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

Knockdown of Arabidopsis ROOT UVB SENSITIVE4 Disrupts Anther Dehiscence by Suppressing Secondary Thickening in the Endothecium

ROOT UV-B SENSITIVE4 (RUS4) encodes a protein with no known function that contains a conserved Domain of Unknown Function 647 (DUF647). The DUF647-containing proteins RUS1 and RUS2 have previously been associated with root UV-B-sensing pathway that plays a major role in Arabidopsis early seedling morphogenesis and development. Here, we show that RUS4 knockdown Arabidopsis plants, referred to as amiR-RUS4, were severely reduced in male fertility with indehiscent anthers. Light microscopy of anther sections revealed a significantly reduced secondary wall thickening in the endothecium of amiR-RUS4 anthers. We further show that transcript abundance of the NAC domain genes NAC SECONDARY WALL THICKENING PROMOTING FACTOR1 (NST1) and NST2, which have been shown to regulate the secondary cell wall thickenings in the anther endothecium, were dramatically reduced in the amiR-RUS4 floral buds. Expression of the secondary cell wall-associated MYB transcription factor genes MYB103 and MYB85 were also strongly reduced in floral buds of the amiR-RUS4 plants. Overexpression of RUS4 led to increased secondary thickening in the endothecium. However, the rus4-2 mutant exhibited no obvious phenotype. Promoter-GUS analysis revealed that RUS4 promoter was highly active in the anthers, supporting its role in anther development. Taken together, these results suggest that RUS4, probably functions redundantly with other genes, may play an important role in the secondary thickening formation in the anther endothecium by indirectly affecting the expression of secondary cell wall biosynthetic genes

S-allylcysteine Improves Blood Flow Recovery and Prevents Ischemic Injury by Augmenting Neovasculogenesis.

Studies suggest that a low level of circulating human endothelial progenitor cells (EPCs) is a risk factor for ischemic injury and coronary artery disease (CAD). Consumption of S-allylcysteine (SAC) is known to prevent CAD. However, the protective effects of SAC on the ischemic injury are not yet clear. In this study, we examined whether SAC could improve blood flow recovery in ischemic tissues through EPC-mediated neovasculogenesis. The results demonstrate that SAC significantly enhances the neovasculogenesis of EPCs in vitro. The molecular mechanisms for SAC enhancement of neovasculogenesis include the activation of Akt/endothelial nitric oxide synthase signaling cascades. SAC increased the expression of c-kit, β-catenin, cyclin D1, and Cyclin-dependent kinase 4 (CDK4) proteins in EPCs. Daily intake of SAC at dosages of 0.2 and 2 mg/kg body weight significantly enhanced c-kit protein levels in vivo. We conclude that dietary consumption of SAC improves blood flow recovery and prevents ischemic injury by inducing neovasculogenesis in experimental models