Determining the CP Violation Angle γ\gamma in BsB_s Decays without Hadronic Uncertainty

We study the rare decays $B_s^0\to D^\pm \pi^\mp$ and $\bar B_s^0\to D^\mp \pi^\pm$, which can occur only via annihilation type $W$ exchange diagrams in the standard model. The time-dependent decay rates of the four channels can provide four CP parameters, which are experimentally measurable. We show that the CKM angle $\phi_3=\gamma$ can be determined from these parameters without any theoretical model dependence. These channels can be measured in future LHCb experiments to provide a clean way for $\gamma$ measurement.Comment: 4 pages, including 2 figures, Revte

Energy dependent chemical potentials of light hadrons and quarks based on transverse momentum spectra and yield ratios of negative to positive particles

We describe the transverse momentum (or mass) spectra of $\pi^\pm$, $K^\pm$, $p$, and $\bar{p}$ produced in central gold-gold (Au-Au), central lead-lead (Pb-Pb), and inelastic proton-proton ($pp$) collisions at different collision energies range from the AGS to LHC by using a two-component (in most cases) Erlang distribution in the framework of multi-source thermal model. The fitting results are consistent with the experimental data and the energy-dependent chemical potentials of light hadrons ($\pi$, $K$, and $p$) and quarks ($u$, $d$, and $s$) in central Au-Au, central Pb-Pb, and inelastic $pp$ collisions from the yield ratios of negative to positive particles obtained from the normalization constants are then extracted. The study shows that most types of energy-dependent chemical potentials decrease with increase of collision energy over a range from the AGS to LHC. The curves of all types of energy-dependent chemical potentials, obtained from the linear fits of yield ratios vs energy, have inflection points at the same energy of 3.526 GeV, which is regarded as the critical energy of phase transition from a hadron liquid-like state to a quark gas-like state in the collision system and indicates that the hadronic interactions play an important role in this period. At the RHIC and LHC, all types of chemical potentials become small and tend to zero at very high energy, which confirms that the collision system possibly changes completely from the hadron-dominant liquid-like state to the quark-dominant gas-like state and the partonic interactions possibly play a dominant role at the LHC

3,8-Dimethyl-4-oxo-3,4-dihydro­quinazoline-6-carbonitrile

In the title compound, C11H9N3O, the quinazoline unit is almost planar, with a mean deviation of 0.006 (1) Å from the least-squares plane defined by the ten constituent atoms. In the crystal, mol­ecules are linked by weak C—H⋯N hydrogen bonds

mGluR5 antagonism inhibits cocaine reinforcement and relapse by elevation of extracellular glutamate in the nucleus accumbens via a CB1 receptor mechanism.

Metabotropic glutamate receptor 5 (mGluR5) antagonism inhibits cocaine self-administration and reinstatement of drug-seeking behavior. However, the cellular and molecular mechanisms underlying this action are poorly understood. Here we report a presynaptic glutamate/cannabinoid mechanism that may underlie this action. Systemic or intra-nucleus accumbens (NAc) administration of the mGluR5 antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) dose-dependently reduced cocaine (and sucrose) self-administration and cocaine-induced reinstatement of drug-seeking behavior. The reduction in cocaine-taking and cocaine-seeking was associated with a reduction in cocaine-enhanced extracellular glutamate, but not cocaine-enhanced extracellular dopamine (DA) in the NAc. MPEP alone, when administered systemically or locally into the NAc, elevated extracellular glutamate, but not DA. Similarly, the cannabinoid CB1 receptor antagonist, rimonabant, elevated NAc glutamate, not DA. mGluR5s were found mainly in striatal medium-spiny neurons, not in astrocytes, and MPEP-enhanced extracellular glutamate was blocked by a NAc CB1 receptor antagonist or N-type Ca++ channel blocker, suggesting that a retrograde endocannabinoid-signaling mechanism underlies MPEP-induced glutamate release. This interpretation was further supported by our findings that genetic deletion of CB1 receptors in CB1-knockout mice blocked both MPEP-enhanced extracellular glutamate and MPEP-induced reductions in cocaine self-administration. Together, these results indicate that the therapeutic anti-cocaine effects of mGluR5 antagonists are mediated by elevation of extracellular glutamate in the NAc via an endocannabinoid-CB1 receptor disinhibition mechanism