma is predicted to be Br(\Xi_b->Xi gamma)=(3.03\pm0.10)\times10^{-4}.Comment: 10 pages, 4 figures; to appear in Phys. Rev.

Search for Zs1+Z^{+}_{s1} and Zs2+Z^{+}_{s2} strangeonium-like structures

Theoretically, it has been presumed from an effective Lagrangian calculation that there could exist two charged strangeonium-like molecular states $Z^{+}_{s1}$ and $Z^{+}_{s2}$, with $K\bar{K}^{*}$ and $K^{*}\bar{K}^{*}$ configurations respectively. In the framework of QCD sum rules, we predict that masses of $Z^{+}_{s1}$ ($K\bar{K}^{*}$) and $Z^{+}_{s2}$ ($K^{*}\bar{K}^{*}$) are $1.85\pm0.14 GeV$ and $2.02\pm0.15 GeV$ respectively, which are both above their respective two meson thresholds. We suggest to put in practice the search for these two charged strangeonium-like structures in future experiments.Comment: 7 pages, 4 eps figures; the version accepted for publication in PRD. arXiv admin note: text overlap with arXiv:1203.070

Semileptonic Decays of B Meson Transition Into D-wave Charmed Meson Doublets

We use QCD sum rules to estimate the leading-order universal form factors describing the semileptonic B decay into orbital excited $D$-wave charmed doublets, including the ($1^{-}$, $2^{-}$) states ($D_{1}^{*}$, $D'_{2}$) and the ($2^{-}$, $3^{-}$) states ($D_{2}$, $D_{3}^{*}$). The decay rates we predict are $\Gamma_{B\to D^{*}_{1}\ell\overline{\nu}}=\Gamma_{B\to D'_{2}\ell\overline{\nu}}=2.4\times10^{-18} {GeV}$, $\Gamma_{B\to D_{2}\ell\overline{\nu}}=6.2\times10^{-17} {GeV}$, and $\Gamma_{B\to D_{3}^{*}\ell\overline{\nu}}=8.6\times10^{-17} {GeV}$. The branching ratios are $\mathcal {B}(B\to D^{*}_{1}\ell\overline{\nu})=\mathcal {B}(B\to D'_{2}\ell\overline{\nu})=6.0\times10^{-6}$, $\mathcal {B}(B\to D_{2}\ell\overline{\nu})=1.5\times10^{-4}$, and $\mathcal {B}(B\to D_{3}^{*}\ell\overline{\nu})=2.1\times10^{-4}$, respectively.Comment: 11 pages, 3 figure

Dissecting Mutational Allosteric Effects in Alkaline Phosphatases Associated with Different Hypophosphatasia Phenotypes: An Integrative Computational Investigation

Hypophosphatasia (HPP) is a rare inherited disorder characterized by defective bone mineralization and is highly variable in its clinical phenotype. The disease occurs due to various loss-of-function mutations in ALPL, the gene encoding tissue-nonspecific alkaline phosphatase (TNSALP). In this work, a data-driven and biophysics-based approach is proposed for the large-scale analysis of ALPL mutations-from nonpathogenic to severe HPPs. By using a pipeline of synergistic approaches including sequence-structure analysis, network modeling, elastic network models and atomistic simulations, we characterized allosteric signatures and effects of the ALPL mutations on protein dynamics and function. Statistical analysis of molecular features computed for the ALPL mutations showed a significant difference between the control, mild and severe HPP phenotypes. Molecular dynamics simulations coupled with protein structure network analysis were employed to analyze the effect of single-residue variation on conformational dynamics of TNSALP dimers, and the developed machine learning model suggested that the topological network parameters could serve as a robust indicator of severe mutations. The results indicated that the severity of disease-associated mutations is often linked with mutation-induced modulation of allosteric communications in the protein. This study suggested that ALPL mutations associated with mild and more severe HPPs can exert markedly distinct effects on the protein stability and long-range network communications. By linking the disease phenotypes with dynamic and allosteric molecular signatures, the proposed integrative computational approach enabled to characterize and quantify the allosteric effects of ALPL mutations and role of allostery in the pathogenesis of HPPs. Author summary By focusing on Hypophosphatasia, a rare inherited disorder we performed a comprehensive computational analysis of mutational effects on protein function in the encoded protein of Tissue Nonspecific Alkaline Phosphatase. This analysis demonstrated that pathogenic mutations can often modulate long-range allosteric interactions and communications in the dynamic protein network and the mechanisms underlying severity of mutational effects can be rationalized based on molecular principles of allostery. We have also developed a machine learning-based method to classify different disease phenotypes, and the interpretability of the classification model was addressed using the structural-functional analysis of network topologically important mutations. The results of this study revealed allosteric molecular signatures of severe mutations, suggesting that allosteric models of protein dynamics and function can be useful in dissecting complex genotype-phenotype relationships