What Motivates People to Purchase NFTs? A Self-Discrepancy Perspective

Non-fungible token (NFT) sales change unpredictably and trend downward, which motivates us to explore the determinants of why people purchase NFTs. To answer this question, we develop a model based on the self-discrepancy theory and symbolic self-completion theory. The model proposes that the desire for self-completion is a key driver for such purchases, and functional properties of attractiveness, price utility, emotional properties of aesthetics and playfulness, and social properties of parasocial interaction and social relationship support are antecedents of the desire for self-completion. We also hypothesize that psychological ownership moderates the relationship between the desire for symbolic self-completion and purchase intention. The model will be validated using survey data collected from some popular NFT platforms. The results are expected to support our hypothesis, which contributes to the understanding of the purchase of NFTs by extending the theory of self-discrepancy and adds a new perspective to research on NFTs

H9N2 Viruses Isolated From Mammals Replicated in Mice at Higher Levels Than Avian-Origin Viruses

H9N2 subtype influenza A virus (IAV) has more than 20 genotypes that are able to cross species barriers and expand from birds to mammals and humans. To better understand the impact of different H9N2 genotypes and their characteristics, five H9N2 viruses from different hosts including chickens, geese, pigs, mink, and humans representing the B69 88(Gs/14, Ck/15, and Mi/14), B35 (Sw/08) and G9 genotypes (Hu/04) were infected in chicken and mice. In mice, mammal-origin viruses replicated at higher levels in the lungs compared to avian viruses. The goose-virus replicated at the lowest levels indicating poor adaptation. Increased pro-inflammatory cytokines were positively correlated with viral loads in the lung. In chickens, all viruses were excreted from cloacal and/or oropharyngeal swabs. Interestingly, Mink-origin virus exhibited higher virulence and replication in mice and chickens. Our data indicate that mammal-origin H9N2 viruses are more adapted and virulent in mice than the avian-origin viruses

Effects of paternal obesity on maternal-neonatal outcomes and long-term prognosis in adolescents

ObjectiveThis study evaluated whether paternal body mass index (BMI) before pregnancy was a risk factor for maternal-neonatal outcomes and long-term prognosis in offspring.MethodsThis study included 29,518 participants from eight cities in Fujian, China using a stratified cluster random sampling method from May to September 2019. They were divided into four groups based on paternal BMI. Univariate and multivariate logistic regression were used to explore the relationship between paternal BMI groups, maternal-neonatal outcomes, and long-term prognosis in offspring. Further subgroup analysis was conducted to examine the stability of the risk. ResultsThe incidences of hypertensive disorder complicating pregnancy (HDCP), cesarean delivery, gestational weight gain (GWG) over guideline, and macrosomia were significantly higher in the paternal overweight and obesity group. Importantly, this study demonstrated that the incidence of asthma, hand-foot-and-mouth disease (HFMD), anemia, dental caries, and obesity of adolescents in paternal obesity increased. Furthermore, logistic regression and subgroup analysis confirm paternal obesity is a risk factor for HDCP, cesarean delivery, and macrosomia. It caused poor long-term prognosis in adolescents, including asthma, dental caries, and HFMD.ConclusionsPaternal obesity is a risk factor for adverse maternal-neonatal outcomes and poor long-term prognosis in adolescents. In addition to focusing on maternal weight, expectant fathers should pay more attention to weight management since BMI is a modifiable risk factor. Preventing paternal obesity can lead to better maternal and child outcomes. It would provide new opportunities for chronic diseases

A VOTING MODEL ON GRAPHS

Bachelor'sBACHELOR OF SCIENCE (HONOURS

Sevoflurane inhibits cholangiocarcinoma via Wnt/β-catenin signaling pathway

Abstract Background Cholangiocarcinoma (CCA) is a refractory malignancy derived from bile duct epithelial cells. This study aimed to explore the role and molecular mechanisms of action of sevoflurane in CCA. Methods CCK-8 assay was used to assess the proliferation of cholangiocarcinoma cells, and flow cytometry was used to detect cholangiocarcinoma cell apoptosis. The effects of sevoflurane on TFK1 and QBC939 cell migration and invasion were investigated using a Transwell assay. Western blotting and RT-qPCR were used to assess the expression of apoptosis-related proteins and genes, and gene expression of the Wnt/β-catenin signaling pathway. Results Our study found that sevoflurane inhibited cholangiocarcinoma cell proliferation in a dose-dependent manner. In addition, sevoflurane induced cholangiocarcinoma cell apoptosis, inhibited cholangiocarcinoma cell migration and invasion, as well as the Wnt/β-catenin signaling pathway evidenced by decreased Wnt3a, β-catenin, c-Myc, and Cyclin D1 protein and mRNA expression, reduced p-GSK3β protein expression and p-GSK3β/GSK3β ratio. Further mechanistic studies revealed that Wnt/β-catenin pathway inducer SKL2001 reversed the inhibitory effect of sevoflurane on cholangiocarcinoma cells. Conclusions Sevoflurane induces apoptosis and inhibits the growth, migration, and invasion of cholangiocarcinoma cells by inhibiting the Wnt/β-catenin signaling pathway. This study not only revealed the role of sevoflurane in the development of CCA but also elucidated new therapeutic agents for CCA

Quantitative Proteomic Analysis of Hepatic Tissue of T2DM Rhesus Macaque

Type 2 diabetes mellitus (T2DM) is a metabolic disorder that severely affects human health, but the pathogenesis of the disease remains unknown. The high-fat/high-sucrose diets combined with streptozotocin- (STZ-) induced nonhuman primate animal model of diabetes are a valuable research source of T2DM. Here, we present a study of a STZ rhesus macaque model of T2DM that utilizes quantitative iTRAQ-based proteomic method. We compared the protein profiles in the liver of STZ-treated macaques as well as age-matched healthy controls. We identified 171 proteins differentially expressed in the STZ-treated groups, about 70 of which were documented as diabetes-related gene in previous studies. Pathway analyses indicated that the biological functions of differentially expressed proteins were related to glycolysis/gluconeogenesis, fatty acid metabolism, complements, and coagulation cascades. Expression change in tryptophan metabolism pathway was also found in this study which may be associations with diabetes. This study is the first to explore genome-wide protein expression in hepatic tissue of diabetes macaque model using HPLC-Q-TOF/MS technology. In addition to providing potential T2DM biomarkers, this quantitative proteomic study may also shed insights regarding the molecular pathogenesis of T2DM