Electroweak corrections to Higgs boson production via Z Z fusion at the future LHeC

An important mechanism for production of the Higgs boson at the prospective Large Hadron-electron Collider (LHeC) is via neutral current (NC) weak boson fusion (WBF) processes. Aside from its role in measurements of Higgs couplings within the standard model, this production mode is particularly useful in searchings of Higgs decays into invisble particles in various models for the Higg portal dark matter. In this work we compute the electroweak corrections for the NC WBF at the LHeC up to the 1-loop level. For a center-of-mass energy of 1.98 TeV, the magnitudes of the relative corrections for the total cross section at next-to-leading (NLO) order are respectively 8% and 17%, in the two renormalization schemes we use. The NLO terms also distort various distributions (notably, those for Higgs and electron observables) computed at the leading order. Along with our previous treatment of the charge current processes, this paper completes the calulation of the NLO EW effects for the dominant Higgs production modes at the LHeC.Comment: 14 pages, 10 figures. arXiv admin note: text overlap with arXiv:2207.1451

Perihelion Precession and Deflection of Light in the General Spherically Symmetric Spacetime

The perihelion precession and deflection of light have been investigated in the 4-dimensional general spherically symmetric spacetime, and the master equation is obtained. As the application of this master equation, the Reissner-Nordstorm-AdS solution and Clifton-Barrow solution in f(R) gravity have been taken as examples. We find that both the electric charge and f(R) gravity can affect the perihelion precession and deflection of light, while the cosmological constant can only effect the perihelion precession. Moreover, we clarify a subtlety in the deflection of light in the solar system that the possible sun’s electric charge is usually used to interpret the gap between the experiment data and theoretical result. However, after also considering the effect from the sun’s same electric charge on the perihelion precession of Mercury, we can find that it is not the truth

Compound Kushen Injection suppresses human breast cancer stem-like cells by down-regulating the canonical Wnt/β-catenin pathway

<p>Abstract</p> <p>Background</p> <p>Cancer stem cells (CSCs) play an important role in cancer initiation, relapse and metastasis. To date, no specific medicine has been found to target CSCs as they are resistant to most conventional therapies and proliferate indefinitely. Compound Kushen Injection (CKI) has been widely used for cancer patients with remarkable therapeutic effects in Chinese clinical settings for many years. This study focused on whether CKI could inhibit MCF-7 SP cells in vitro and in vivo.</p> <p>Methods</p> <p>The analysis of CKI on SP population and the main genes of Wnt signaling pathway were studied first. Then we studied the tumorigenicity of SP cells and the effects of CKI on SP cells in vivo. The mice inoculated with 10,000 SP cells were randomly divided into three groups (6 in each group) and treated with CKI, cisplatin and saline (as a control) respectively for 7 weeks. The tumor formation rates of each group were compared. The main genes and proteins of the Wnt signaling pathway were analyzed by RT-PCR and western blot.</p> <p>Results</p> <p>CKI suppressed the size of SP population (approximately 90%), and down-regulated the main genes of Wnt signaling pathway. We also determined that MCF-7 SP cells were more tumorigenic than non-SP and unsorted cells. The Wnt signaling pathway was up-regulated in tumors derived from SP cells compared with that in tumors from non-SP cells. The tumor formation rate of the CKI Group was 33% (2/6, <it>P </it>< 0.05), and that of Cisplatin Group was 50%(3/6, <it>P </it>< 0.05), whereas that of the Control Group was 100% (6/6).The RT-PCR and western blot results indicated that CKI suppressed tumor growth by down-regulating the Wnt/β-catenin pathway, while cisplatin activated the Wnt/β-catenin pathway and might spare SP cells.</p> <p>Conclusions</p> <p>It suggested that CKI may serve as a novel drug targeting cancer stem-like cells, though further studies are recommended.</p

Long Non-coding RNAs Contribute to the Inhibition of Proliferation and EMT by Pterostilbene in Human Breast Cancer

Background: There is increasing evidence that long non-coding RNAs (lncRNAs) are involved in the process of carcinogenesis and treatment using chemotherapy. Pterostilbene, a phytochemical agent with natural antioxidant and anti-inflammatory properties, has been shown to modulate oncogenic processes in many cancers. However, there has been limited research on the association between pterostilbene and the expression of lncRNAs.Methods: MCF7 breast cancer cells were treated with various concentrations of pterostilbene and their gene expression profile was analyzed by quantitative real-time PCR, Western blotting and immunofluorescence.Results: Treatment with pterostilbene inhibited cell proliferation and epithelial-to-mesenchymal transition (EMT), and increased cell apoptosis, autophagy and ER stress. The Akt/mTOR pathway was downregulated, but p38 MAPK/Erk signaling was activated in cells following treatment with pterostilbene. Pterostilbene increased the expression of the lncRNAs MEG3, TUG1, H19, and DICER1-AS1 whereas the expression of LINC01121, PTTG3P, and HOTAIR declined. Knockdown of lncRNA H19 resulted in a reduction of the cell invasion, with the cells becoming more sensitive to pterostilbene therapy.Conclusions: These results suggest that efficient optimum disruption of lncRNA expression might possibly improve the anti-tumor effects of phytochemical agents, thus serving as a potential therapy for breast cancer

