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

Ankyrin repeat and SOCS box containing protein 4 (Asb-4) colocalizes with insulin receptor substrate 4 (IRS4) in the hypothalamic neurons and mediates IRS4 degradation

Abstract Background The arcuate nucleus of the hypothalamus regulates food intake. Ankyrin repeat and SOCS box containing protein 4 (Asb-4) is expressed in neuropeptide Y and proopiomelanocortin (POMC) neurons in the arcuate nucleus, target neurons in the regulation of food intake and metabolism by insulin and leptin. However, the target protein(s) of Asb-4 in these neurons remains unknown. Insulin receptor substrate 4 (IRS4) is an adaptor molecule involved in the signal transduction by both insulin and leptin. In the present study we examined the colocalization and interaction of Asb-4 with IRS4 and the involvement of Asb-4 in insulin signaling. Results In situ hybridization showed that the expression pattern of Asb-4 was consistent with that of IRS4 in the rat brain. Double in situ hybridization showed that IRS4 colocalized with Asb-4, and both Asb-4 and IRS4 mRNA were expressed in proopiomelanocortin (POMC) and neuropeptide Y (NPY) neurons within the arcuate nucleus of the hypothalamus. In HEK293 cells co-transfected with Myc-tagged Asb-4 and Flag-tagged IRS4, Asb-4 co-immunoprecipitated with IRS4; In these cells endogenous IRS4 also co-immunoprecipitated with transfected Myc-Asb-4; Furthermore, Asb-4 co-immunoprecipitated with IRS4 in rat hypothalamic extracts. In HEK293 cells over expression of Asb-4 decreased IRS4 protein levels and deletion of the SOCS box abolished this effect. Asb-4 increased the ubiquitination of IRS4; Deletion of SOCS box abolished this effect. Expression of Asb-4 decreased both basal and insulin-stimulated phosphorylation of AKT at Thr308. Conclusions These data demonstrated that Asb-4 co-localizes and interacts with IRS4 in hypothalamic neurons. The interaction of Asb-4 with IRS4 in cell lines mediates the degradation of IRS4 and decreases insulin signaling

Loss of Omi mitochondrial protease activity causes the neuromuscular disorder of mnd2 mutant mice

The mouse mutant mnd2 (motor neuron degeneration 2) exhibits muscle wasting, neurodegeneration, involution of the spleen and thymus, and death by 40 days of age(1,2). Degeneration of striatal neurons, with astrogliosis and microglia activation, begins at around 3 weeks of age, and other neurons are affected at later stages'. Here we have identified the mnd2 mutation as the missense mutation Ser276Cys in the protease domain of the nuclear-encoded mitochondrial serine protease Omi (also known as HtrA2 or Prss25). Protease activity of Omi is greatly reduced in tissues of mnd2 mice but is restored in mice rescued by a bacterial artificial chromosome transgene containing the wildtype Omi gene. Deletion of the PDZ domain partially restores protease activity to the inactive recombinant Omi protein carrying the Ser276Cys mutation, suggesting that the mutation impairs substrate access or binding to the active site pocket. Loss of Omi protease activity increases the susceptibility of mitochondria to induction of the permeability transition, and increases the sensitivity of mouse embryonic fibroblasts to stress-induced cell death. The neurodegeneration and juvenile lethality in mnd2 mice result from this defect in mitochondrial Omi protease.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62561/1/nature02052.pd

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

Integrated Bioinformatic Analysis Identifies Networks and Promising Biomarkers for Hepatitis B Virus-Related Hepatocellular Carcinoma

Chronic infection with hepatitis B virus (HBV) has long been recognized as a dominant hazard factor for hepatocellular carcinoma (HCC) and accounts for at least half of HCC instances globally. However, the underlying molecular mechanism of HBV-linked HCC has not been completely elucidated. Here, three microarray datasets, totally containing 170 tumoral samples and 181 adjacent normal tissues from the liver of patients suffering from HBV-related HCC assembled from the Gene Expression Omnibus (GEO) database, were subjected to integrated analysis of differentially expressed genes (DEGs). Subsequently, the analysis of function and pathway enrichment as well as the protein-protein interaction network (PPI) was performed. The ten hub genes screened out from the PPI network were further subjected to expression profile and survival analysis. Overall, 329 DEGs (67 upregulated and 262 downregulated) were identified. Ten DEGs with the highest degree of connectivity included cyclin-dependent kinase 1 (CDK1), cyclin B1 (CCNB1), cyclin B2 (CCNB2), PDZ-binding kinase (PBK), abnormal spindle microtubule assembly (ASPM), nuclear division cycle 80 (NDC80), aurora kinase A (AURKA), targeting protein for xenopus kinesin-like protein 2 (TPX2), kinesin family member 2C (KIF2C), and centromere protein F (CENPF). Kaplan-Meier analysis unveiled that overexpression levels of KIF2C and TPX2 were relevant to both the poor overall survival and relapse-free survival. In summary, the hub genes validated in the present study may provide promising targets for the diagnosis, prognosis, and therapy of HBV-associated HCC. Additionally, our work uncovers various crucial biological components (e.g., extracellular exosome) and signaling pathways that participate in the progression of HCC induced by HBV, serving comprehensive knowledge of the mechanisms regarding HBV-related HCC

