Search for heavy Majorana neutrinos at future lepton colliders

The nonzero neutrino mass can be a signal for new physics beyond the standard model. To explain the tiny neutrino mass, we can extend the standard model with right-handed Majorana neutrinos in a low-scale seesaw mechanism, while the CP violation effect can be induced due to the CP phase in the interference of heavy Majorana neutrinos. The existence of heavy Majorana neutrinos may lead to lepton number violation processes, which can be used as a probe to search for the signal of heavy Majorana neutrinos. In this paper, we focus on the CP violation effect related to two generations of heavy Majorana neutrinos for $15$ GeV $<m_N<$ $70$ GeV in the pair production of W bosons and rare decays. It is valuable to investigate the Majorana neutrino production signals and the related CP violation effects in the W boson rare decays at future lepton colliders.Comment: 12 pages, 8 figure

The First Human Infection with Severe Fever with Thrombocytopenia Syndrome Virus in Shaanxi Province, China

Background: Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease discovered in China in 2009. In July 2013, the first human infection with SFTS virus (SFTSV) was detected in Shaanxi Province, Western China. Methods: A seroprevalence study among humans was carried out in an SFTS endemic village; specifically, serum samples were collected from 363 farmers in an SFTS endemic village in Shaanxi Province. The presence of SFTSV antibodies in serum was determined using an ELISA. Results: SFTSV antibodies were found in a total of 20 people (5.51%), with no significant difference between males and females (6.93% and 4.42%, respectively; Chi-square = 1.29, p = 0.25). Moreover, the SFTSV antibody positive rate was not significantly different across different age groups (Chisquare = 2.23, p = 0.69). Conclusions: SFTSV readily infects humans with outdoor exposure. The results of the serological study indicate that the virus circulates widely in Shaanxi Province. SFTSV represents a public health threat in China

Evidence for a synergistic effect of post-translational modifications and genomic composition of eEF-1 alpha on the adaptation of Phytophthora infestans

Genetic variation plays a fundamental role in pathogen's adaptation to environmental stresses. Pathogens with low genetic variation tend to survive and proliferate more poorly due to their lack of genotypic/phenotypic polymorphisms in responding to fluctuating environments. Evolutionary theory hypothesizes that the adaptive disadvantage of genes with low genomic variation can be compensated for structural diversity of proteins through post-translation modification (PTM) but this theory is rarely tested experimentally and its implication to sustainable disease management is hardly discussed. In this study, we analyzed nucleotide characteristics of eukaryotic translation elongation factor-1 alpha (eEF-l alpha) gene from 165 Phytophthora infestans isolates and the physical and chemical properties of its derived proteins. We found a low sequence variation of eEF-l alpha protein, possibly attributable to purifying selection and a lack of intra-genic recombination rather than reduced mutation. In the only two isoforms detected by the study, the major one accounted for >95% of the pathogen collection and displayed a significantly higher fitness than the minor one. High lysine representation enhances the opportunity of the eEF-1 alpha protein to be methylated and the absence of disulfide bonds is consistent with the structural prediction showing that many disordered regions are existed in the protein. Methylation, structural disordering, and possibly other PTMs ensure the ability of the protein to modify its functions during biological, cellular and biochemical processes, and compensate for its adaptive disadvantage caused by sequence conservation. Our results indicate that PTMs may function synergistically with nucleotide codes to regulate the adaptive landscape of eEF-1 alpha, possibly as well as other housekeeping genes, in P. infestans. Compensatory evolution between pre- and post-translational phase in eEF-1 alpha could enable pathogens quickly adapting to disease management strategies while efficiently maintaining critical roles of the protein playing in biological, cellular, and biochemical activities. Implications of these results to sustainable plant disease management are discussed

Hypochlorite-Modified Albumin Upregulates ICAM-1 Expression via

Hypochlorite-modified albumin (HOCl-alb) has been linked to endothelial dysfunction, which plays an important role in the development of hypertension, diabetes, and chronic kidney disease. However, whether HOCl-alb induces endothelial dysfunction via vascular inflammation and whether a signaling pathway is involved are unknown and have not been investigated. HOCl-alb was found to upregulate ICAM-1 expression in human umbilical vein endothelial cells (HUVECs) in a time- and dose-dependent manner. HOCl-alb time-dependently phosphorylated ERK1/2 and p38MAPK. HOCl-alb also activated NF-κB. ICAM-1 expression was dose-dependently inhibited by U0126 (a specific inhibitor of MEK1/2, a signal upstream from ERK1/2), SB203580 (a specific inhibitor of p38MAPK), and SN50 (a specific inhibitor of NF-κB). U0126 and SB203580 both counteracted the activation of NF-κB, whereas the phosphorylation of ERK1/2 and p38MAPK was not blocked by SN50. ERK1/2 phosphorylation was blocked by U0126 but not by SB203580, and p38MAPK activity was reduced by SB203580 but not by U0126. Apocynin, a specific NADPH oxidase (NOX) inhibitor, inhibited ICAM-1 expression and the activity of ERK1/2, p38MAPK, and NF-κB. These results indicate that HOCl-alb-induced ICAM-1 expression is caused by the activation of a redox-sensitive intracellular signal cascade involving ERK1/2 and p38MAPK, culminating in the activation of NF-κB and involving NOXs among the upstream signals