Psychological contract’s effect on job mobility: Evidence from Chinese construction worker

The subject of this study is that the psychological contract (PC) approaches to job mobility within the construction industry with special reference to migrant construction workers in China. Using a semi-structured interview to elicit a full range of the PC’s con- tent of construction worker, we unravel the mechanism of such contract to influence the informal job mobility of workers through the lens of the evolutionary game framework. The results demonstrate that, in the case of fulfilling PC, the informal job mobility of workers is under control, and both workers and employers benefit from this situation. This study deepens the understanding of the PC’s effect on the job mobility of construction workers in China during the course of economic change. The theoretical and practical implications are discusse

Perinatal Blockade of B7-1 and B7-2 Inhibits Clonal Deletion of Highly Pathogenic Autoreactive T Cells

A number of in vitro studies have suggested that costimulatory molecules B7-1 and B7-2 and their receptor CD28 can promote clonal deletion, and limited in vivo studies have indicated that CD28 is involved in the clonal deletion of some T cells. However, the significance of B7-mediated clonal deletion in preventing autoimmune diseases has not been studied systematically. Here we report that the perinatal blockade of B7-1 and B7-2 substantially inhibits the clonal deletion of T cells in the thymus and leads to an accumulation of T cells capable of inducing fatal multiorgan inflammation. These results reveal a critical role for costimulatory molecules B7-1 and B7-2 in deleting pathogenic autoreactive T cells in the thymus. The critical role of B7-1 and B7-2 in T cell clonal deletion may explain, at least in part, the paradoxical increase of autoimmune disease in mice deficient for this family of costimulatory molecules, such as cytotoxic T lymphocyte associated molecule 4, CD28, and B7-2. The strong pathogenicity of the self-reactive T cells supports a central hypothesis in immunology, which is that clonal deletion plays an important role in preventing autoimmune diseases

MTHFD2 Overexpression Predicts Poor Prognosis in Renal Cell Carcinoma and is Associated with Cell Proliferation and Vimentin-Modulated Migration and Invasion

Background/Aims: To investigate the role of methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) in the clinical prognosis and cell biology of renal cell carcinoma (RCC). Methods: A total of 137 RCC tissues were evaluated by immunohistochemistry. The relationship between MTHFD2 overexpression and clinical parameters and vimentin expression was assessed. Kaplan-Meier curves and the log-rank test were applied for survival analysis according to MTHFD2 and vimentin expression in RCC tissues. The expression of MTHFD2 mRNA and protein was examined by quantitative reverse transcription PCR and western blotting, respectively. To determine further the biological activity of MTHFD2 in RCC, 786-O cells were transfected with short hairpin RNA specifically targeting MTHFD2 (shMTHFD2) with or without tumor necrosis factor (TNF)-α stimulation. Cell proliferation, cell migration and invasion and drug sensitivity were subsequently assessed using Cell Counting Kit-8, wound healing, and Transwell assays. Results: Immunohistochemical analysis demonstrated that both MTHFD2 and vimentin overexpression was positively associated with clinical staging, pathological grade, and poor overall survival (all P < 0.05). MTHFD2 expression was closely correlated with vimentin overexpression in RCC (r = 0.402, P < 0.001). After knocking down MTHFD2 expression in 786-O cells, decreased cell proliferation, migration, and invasion were observed and accompanied by the reduced expression of vimentin. The effects of MTHFD2 down-regulation could be partially restrained by TNF-α treatment. Vimentin expression and cell migration and invasion, but not cell proliferation, were reversed by TNF-α stimulation. Furthermore, treatment of 786-O cells with shMTHFD2 increased their sensitivity to chemotherapy drugs. Conclusion: The current results demonstrated that MTHFD2 was overexpressed in RCC and associated with poor clinical characteristics, vimentin expression, and cellular features connected to malignant disease, thus, implicating MTHFD2 as a potential target for RCC therapy