Multicascaded Feature Fusion-Based Deep Learning Network for Local Climate Zone Classification Based on the So2Sat LCZ42 Benchmark Dataset

A detailed investigation of the microclimate is beneficial for optimizing the urban inner/spatial pattern to enhance thermal comfort or even reduce heatwave disasters, whereas accurately classifying local climate zones (LCZs) severely restricts analysis of thermal characterization. Generally, deep learning-based approaches are effective for adaptive LCZ mapping, yet they often have poor accuracy because inadequate cascade feature extraction patterns may not adapt to the fuzzy LCZ boundaries produced by intricate urban textures, especially when using large-scale datasets. To address these issues, we propose a novel CNN model in which we design a strategy that incorporates a triple feature fusion pattern to enhance LCZ recognition based on the So2sat LCZ 42 large-scale annotated dataset. The approach connects multilayer cascaded information to participate in category judgment, which avoids the loss of effective feature information via continuous cascade transformation as much as possible. The results show that the overall accuracy and kappa coefficient of the proposed model reach 0.70 and 0.68, respectively, manifesting an improvement of approximately 4.47% and 6.25% over advanced LCZ classification approaches. In particular, the accuracy of the proposed approach improves even further after the fusion structure or layer depth is partially removed or reduced, respectively. Finally, we discuss several items, including the effectiveness of different parameters and cascaded feature fusion patterns, the superiority of multilayer cascade feature fusion, the mapping impact of seasons and cloud cover, and even some other issues in LCZ mapping. This article will facilitate improvements in the research precision of urban thermal environments

Anti-Inflammatory and Anti-Oxidative Activity of Indole-3-Acetic Acid Involves Induction of HO-1 and Neutralization of Free Radicals in RAW264.7 Cells

The cellular and molecular mechanisms by which indole-3-acetic acid (IAA), a tryptophan-derived metabolite from gut microbiota, attenuates inflammation and oxidative stress has not been fully elucidated. The present study was to unearth the protective effect and underlying mechanism of IAA against lipopolysaccharide (LPS)-induced inflammatory response and free radical generation in RAW264.7 macrophages. IAA significantly ameliorated LPS-induced expression of interleukin-1β (IL-1β), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1) as well as generation of reactive oxidative species (ROS) and nitric oxide (NO). LPS-triggered nuclear translocation of nuclear factor kappa B (NF-κB) p65 was mitigated by IAA treatment. Further, an up-regulation of heme oxygenase-1 (HO-1) was observed in IAA-treated cells in dose-dependent manner under both normal and LPS-stimulated condition. Interference of HO-1 activity by tin protoporphyrin IX (SnPP) impeded the alleviative effects of IAA on expression of IL-1β and IL-6 induced by LPS, whereas demonstrated no effect on its suppression of ROS and NO production. This result suggests a HO-1-dependent anti-inflammatory effect of IAA and its direct scavenging action on free radicals. Treatment with CH-223191, a specific antagonist of aryl hydrocarbon receptor (AhR), showed no significant effects on the beneficial role of IAA against inflammation and free radical generation. In summary, our findings indicate that IAA alleviates LPS-elicited inflammatory response and free radical generation in RAW264.7 macrophages by induction of HO-1 and direct neutralization of free radicals, a mechanism independent of AhR

Graph-Based Transformer with Cross-Candidate Verification for Semantic Parsing

In this paper, we present a graph-based Transformer for semantic parsing. We separate the semantic parsing task into two steps: 1) Use a sequence-to-sequence model to generate the logical form candidates. 2) Design a graph-based Transformer to rerank the candidates. To handle the structure of logical forms, we incorporate graph information to Transformer, and design a cross-candidate verification mechanism to consider all the candidates in the ranking process. Furthermore, we integrate BERT into our model and jointly train the graph-based Transformer and BERT. We conduct experiments on 3 semantic parsing benchmarks, ATIS, JOBS and Task Oriented semantic Parsing dataset (TOP). Experiments show that our graph-based reranking model achieves results comparable to state-of-the-art models on the ATIS and JOBS datasets. And on the TOP dataset, our model achieves a new state-of-the-art result

DQX1, an RNA-dependent ATPase homolog with a novel DEAQ box: expression pattern and genomic sequence comparison of the human and mouse genes

DQX1 is a novel gene related to the RNA-dependent ATPases. The gene was classified as a member of the DEAD/H family on the basis of the conserved order and spacing of ten short protein motifs. The unique features of DQX1 include replacement of the signature DEAH motif with DEAQ and the absence of the helicase motif. We determined the coding sequences of human and mouse DQX1, which encode proteins of 717 and 718 amino acids with 84% amino acid sequence identity. The 3.2-kb Dqx1 transcript has highest expression in muscle and liver. DQX1 is located between AUP1 and HOX11L1 in a gene-dense region of human Chromosome (Chr) 2p13 and mouse Chr 6. Although DQX1 is within the nonrecombinant region for the mouse neuromuscular mutant mnd2, no difference in coding sequence, transcript length, or transcript abundance was observed between normal mice and mnd2 mutant mice. The ubiquitous expression of DQX1 and its close phylogenetic relationship to the yeast pre-mRNA processing (Prp) proteins suggest a role in cellular RNA metabolism.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42125/1/335-12-6-456_10120456.pd