B0→D0Dˉ0K0B^0 \to D^0 \bar D^0 K^0, B+→D0Dˉ0K+B^+ \to D^0 \bar D^0 K^+ and the scalar DDˉD \bar D bound state

We study the $B^0$ decay to $D^0 \bar D^0 K^0$ based on the chiral unitary model that generates the X(3720) resonance, and make predictions for the $D^0 \bar D^0$ invariant mass distribution. From the shape of the distribution, the existence of the resonance below threshold could be induced. We also predict the rate of production of the X(3720) resonance to the $D^0 \bar D^0$ mass distribution with no free parameters.Comment: 9 pages, 17 figure

Robust observer for uncertain linear quantum systems

In the theory of quantum dynamical filtering, one of the biggest issues is that the underlying system dynamics represented by a quantum stochastic differential equation must be known exactly in order that the corresponding filter provides an optimal performance; however, this assumption is generally unrealistic. Therefore, in this paper, we consider a class of linear quantum systems subjected to time-varying norm-bounded parametric uncertainties and then propose a robust observer such that the variance of the estimation error is guaranteed to be within a certain bound. Although in the linear case much of classical control theory can be applied to quantum systems, the quantum robust observer obtained in this paper does not have a classical analogue due to the system's specific structure with respect to the uncertainties. Moreover, by considering a typical quantum control problem, we show that the proposed robust observer is fairly robust against a parametric uncertainty of the system even when the other estimators--the optimal Kalman filter and risk-sensitive observer--fail in the estimation.Comment: 11 pages, 1 figur

Gonadotropin and kisspeptin gene expression, but not GnRH, are impaired in cFOS deficient mice.

cFOS is a pleiotropic transcription factor, which binds to the AP1 site in the promoter of target genes. In the pituitary gonadotropes, cFOS mediates induction of FSHβ and GnRH receptor genes. Herein, we analyzed reproductive function in the cFOS-deficient mice to determine its role in vivo. In the pituitary cFOS is necessary for gonadotropin subunit expression, while TSHβ is unaffected. Additionally, cFOS null animals have the same sex-steroid levels, although gametogenesis is impeded. In the brain, cFOS is not necessary for GnRH neuronal migration, axon targeting, cell number, or mRNA levels. Conversely, cFOS nulls, particularly females, have decreased Kiss1 neuron numbers and lower Kiss1 mRNA levels. Collectively, our novel findings suggest that cFOS plays a cell-specific role at multiple levels of the hypothalamic-pituitary-gonadal axis, affecting gonadotropes but not thyrotropes in the pituitary, and kisspeptin neurons but not GnRH neurons in the hypothalamus, thereby contributing to the overall control of reproduction