BRST Cohomology is Lie Algebroid Cohomology

In this paper we demonstrate that the exterior algebra of an Atiyah Lie algebroid generalizes the familiar notions of the physicist's BRST complex. To reach this conclusion, we develop a general picture of Lie algebroid morphisms as commutative diagrams between algebroids preserving the geometric structure encoded in their brackets. We illustrate that a necessary and sufficient condition for such a diagram to define a morphism is that the two algebroids possess gauge-equivalent connections. This observation indicates that the set of Lie algebroid morphisms should be regarded as equivalent to the set of local diffeomorphisms and gauge transformations. Moreover, a Lie algebroid morphism being a chain map in the exterior algebra sense ensures that morphic algebroids are cohomologically equivalent. The Atiyah Lie algebroids derived from principal bundles with common base manifolds and structure groups may therefore be divided into equivalence classes of morphic algebroids. Each equivalence class possesses a representative which we refer to as the trivialized Lie algebroid, and we show that the exterior algebra of the trivialized algebroid gives rise to the BRST complex. We conclude by illustrating the usefulness of Lie algebroid cohomology in computing quantum anomalies. In particular, we pay close attention to the fact that the geometric intuition afforded by the Lie algebroid (which was absent in the naive BRST complex) provides hints of a deeper picture that simultaneously geometrizes the consistent and covariant forms of the anomaly. In the algebroid construction, the difference between the consistent and covariant anomalies is simply a different choice of basis.Comment: 24 pages, 1 figure, LaTe

Is the Pareto-Lévy law a good representation of income distributions?

Mandelbrot (1960) proposed using the so-called Pareto-Lévy class of distributions as a framework for representing income distributions. We argue in this paper that the Pareto-Lévy distribution is an interesting candidate for representing income distribution because its parameters are easy to interpret and it satisfies a specific invariance-under-aggregation property. We also demonstrate that the Gini coefficient can be expressed as a simple formula of the parameters of the Pareto-Lévy distribution. We subsequently use wage and income data for Norway and seven other OECD countries to fit the Pareto- Lévy distribution as well as the Generalized Beta type II (GB2) distribution. The results show that the Pareto-Lévy distribution fits the data better than the GB2 distribution for most countries, despite the fact that GB2 distribution has four parameters whereas the Pareto-Lévy distribution has only three

Compassion, Discrimination, and Prosocial Behaviors: Young Diasporic Chinese During the COVID-19 Pandemic

The coronavirus disease 2019 (COVID-19) pandemic has fueled anti-Asian, especially anti-Chinese sentiments worldwide, which may negatively impact diasporic Chinese youths\u27 adjustment and prosocial development. This study examined the association between compassion, discrimination and prosocial behaviors in diasporic Chinese youths during the COVID-19 pandemic. 360 participants participated and completed the multi-country, cross-sectional, web-based survey between April 22 and May 9, 2020, the escalating stage of the pandemic. This study found compassion as prosocial behaviors\u27 proximal predictor, while discrimination independently predicted participation in volunteering, and could potentially enhance the association between compassion and charitable giving. These findings suggest that prosociality among young people is sensitive to social context, and that racial discrimination should be considered in future prosocial studies involving young members of ethnic and racial minorities

Cancer apelin receptor suppresses vascular mimicry in malignant melanoma

Several reports indicate that apelin is often over-expressed in tumors, and therefore it has been suggested that the apelin–apelin receptor (APJ) system may induce tumor progression. In contrast, our previous research revealed high expression of the apelin–APJ system in tumor blood vessels, suggesting its involvement in the regulation of tumor vessel formation and normalization, resulting in the suppression of tumor growth by promoting the infiltration of T cells. Thus, the effect of the apelin–APJ system on tumors remains controversial. In this report, to clarify the effect of apelin in tumor cells, we analyzed the function of APJ in tumor cells using APJ knock out (KO) mice. In APJ-KO mice, Apelin overexpression in B16/BL6 (B16) melanoma cells induced greater tumor growth than controls. In an APJ-KO melanoma inoculation model, although angiogenesis is suppressed compared to wild type, no difference is evident in tumor growth. We found that APJ deficiency promoted vascular mimicry in tumors. In vitro, cultured APJ-KO B16 cells demonstrated a spindle-like shape. This phenotypic change was thought to be induced by epithelial–mesenchymal transition (EMT) based on evidence that APJ-KO B16 cells show persistently high levels of the mesenchymal maker, Zeb1; however, we found that EMT did not correlate with the transforming growth factor-β/smad signaling pathway in our model. We propose that apelin-APJ system in cancer cells induces tumor growth but negatively regulates EMT and tumor malignancy

Mutations in sphingosine-1-phosphate lyase cause nephrosis with ichthyosis and adrenal insufficiency

