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

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.

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

PeSOTIF: a Challenging Visual Dataset for Perception SOTIF Problems in Long-tail Traffic Scenarios

Perception algorithms in autonomous driving systems confront great challenges in long-tail traffic scenarios, where the problems of Safety of the Intended Functionality (SOTIF) could be triggered by the algorithm performance insufficiencies and dynamic operational environment. However, such scenarios are not systematically included in current open-source datasets, and this paper fills the gap accordingly. Based on the analysis and enumeration of trigger conditions, a high-quality diverse dataset is released, including various long-tail traffic scenarios collected from multiple resources. Considering the development of probabilistic object detection (POD), this dataset marks trigger sources that may cause perception SOTIF problems in the scenarios as key objects. In addition, an evaluation protocol is suggested to verify the effectiveness of POD algorithms in identifying the key objects via uncertainty. The dataset never stops expanding, and the first batch of open-source data includes 1126 frames with an average of 2.27 key objects and 2.47 normal objects in each frame. To demonstrate how to use this dataset for SOTIF research, this paper further quantifies the perception SOTIF entropy to confirm whether a scenario is unknown and unsafe for a perception system. The experimental results show that the quantified entropy can effectively and efficiently reflect the failure of the perception algorithm.Comment: 7 pages, 5 figures, 4 tables, submitted to 2023 ICR

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