Robust continuous-variable entanglement of microwave photons with cavity electromechanics

We investigate the controllable generation of robust photon entanglement with a circuit cavity electromechanical system, consisting of two superconducting coplanar waveguide cavities (CPWC's) capacitively coupled by a nanoscale mechanical resonator (MR). We show that, with this electromechanical system, two-mode continuous-variable entanglement of cavity photons can be engineered deterministically either via coherent control on the dynamics of the system, or through a dissipative quantum dynamical process. The first scheme, operating in the strong coupling regime, explores the excitation of the cavity Bogoliubov modes, and is insensitive to the initial thermal noise. The second one is based on the reservoir-engineering approach, which exploits the mechanical dissipation as a useful resource to perform ground state cooling of two delocalized cavity Bogoliubov modes. The achieved amount of entanglement in both schemes is determined by the relative ratio of the effective electromechanical coupling strengths, which thus can be tuned and made much lager than that in previous studies.Comment: To appear in PRA, published versio

Searching for the signal of dark matter and photon associated production at the LHC beyond leading order

We study the signal of dark matter and photon associated production induced by the vector and axial-vector operators at the LHC, including the QCD next-to-leading order (NLO) effects. We find that the QCD NLO corrections reduce the dependence of the total cross sections on the factorization and renormalization scales, and the $K$ factors increase with the increasing of the dark matter mass, which can be as large as about 1.3 for both the vector and axial-vector operators. Using our QCD NLO results, we improve the constraints on the new physics scale from the results of the recent CMS experiment. Moreover, we show the Monte Carlo simulation results for detecting the \gamma+\Slash{E}_{T} signal at the QCD NLO level, and present the integrated luminosity needed for a $5\sigma$ discovery at the 14 TeV LHC . If the signal is not observed, the lower limit on the new physics scale can be set.Comment: 19 pages, 18 figures, 2 tables, version published in Phys.Rev.

Phenomenology of an Extended Higgs Portal Inflation Model after Planck 2013

We consider an extended inflation model in the frame of Higgs portal model, assuming a nonminimal coupling of the scalar field to the gravity. Using the new data from Planck $2013$ and other relevant astrophysical data, we obtain the relation between the nonminimal coupling $\xi$ and the self-coupling $\lambda$ needed to drive the inflation, and find that this inflationary model is favored by the astrophysical data. Furthermore, we discuss the constraints on the model parameters from the experiments of particle physics, especially the recent Higgs data at the LHC.Comment: 21 pages, 8 figures; Version published in EPJ

Constraints on flavor-changing neutral-current HtqHtq couplings from the signal of tHtH associated production with QCD next-to-leading order accuracy at the LHC

We study a generic Higgs boson and a top quark associated production via model-independent flavor-changing neutral-current couplings at the LHC, including complete QCD next-to-leading order (NLO) corrections to the production and decay of the top quark and the Higgs boson. We find that QCD NLO corrections can increase the total production cross sections by about 48.9% and 57.9% for the $Htu$ and $Htc$ coupling induced processes at the LHC, respectively. After kinematic cuts are imposed on the decay products of the top quark and the Higgs boson, the QCD NLO corrections are reduced to 11% for the $Htu$ coupling induced process and almost vanish for the $Htc$ coupling induced process. Moreover, QCD NLO corrections reduce the dependence of the total cross sections on the renormalization and factorization scales. We also discuss signals of the $tH$ associated production with the decay mode t \rightarrow bl^{+}E \slash_{T}, H \rightarrow b\bar{b} and $t\bar{t}$ production with the decay mode \bar{t} \rightarrow H\bar{q}, t\rightarrow bl^{+}E \slash_{T}. Our results show that, in some parameter regions, the LHC may observe the above signals at the $5\sigma$ level. Otherwise, the upper limits on the FCNC $Htq$ couplings can be set.Comment: 28 pages, 14 figures, 5 tables; version published in PR

Inhibition of Autophagy Signaling via 3-methyladenine Rescued Nicotine-Mediated Cardiac Pathological Effects and Heart Dysfunctions.

Rationale: Cigarette smoking is a well-established risk factor for myocardial infarction and sudden cardiac death. The deleterious effects are mainly due to nicotine, but the mechanisms involved and theranostics remain unclear. Thus, we tested the hypothesis that nicotine exposure increases the heart sensitivity to ischemia/reperfusion injury and dysfunction, which can be rescued by autophagy inhibitor. Methods: Nicotine or saline was administered to adult rats via subcutaneous osmotic minipumps in the absence or presence of an autophagy inhibitor, 3-methyladenine (3-MA). After 30 days of nicotine treatment, the rats underwent the cardiac ischemia/reperfusion (I/R) procedure and echocardiography analysis, and the heart tissues were isolated for molecular biological studies. Results: Nicotine exposure increased I/R-induced cardiac injury and cardiac dysfunction as compared to the control. The levels of autophagy-related proteins including LC3 II, P62, Beclin1, and Atg5 were upregulated in the reperfused hearts isolated from nicotine-treated group. In addition, nicotine enhanced cardiac and plasma ROS production, and increased the phosphorylation of GSK3β (ser9) in the left ventricle tissues. Treatment with 3-MA abolished nicotine-mediated increase in the levels of autophagy-related proteins and phosphorylation of GSK3β, but had no effect on ROS production. Of importance, 3-MA ameliorated the augmented I/R-induced cardiac injury and dysfunction in the nicotine-treated group as compared to the control. Conclusion: Our results demonstrate that nicotine exposure enhances autophagy signaling pathway, resulting in development of ischemic-sensitive phenotype of heart. It suggests a potentially novel therapeutic strategy of autophagy inhibition for the treatment of ischemic heart disease