Searching for Majorana Neutrinos at a Same-Sign Muon Collider

Majorana properties of neutrinos have long been a focus in the pursuit of possible new physics beyond the standard model, which has motivated lots of dedicated theoretical and experimental studies. A future same-sign muon collider is an ideal platform to search for Majorana neutrinos through the Lepton Number Violation process. Specifically, this t-channel kind of process is less kinematically suppressed and has a good advantage in probing Majorana neutrinos at high mass regions up to 10 TeV. In this paper, we perform a detailed fast Monte Carlo simulation study through examining three different final states: 1) pure-leptonic state with electrons or muons, 2) semi-leptonic state, and 3) pure-hadronic state in the resolved or merged categories. Furthermore, we perform a full simulation study on the pure-leptonic final state to validate our fast simulation results.Comment: 15 pages, 8 figure

A Comparative Study of Z′^{\prime} mediated Charged Lepton Flavor Violation at future lepton colliders

Charged lepton flavor violation (CLFV) represents a transition between charged leptons of different generations that violates lepton flavor conservation, which is a clear signature of possible new physics beyond the standard model. By exploiting a typical example model of extra Z$^{\prime}$ gauge boson, we perform a detailed comparative study on CLFV searches at several future lepton colliders, including a 240 GeV electron-positron collider and a TeV scale muon collider. Based on detailed signal and background Monte-Carlo studies with fast detector simulations, we derive the potentials in searching for Z$^{\prime}$ mediated CLFV couplings with $e\mu$, $e\tau$ and $\mu\tau$ of different future colliders. The results are compared with the current limits set by either low-energy experiments or the high-energy LHC experiments. We find that the sensitivity of the $\tau$ related CLFV coupling strength at future lepton colliders will be significantly improved comparing with the current best constraints.Comment: 11 pages, 5 figure

Ku80 cooperates with CBP to promote COX-2 expression and tumor growth.

Cyclooxygenase-2 (COX-2) plays an important role in lung cancer development and progression. Using streptavidin-agarose pulldown and proteomics assay, we identified and validated Ku80, a dimer of Ku participating in the repair of broken DNA double strands, as a new binding protein of the COX-2 gene promoter. Overexpression of Ku80 up-regulated COX-2 promoter activation and COX-2 expression in lung cancer cells. Silencing of Ku80 by siRNA down-regulated COX-2 expression and inhibited tumor cell growth in vitro and in a xenograft mouse model. Ku80 knockdown suppressed phosphorylation of ERK, resulting in an inactivation of the MAPK pathway. Moreover, CBP, a transcription co-activator, interacted with and acetylated Ku80 to co-regulate the activation of COX-2 promoter. Overexpression of CBP increased Ku80 acetylation, thereby promoting COX-2 expression and cell growth. Suppression of CBP by a CBP-specific inhibitor or siRNA inhibited COX-2 expression as well as tumor cell growth. Tissue microarray immunohistochemical analysis of lung adenocarcinomas revealed a strong positive correlation between levels of Ku80 and COX-2 and clinicopathologic variables. Overexpression of Ku80 was associated with poor prognosis in patients with lung cancers. We conclude that Ku80 promotes COX-2 expression and tumor growth and is a potential therapeutic target in lung cancer

Experimental Investigation of the Matching Relationship between Asphalt Particle and Reservoir Pore in Profile Control Process

Modified sulfonated asphalt particles have a bright application prospect of the profile control of thick reservoirs due to the low cost, extensive sources, and good compatibility with reservoir. Nevertheless, the matching relationship between asphalt particles and reservoir pore has seldom been investigated till now. Oversized particles always block the near-wellbore area, which causes high injection pressures, while undersized particles cannot plug large pores. We designed a core for this experiment which has a high permeability zone in front of it and many pressure measuring points. We could quantitatively assess the matching relationship by measuring the on-way resistance coefficient, residual resistance factor, and relative change of permeability of man-made cores after injecting asphalt. Experimental results indicate that asphalt particles with sizes of 0.02 mm, 0.02–0.06 mm, and 0.08–0.1 mm match with reservoir permeability of 500 mD, 1000 mD, and 2000 mD, respectively. Undersized or oversized particles can reduce the conformance control effect, and the concentration of asphalt particles in the injectant can limit their migration ability. When the concentration of asphalt particles increases to 3000 mg/L, accumulations of asphalt particles can be caused in the formation, in which a scheme with asphalt particles alternative water injection is proposed to avoid the accumulation

Viral subversion of selective autophagy is critical for biogenesis of virus replication organelles

Infection by many (+)RNA viruses is accompanied by ER-expansion and membrane remodelling to form viral replication organelles, followed by assembly and secretion of viral progenies. We previously identified that virus-triggered lipophagy was critical for flaviviral assembly, and is driven by the lipid droplet associated protein Ancient ubiquitin protein 1 (Aup1). A ubiquitin conjugating protein Ube2g2 that functions as a co-factor for Aup1 was identified as a host dependency factor in our study. Here we characterized its function: Ube2g2-deficient cells displayed a dramatic reduction in virus production, which could be rescued by reconstituting the wild-type but not the catalytically deficient (C89K) mutant of Ube2g2, suggesting that its enzymatic activity is necessary. Ube2g2 deficiency did not affect entry of virus particles but resulted in a profound loss in formation of replication organelles, and production of infectious progenies. This phenomenon resulted from its dual activity in (i) triggering lipophagy in conjunction with Aup1, and (ii) degradation of ER chaperones such as Herpud1, SEL1L, Hrd1, along with Sec62 to restrict ER-phagy upon Xbp1-IRE1 triggered ER expansion. Our results therefore underscore an exquisite fine-tuning of selective autophagy by flaviviruses that drive host membrane reorganization during infection to enable biogenesis of viral replication organelles