Steroid-resistant nephrotic syndrome (SRNS) causes 15% of chronic kidney disease cases. A mutation in 1 of over 40 monogenic genes can be detected in approximately 30% of individuals with SRNS whose symptoms manifest before 25 years of age. However, in many patients, the genetic etiology remains unknown. Here, we have performed whole exome sequencing to identify recessive causes of SRNS. In 7 families with SRNS and facultative ichthyosis, adrenal insufficiency, immunodeficiency, and neurological defects, we identified 9 different recessive mutations in SGPL1, which encodes sphingosine-1-phosphate (S1P) lyase. All mutations resulted in reduced or absent SGPL1 protein and/or enzyme activity. Overexpression of cDNA representing SGPL1 mutations resulted in subcellular mislocalization of SGPL1. Furthermore, expression of WT human SGPL1 rescued growth of SGPL1-deficient dpl1. yeast strains, whereas expression of disease-associated variants did not. Immunofluorescence revealed SGPL1 expression in mouse podocytes and mesangial cells. Knockdown of Sgpl1 in rat mesangial cells inhibited cell migration, which was partially rescued by VPC23109, an S1P receptor antagonist. In Drosophila, Sply mutants, which lack SGPL1, displayed a phenotype reminiscent of nephrotic syndrome in nephrocytes. WT Sply, but not the disease-associated variants, rescued this phenotype. Together, these results indicate that SGPL1 mutations cause a syndromic form of SRNS

Genome-Wide Association Studies in an Isolated Founder Population from the Pacific Island of Kosrae

It has been argued that the limited genetic diversity and reduced allelic heterogeneity observed in isolated founder populations facilitates discovery of loci contributing to both Mendelian and complex disease. A strong founder effect, severe isolation, and substantial inbreeding have dramatically reduced genetic diversity in natives from the island of Kosrae, Federated States of Micronesia, who exhibit a high prevalence of obesity and other metabolic disorders. We hypothesized that genetic drift and possibly natural selection on Kosrae might have increased the frequency of previously rare genetic variants with relatively large effects, making these alleles readily detectable in genome-wide association analysis. However, mapping in large, inbred cohorts introduces analytic challenges, as extensive relatedness between subjects violates the assumptions of independence upon which traditional association test statistics are based. We performed genome-wide association analysis for 15 quantitative traits in 2,906 members of the Kosrae population, using novel approaches to manage the extreme relatedness in the sample. As positive controls, we observe association to known loci for plasma cholesterol, triglycerides, and C-reactive protein and to a compelling candidate loci for thyroid stimulating hormone and fasting plasma glucose. We show that our study is well powered to detect common alleles explaining ≥5% phenotypic variance. However, no such large effects were observed with genome-wide significance, arguing that even in such a severely inbred population, common alleles typically have modest effects. Finally, we show that a majority of common variants discovered in Caucasians have indistinguishable effect sizes on Kosrae, despite the major differences in population genetics and environment

Mutations in KEOPS-Complex Genes Cause Nephrotic Syndrome with Primary Microcephaly

Galloway-Mowat syndrome (GAMOS) is an autosomal-recessive disease characterized by the combination of early-onset nephrotic syndrome (SRNS) and microcephaly with brain anomalies. Here we identified recessive mutations in OSGEP, TP53RK, TPRKB, and LAGE3, genes encoding the four subunits of the KEOPS complex, in 37 individuals from 32 families with GAMOS. CRISPR-Cas9 knockout in zebrafish and mice recapitulated the human phenotype of primary microcephaly and resulted in early lethality. Knockdown of OSGEP, TP53RK, or TPRKB inhibited cell proliferation, which human mutations did not rescue. Furthermore, knockdown of these genes impaired protein translation, caused endoplasmic reticulum stress, activated DNA-damage-response signaling, and ultimately induced apoptosis. Knockdown of OSGEP or TP53RK induced defects in the actin cytoskeleton and decreased the migration rate of human podocytes, an established intermediate phenotype of SRNS. We thus identified four new monogenic causes of GAMOS, describe a link between KEOPS function and human disease, and delineate potential pathogenic mechanisms

The effect of pension wealth on private savings. Results from an extended life cycle model

An extended life cycle model is used to investigate how variation in the level of expected pensions influences non-pension wealth accumulation. We try to explain why the offset effects between pension wealth and private savings are not one to one by accounting for different risks and market imperfections, which includes uninsured risk on earnings, mortality risk, borrowing constraints and bequest motive. The model is calibrated on Norwegian household data from 1992 to 2005. Based on the calibrated model, simulations are performed to explore consequences of introducing these factors. The result shows that by simply accounting these risks and constraints, we can explain most of the departure between empirical findings and theoretical prediction.publishedVersio