Higgs production at future e+e−e^+e^- colliders in the Georgi-Machacek model

We study how the dominant single and double SM-like Higgs ($h$) production at future $e^+e^-$ colliders is modified in the Georgi-Machacek (GM) model. On imposing theoretical, indirect and direct constraints, significant deviations of $h$-couplings from their SM values are still possible; for instance, the Higgs-gauge coupling coupling can be corrected by a factor $\kappa_{hVV}\in[0.93,1.15]$ in the allowed parameter space. For the Higgs-strahlung $e^+e^-\to hZ$ and vector boson fusion processes $e^+e^-\to h\nu\bar{\nu},~he^+e^-$, the cross section could increase by $32\%$ or decrease by $13\%$. In the case of associated production with a top quark pair $e^+e^-\to ht\bar{t}$, the cross section can be enhanced up to several times when the custodial triplet scalar $H_3^0$ is resonantly produced. In the meanwhile, the double Higgs production $e^+e^-\to hhZ~(hh\nu\bar{\nu})$ can be maximally enhanced by one order of magnitude at the resonant $H_{1,3}^0$ production. We also include exclusion limits expected from future LHC runs at higher energy and luminosity and discuss their further constraints on the relevant model parameters. We find that the GM model can result in likely measurable deviations of Higgs production from the SM at future $e^+e^-$ colliders.Comment: 31 pages, 17 figures, published in JHE

Hunting for Heavy Majorana Neutrinos with Lepton Number Violating Signatures at LHC

The neutrinophilic two-Higgs-doublet model ($\nu$2HDM) provides a natural way to generate tiny neutrino mass from interactions with the new doublet scalar $\Phi_\nu$ ($H^\pm,~H,~A$) and singlet neutrinos $N_R$ of TeV scale. In this paper, we perform detailed simulations for the lepton number violating (LNV) signatures at LHC arising from cascade decays of the new scalars and neutrinos with the mass order $m_{N_R}<m_{\Phi_\nu}$. Under constraints from lepton flavor violating processes and direct collider searches, their decay properties are explored and lead to three types of LNV signatures: $2\ell^\pm 4j+\cancel{E}_T$, $3\ell^\pm 4j+\cancel{E}_T$, and $3\ell^\pm\ell^\mp 4j$. We find that the same-sign trilepton signature $3\ell^\pm4j+\cancel{E}_T$ is quite unique and is the most promising discovery channel at the high-luminosity LHC. Our analysis also yields the $95\%$ C.L. exclusion limits in the plane of the $\Phi_\nu$ and $N_R$ masses at 13 (14) TeV LHC with an integrated luminosity of 100~(3000)/fb.Comment: 31 pages, 17 figures, 6 tables; v2: added a few refs and updated one ref, without other change

Amending coherence-breaking channels via unitary operations

The coherence-breaking channels play a significant role in quantum information theory. We study the coherence-breaking channels and give a method to amend the coherence-breaking channels by applying unitary operations. For given incoherent channel $\Phi$, we give necessary and sufficient conditions for the channel to be a coherence-breaking channel and amend it via unitary operations. For qubit incoherent channels $\Phi$ that are not coherence-breaking ones, we consider the mapping $\Phi\circ\Phi$ and present the conditions for coherence-breaking and channel amendment as well.Comment: 8 page

Benzoxime inhibits matrix metalloproteinase-13 activation and cartilage damage in osteoarthritis rats via inhibition of NF-κB pathway

Purpose: To investigate the effect of benzoxime on degradation of  articular cartilage in a rat model of osteoarthritis (OA), and the mechanism involved.Methods: The OA rat model was prepared by injecting monosodium  iodoacetate (MIA) intra-articularly to Wistar rats. Rats in the treatment group were given benzoxime (5 mg/kg) daily for 21 days through the intra-articular route. The animals were then examined for behavioral changes by assessment of asymmetry in bearing weight and paw  withdrawal threshold of the hind limb. Western blot assay was used for the analysis of inflammatory cytokine expressions.Results: The expression of P2X purinoceptor 7 receptor (P2X7R) mRNA was significantly elevated in the OA rats (p &lt; 0.02). However, benzoxime treatment caused a marked decrease in the level of P2X1-8R mRNA. Benzoxime treatment also prevented asymmetry in bearing weight, decreased paw withdrawal threshold, and inhibited the expressions of interleukin-1β, interleukin-6 and tumor necrosis factor-α in plasma and cartilage. Moreover, benzoxime exhibited significant inhibitory effects on the expressions of P2X7R, matrix metalloproteinase (MMP)-13 and prostaglandin E2 (PGE2) in cartilage tissue. It also significantly  suppressed OA-induced increases in the levels of inhibitor of nuclear factor-κB (NF-κB) kinase (IKK)α, IKKβ, IκBα and NF-κB p65, and blocked OA-induced increases in the expressions of P2X7R, MMP-13 and PGE2.Conclusion: These results demonstrate that benzoxime prevents cartilage degradation in OA rats by targeting NF-κB signaling pathway. Thus, benzoxime possesses clinical and therapeutic potentials for the prevention of cartilage degradation in OA.Keywords: Interleukin-1β, Purinoceptor-7, Benzoxime, Osteoarthritis, Prostaglandin, Matrix metalloproteinase