CHY representations for gauge theory and gravity amplitudes with up to three massive particles

We show that a wide class of tree-level scattering amplitudes involving scalars, gauge bosons, and gravitons, up to three of which may be massive, can be expressed in terms of a Cachazo-He-Yuan representation as a sum over solutions of the scattering equations. These amplitudes, when expressed in terms of the appropriate kinematic invariants, are independent of the masses and therefore identical to the corresponding massless amplitudes.Comment: 20 pages, 1 figure; v2: minor typos corrected, published versio

Applying the effort-reward imbalance model to household and family work: a population-based study of German mothers

<p>Abstract</p> <p>Background</p> <p>This paper reports on results of a newly developed questionnaire for the assessment of effort-reward imbalance (ERI) in unpaid household and family work. Methods: Using a cross-sectional population-based survey of German mothers (n = 3129) the dimensional structure of the theoretical ERI model was validated by means of Confirmatory Factor Analysis (CFA). Analyses of Variance were computed to examine relationships between ERI and social factors and health outcomes.</p> <p>Results</p> <p>CFA revealed good psychometric properties indicating that the subscale 'effort' is based on one latent factor and the subscale 'reward' is composed of four dimensions: 'intrinsic value of family and household work', 'societal esteem', 'recognition from the partner', and 'affection from the child(ren)'. About 19.3% of mothers perceived lack of reciprocity and 23.8% showed high rates of overcommitment in terms of inability to withdraw from household and family obligations. Socially disadvantaged mothers were at higher risk of ERI, in particular with respect to the perception of low societal esteem. Gender inequality in the division of household and family work and work-family conflict accounted most for ERI in household and family work. Analogous to ERI in paid work we could demonstrate that ERI affects self-rated health, somatic complaints, mental health and, to some extent, hypertension.</p> <p>Conclusions</p> <p>The newly developed questionnaire demonstrates satisfied validity and promising results for extending the ERI model to household and family work.</p

Impacts of climate change on plant diseases – opinions and trends

There has been a remarkable scientific output on the topic of how climate change is likely to affect plant diseases in the coming decades. This review addresses the need for review of this burgeoning literature by summarizing opinions of previous reviews and trends in recent studies on the impacts of climate change on plant health. Sudden Oak Death is used as an introductory case study: Californian forests could become even more susceptible to this emerging plant disease, if spring precipitations will be accompanied by warmer temperatures, although climate shifts may also affect the current synchronicity between host cambium activity and pathogen colonization rate. A summary of observed and predicted climate changes, as well as of direct effects of climate change on pathosystems, is provided. Prediction and management of climate change effects on plant health are complicated by indirect effects and the interactions with global change drivers. Uncertainty in models of plant disease development under climate change calls for a diversity of management strategies, from more participatory approaches to interdisciplinary science. Involvement of stakeholders and scientists from outside plant pathology shows the importance of trade-offs, for example in the land-sharing vs. sparing debate. Further research is needed on climate change and plant health in mountain, boreal, Mediterranean and tropical regions, with multiple climate change factors and scenarios (including our responses to it, e.g. the assisted migration of plants), in relation to endophytes, viruses and mycorrhiza, using long-term and large-scale datasets and considering various plant disease control methods

Do agreements between adolescent and parent reports on family socioeconomic status vary with household financial stress?

<p>Abstract</p> <p>Background</p> <p>Many studies compared the degree of concordance between adolescents' and parents' reports on family socioeconomic status (SES). However, none of these studies analyzed whether the degree of concordance varies by different levels of household financial stress. This research examines whether the degree of concordance between adolescents' and parent reports for the three traditional SES measures (parental education, parental occupation and household income) varied with parent-reported household financial stress and relative standard of living.</p> <p>Methods</p> <p>2,593 adolescents with a mean age of 13 years, and one of their corresponding parents from the Taiwan Longitudinal Youth Project conducted in 2000 were analyzed. Consistency of adolescents' and parents' reports on parental educational attainment, parental occupation and household income were examined by parent-reported household financial stress and relative standard of living.</p> <p>Results</p> <p>Parent-reported SES variables are closely associated with family financial stress. For all levels of household financial stress, the degree of concordance between adolescent's and parent's reports are highest for parental education (κ ranging from 0.87 to 0.71) followed by parental occupation (κ ranging from 0.50 to 0.34) and household income (κ ranging from 0.43 to 0.31). Concordance for father's education and parental occupation decreases with higher parent-reported financial stress. This phenomenon was less significant for parent-reported relative standard of living.</p> <p>Conclusions</p> <p>Though the agreement between adolescents' and parents' reports on the three SES measures is generally judged to be good in most cases, using adolescents reports for family SES may still be biased if analysis is not stratified by family financial stress.</p

The Spin Structure of the Nucleon

We present an overview of recent experimental and theoretical advances in our understanding of the spin structure of protons and neutrons.Comment: 84 pages, 29 figure

Differentiation Generates Paracrine Cell Pairs That Maintain Basaloid Mouse Mammary Tumors: Proof of Concept