A Dinucleotide Deletion in CD24 Confers Protection against Autoimmune Diseases

It is generally believed that susceptibility to both organ-specific and systemic autoimmune diseases is under polygenic control. Although multiple genes have been implicated in each type of autoimmune disease, few are known to have a significant impact on both. Here, we investigated the significance of polymorphisms in the human gene CD24 and the susceptibility to multiple sclerosis (MS) and systemic lupus erythematosus (SLE). We used cases/control studies to determine the association between CD24 polymorphism and the risk of MS and SLE. In addition, we also considered transmission disequilibrium tests using family data from two cohorts consisting of a total of 150 pedigrees of MS families and 187 pedigrees of SLE families. Our analyses revealed that a dinucleotide deletion at position 1527∼1528 (P1527(del)) from the CD24 mRNA translation start site is associated with a significantly reduced risk (odds ratio = 0.54 with 95% confidence interval = 0.34–0.82) and delayed progression (p = 0.0188) of MS. Among the SLE cohort, we found a similar reduction of risk with the same polymorphism (odds ratio = 0.38, confidence interval = 0.22–0.62). More importantly, using 150 pedigrees of MS families from two independent cohorts and the TRANSMIT software, we found that the P1527(del) allele was preferentially transmitted to unaffected individuals (p = 0.002). Likewise, an analysis of 187 SLE families revealed the dinucleotide-deleted allele was preferentially transmitted to unaffected individuals (p = 0.002). The mRNA levels for the dinucleotide-deletion allele were 2.5-fold less than that of the wild-type allele. The dinucleotide deletion significantly reduced the stability of CD24 mRNA. Our results demonstrate that a destabilizing dinucleotide deletion in the 3′ UTR of CD24 mRNA conveys significant protection against both MS and SLE

Lithofacies logging identification for strongly heterogeneous deep-buried reservoirs based on improved Bayesian inversion: The Lower Jurassic sandstone, Central Junggar Basin, China

The strong heterogeneity characteristics of deep-buried clastic low-permeability reservoirs may lead to great risks in hydrocarbon exploration and development, which makes the accurate identification of reservoir lithofacies crucial for improving the obtained exploration results. Due to the very limited core data acquired from deep drilling, lithofacies logging identification has become the most important method for comprehensively obtaining the rock information of deep-buried reservoirs and is a fundamental task for carrying out reservoir characterization and geological modeling. In this study, a machine learning method is introduced to lithofacies logging identification, to explore an accurate lithofacies identification method for deep fluvial-delta sandstone reservoirs with frequent lithofacies changes. Here Sangonghe Formation in the Central Junggar Basin of China is taken as an example. The K-means-based synthetic minority oversampling technique (K-means SMOTE) is employed to solve the problem regarding the imbalanced lithofacies data categories used to calibrate logging data, and a probabilistic calibration method is introduced to correct the likelihood function. To address the situation in which traditional machine learning methods ignore the geological deposition process, we introduce a depositional prior for controlling the vertical spreading process based on a Markov chain and propose an improved Bayesian inversion process for training on the log data to identify lithofacies. The results of a series of experiments show that, compared with the traditional machine learning method, the new method improves the recognition accuracy by 20%, and the predicted petrographic vertical distribution results are consistent with geological constraints. In addition, SMOTE and probabilistic calibration can effectively handle data imbalance problems so that different categories can be adequately learned. Also the introduction of geological prior has a positive impact on the overall distribution, which significantly improves the accuracy and recall rate of the method. According to this comprehensive analysis, the proposed method greatly enhanced the identification of the lithofacies distributions in the Sangonghe Formation. Therefore, this method can provide a tool for logging lithofacies interpretation of deep and strongly heterogeneous clastic reservoirs in fluvial-delta and other depositional environments

Intracellular CD24 disrupts the ARF–NPM interaction and enables mutational and viral oncogene-mediated p53 inactivation

CD24 is overexpressed in nearly 70% human cancers, whereas TP53 is the most frequently mutated tumour-suppressor gene that functions in a context-dependent manner. Here we show that both targeted mutation and short hairpin RNA (shRNA) silencing of CD24 retard the growth, progression and metastasis of prostate cancer. CD24 competitively inhibits ARF binding to NPM, resulting in decreased ARF, increase MDM2 and decrease levels of p53 and the p53 target p21/CDKN1A. CD24 silencing prevents functional inactivation of p53 by both somatic mutation and viral oncogenes, including the SV40 large T antigen and human papilloma virus 16 E6-antigen. In support of the functional interaction between CD24 and p53, in silico analyses reveal that TP53 mutates at a higher rate among glioma and prostate cancer samples with higher CD24 mRNA levels. These data provide a general mechanism for functional inactivation of ARF and reveal an important cellular context for genetic and viral inactivation of TP53. P53 is a tumour suppressor that is frequently mutated or downregulated in cancer. Here, Wang et al. show that CD24, a molecule frequently overexpressed in cancer, promotes p53 degradation by disrupting a regulatory ARF–MDM2 interaction, and silencing CD24 prevents the downregulation of p53