Genetic determinants of telomere length from 109,122 ancestrally diverse whole-genome sequences in TOPMed

Genetic studies on telomere length are important for understanding age-related diseases. Prior GWAS for leukocyte TL have been limited to European and Asian populations. Here, we report the first sequencing-based association study for TL across ancestrally-diverse individuals (European, African, Asian and Hispanic/Latino) from the NHLBI Trans-Omics for Precision Medicine (TOPMed) program. We used whole genome sequencing (WGS) of whole blood for variant genotype calling and the bioinformatic estimation of telomere length in n=109,122 individuals. We identified 59 sentinel variants (p-value OBFC1indicated the independent signals colocalized with cell-type specific eQTLs for OBFC1 (STN1). Using a multi-variant gene-based approach, we identified two genes newly implicated in telomere length, DCLRE1B (SNM1B) and PARN. In PheWAS, we demonstrated our TL polygenic trait scores (PTS) were associated with increased risk of cancer-related phenotypes

DNA Methylation Signatures of Depressive Symptoms in Middle-aged and Elderly Persons:Meta-analysis of Multiethnic Epigenome-wide Studies

IMPORTANCE Depressive disorders arise from a combination of genetic and environmental risk factors. Epigenetic disruption provides a plausible mechanism through which gene-environment interactions lead to depression. Large-scale, epigenome-wide studies on depression are missing, hampering the identification of potentially modifiable biomarkers.OBJECTIVE To identify epigenetic mechanisms underlying depression in middle-aged and elderly persons, using DNA methylation in blood.DESIGN, SETTING, AND PARTICIPANTS To date, the first cross-ethnic meta-analysis of epigenome-wide association studies (EWAS) within the framework of the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium was conducted. The discovery EWAS included 7948 individuals of European origin from 9 population-based cohorts. Participants who were assessed for both depressive symptoms and whole-blood DNA methylation were included in the study. Results of EWAS were pooled using sample-size weighted meta-analysis. Replication of the top epigenetic sites was performed in 3308 individuals of African American and European origin from 2 population-based cohorts.MAIN OUTCOMES AND MEASURES Whole-blood DNA methylation levels were assayed with Illumina-Infinium Human Methylation 450K BeadChip and depressive symptoms were assessed by questionnaire.RESULTS The discovery cohorts consisted of 7948 individuals (4104 [51.6%] women) with a mean (SD) age of 65.4 (5.8) years. The replication cohort consisted of 3308 individuals (2456 [74.2%) women) with a mean (SD) age of 60.3 (6.4) years. The EWAS identified methylation of 3 CpG sites to be significantly associated with increased depressive symptoms: cg04987734 (P = 1.57 x 10(-)(08); n = 11 256; CDC42BPB gene), cg12325605 (P = 5.24 x 10(-09); n = 11256; ARHGEF3 gene), and an intergenic CpG site cg14023999 (P = 5.99 x 10(-)(08); n = 11256; chromosome = 15q261). The predicted expression of the CDC42BPB gene in the brain (basal ganglia) (effect, 0.14; P = 2.7 x 10(-03)) and of ARHGEF3 in fibroblasts (effect. -0.48; P = 9.8 x 10(-)(04) ) was associated with major depression.CONCLUSIONS AND RELEVANCE This study identifies 3 methylated sites associated with depressive symptoms. All 3 findings point toward axon guidance as the common disrupted pathway in depression. The findings provide new insights into the molecular mechanisms underlying the complex pathophysiology of depression. Further research is warranted to determine the utility of these findings as biomarkers of depression and evaluate any potential role in the pathophysiology of depression and their downstream clinical effects. (C) 2018 American Medical Association. All lights reserved

Origin of anomalous instability of grid‐forming converters tied to stiff grid

Abstract Grid‐forming (GFM) converter is believed to be highly promising in the future power systems, due to its ability of providing voltage and frequency support. However, some recent studies have shown that the GFM converter may suffer from instability in stiff grids, which seriously hampers its application. In this paper, the mechanism of this anomalous effect is studied by using the small‐signal stability analysis in detail. First, a detailed state‐space model of a single converter grid‐tied system is established from the first principle, and by using the participation factor analysis, the interaction between the terminal voltage loop and the power synchronization loop is identified as the major cause for the system instability. Then relying on a reduced‐order model containing only these two controls and using two classical analytical methods including the Routh criterion analysis and the Phillips– Heffron model of complex torque analysis, the origin of this anomalous instability of GFM converters tied to stiff grid coming from the negative damping provided by the terminal voltage loop is well uncovered and the critical grid strength is well predicted. In addition, these results may provide ideas for subsequent control optimization and stability improvement of GFM converters under various situations