There is a paradox offered up by the cancer stem cell hypothesis. How are the mixed populations that are characteristic of heterogeneous solid tumors maintained at constant proportion, given their high, and different, mitotic indices? In this study, we evaluate a well-characterized mouse model of human basaloid tumors (induced by the oncogene Wnt1), which comprise mixed populations of mammary epithelial cells resembling their normal basal and luminal counterparts. We show that these cell types are substantially inter-dependent, since the MMTV LTR drives expression of Wnt1 ligand in luminal cells, whereas the functional Wnt1-responsive receptor (Lrp5) is expressed by basal cells, and both molecules are necessary for tumor growth. There is a robust tumor initiating activity (tumor stem cell) in the basal cell population, which is associated with the ability to differentiate into luminal and basal cells, to regenerate the oncogenic paracrine signaling cell pair. However, we found an additional tumor stem cell activity in the luminal cell population. Knowing that tumors depend upon Wnt1-Lrp5, we hypothesized that this stem cell must express Lrp5, and found that indeed, all the stem cell activity could be retrieved from the Lrp5-positive cell population. Interestingly, this reflects post-transcriptional acquisition of Lrp5 protein expression in luminal cells. Furthermore, this plasticity of molecular expression is reflected in plasticity of cell fate determination. Thus, in vitro, Wnt1-expressing luminal cells retro-differentiate to basal cell types, and in vivo, tumors initiated with pure luminal cells reconstitute a robust basal cell subpopulation that is indistinguishable from the populations initiated by pure basal cells. We propose this is an important proof of concept, demonstrating that bipotential tumor stem cells are essential in tumors where oncogenic ligand-receptor pairs are separated into different cell types, and suggesting that Wnt-induced molecular and fate plasticity can close paracrine loops that are usually separated into distinct cell types

Linker-extended native cyanovirin-N facilitates PEGylation and potently inhibits HIV-1 by targeting the glycan ligand

Cyanovirin-N (CVN) potently inhibits human immunodeficiency virus type 1 (HIV-1) infection, but both cytotoxicity and immunogenicity have hindered the translation of this protein into a viable therapeutic. A molecular docking analysis suggested that up to 12 residues were involved in the interaction of the reverse parallel CVN dimer with the oligosaccharide targets, among which Leu-1 was the most prominent hot spot residue. This finding provided a possible explanation for the lack of anti-HIV-1 activity observed with N-terminal PEGylated CVN. Therefore, linker-CVN (LCVN) was designed as a CVN derivative with a flexible and hydrophilic linker (Gly4Ser)3 at the N-terminus. The N-terminal α-amine of LCVN was PEGylated to create 10 K PEG-aldehyde (ALD)-LCVN. LCVN and 10 K PEG-ALD-LCVN retained the specificity and affinity of CVN for high mannose N-glycans. Moreover, LCVN exhibited significant anti-HIV-1 activity with attenuated cytotoxicity in the HaCaT keratinocyte cell line and MT-4 T lymphocyte cell lines. 10 K PEG-ALD-LCVN also efficiently inactivated HIV-1 with remarkably decreased cytotoxicity and pronounced cell-to-cell fusion inhibitory activity in vitro. The linker-extended CVN and the mono-PEGylated derivative were determined to be promising candidates for the development of an anti-HIV-1 agent. This derivatization approach provided a model for the PEGylation of biologic candidates without introducing point mutations. © 2014 Chen et al

Adenoviral Vector Driven by a Minimal Rad51 Promoter Is Selective for p53-Deficient Tumor Cells

Background: The full length Rad51 promoter is highly active in cancer cells but not in normal cells. We therefore set out to assess whether we could confer this tumor-selectivity to an adenovirus vector. Methodology/Principal Findings: Expression of an adenovirally-vectored luciferase reporter gene from the Rad51 promoter was up to 50 fold higher in cancer cells than in normal cells. Further evaluations of a panel of truncated promoter mutants identified a 447 bp minimal core promoter element that retained the full tumor selectivity and transcriptional activity of the original promoter, in the context of an adenovirus vector. This core Rad51 promoter was highly active in cancer cells that lack functional p53, but less active in normal cells and in cancer cell lines with intact p53 function. Exogenous expression of p53 in a p53 null cell line strongly suppressed activity of the Rad51 core promoter, underscoring the selectivity of this promoter for p53-deficient cells. Follow-up experiments showed that the p53-dependent suppression of the Rad51 core promoter was mediated via an indirect, p300 coactivator dependent mechanism. Finally, transduction of target cells with an adenovirus vector encoding the thymidine kinase gene under transcriptional control of the Rad51 core promoter resulted in efficient killing of p53 defective cancer cells, but not of normal cells, upon addition of ganciclovir. Conclusions/Significance: Overall, these experiments demonstrated that a small core domain of the Rad51 promoter ca

In Silico Whole Genome Association Scan for Murine Prepulse Inhibition

Background The complex trait of prepulse inhibition (PPI) is a sensory gating measure related to schizophrenia and can be measured in mice. Large-scale public repositories of inbred mouse strain genotypes and phenotypes such as PPI can be used to detect Quantitative Trait Loci (QTLs) in silico. However, the method has been criticized for issues including insufficient number of strains, not controlling for false discoveries, the complex haplotype structure of inbred mice, and failing to account for genotypic and phenotypic subgroups. Methodology/Principal Findings We have implemented a method that addresses these issues by incorporating phylogenetic analyses, multilevel regression with mixed effects, and false discovery rate (FDR) control. A genome-wide scan for PPI was conducted using over 17,000 single nucleotide polymorphisms (SNPs) in 37 strains phenotyped. Eighty-nine SNPs were significant at a false discovery rate (FDR) of 5%. After accounting for long-range linkage disequilibrium, we found 3 independent QTLs located on murine chromosomes 1 and 13. One of the PPI positives corresponds to a region of human chromosome 6p which includes DTNBP1, a gene implicated in schizophrenia. Another region includes the gene Tsn which alters PPI when knocked out. These genes also appear to have correlated expression with PPI. Conclusions/Significance These results support the usefulness of using an improved in silico mapping method to identify QTLs for complex traits such as PPI which can be then be used for to help identify loci influencing schizophrenia in humans