Chinese university students’ preferences for physical activity incentive programs: a discrete choice experiment

PurposeThis study aims to explore and compare Chinese university students’ preferences for various physical activity motivation programs.Patients and methodsA cross-sectional study was conducted in China from February 25 to March 25, 2022. Participants anonymously completed an online questionnaire based on a DCE. A total of 1,358 university students participated in the survey. The conditional logit model (CLM), willingness to accept (WTA), and propensity score matching (PSM) were used to assess college students’ preferences for different attributes and levels of physical activity incentive programs.ResultsRespondents identified the number of bonus, exercise time, and academic rewards as the three most significant attributes of the athletic incentive program. The importance of each attribute varied based on individual characteristics such as gender and BMI. In CLM, college students displayed a preference for a “¥4” bonus amount (OR: 2.04, 95% CI 1.95–2.13), “20 min” of exercise time (OR: 1.85, 95% CI 1.79–1.92), and “bonus points for comprehensive test scores” as academic rewards (OR: 1.33, 95% CI 1.28–1.37). According to the WTA results, college students were willing to accept the highest cost to obtain academic rewards tied to composite test scores.ConclusionThe number of bonus, exercise time, and academic rewards emerge as the three most crucial attributes of physical activity incentive programs. Furthermore, college students with different characteristics exhibit heterogeneity in their preferences for such programs. These findings can guide the development of programs and policies aimed at motivating college students to engage in physical activities

Modulation of NKT Cell Development by B7-CD28 Interaction: An Expanding Horizon for Costimulation

It has been demonstrated that the development of NKT cells requires CD1d. The contribution of costimulatory molecules in this process has not been studied. Here we show that in mice with targeted mutations of B7-1/2 and CD28, the TCRβ+α-Galcer/CD1d + (iVα14 NKT) subset is significantly reduced in the thymus, spleen and liver. This is mainly due to decreased cell proliferation; although increased cell death in the thymi of CD28-deficient mice was also observed. Moreover, in the B7-1/2- and CD28-deficient mice, we found a decreased percentage of the CD4−NK1.1+ subset and a correspondingly increased portion of the CD4+NK1.1− subset. In addition, the mice with a targeted mutation of either B7 or CD28 had a reduced susceptibility to Con A induced hepatitis, which is known to be mediated by NKT cells. Our results demonstrate that the development, maturation and function of NKT cell are modulated by the costimulatory pathway and thus expand the horizon of costimulation into NKT, which is widely viewed as a bridge between innate and adaptive immunity. As such, costimulation may modulate all major branches of cell-mediated immunity, including T cells, NK cells and NKT cells

Modulation of NKT Cell Development by B7-CD28 Interaction: An Expanding Horizon for Costimulation

It has been demonstrated that the development of NKT cells requires CD1d. The contribution of costimulatory molecules in this process has not been studied. Here we show that in mice with targeted mutations of B7-1/2 and CD28, the TCRβ+α-Galcer/CD1d + (iVα14 NKT) subset is significantly reduced in the thymus, spleen and liver. This is mainly due to decreased cell proliferation; although increased cell death in the thymi of CD28-deficient mice was also observed. Moreover, in the B7-1/2- and CD28-deficient mice, we found a decreased percentage of the CD4−NK1.1+ subset and a correspondingly increased portion of the CD4+NK1.1− subset. In addition, the mice with a targeted mutation of either B7 or CD28 had a reduced susceptibility to Con A induced hepatitis, which is known to be mediated by NKT cells. Our results demonstrate that the development, maturation and function of NKT cell are modulated by the costimulatory pathway and thus expand the horizon of costimulation into NKT, which is widely viewed as a bridge between innate and adaptive immunity. As such, costimulation may modulate all major branches of cell-mediated immunity, including T cells, NK cells and NKT cells.</p