The effect of students' effort-reward imbalance on learning engagement: the mediating role of learned helplessness and the moderating role of social support.

Introduction: To explore the predictive effect of effort-reward imbalance on students' learning engagement and to elucidate the underlying mechanism, 796 students were selected for a survey. Methods: The participants were required to complete four scales: the Effort-reward Imbalance Scale, the Learning Engagement Scale, the Learned Helplessness Questionnaire, and the Perceived Social Support Scale. Results: (1) Students' effort-reward imbalance significantly and negatively predicts their learning engagement; (2) Learned helplessness serves as a mediator in the relationship between students' effort-reward imbalance and learning engagement; (3) Social support plays a moderating role in the association between effort-reward imbalance and learned helplessness. High levels of social support can buffer the impact of an effort-reward imbalance on learned helplessness, and the protective effect of social support is more obvious when the effort-reward imbalance is low. Discussion: The present study revealed how an effort-reward imbalance affects learning engagement among students through the dimensions of learned helplessness and perceived social support. The constructed model not only further clarifies the mechanism underlying the relationship between effort-reward imbalance and learning engagement but also holds significant implications for guiding students' education.

Prediction and validation of common targets in atherosclerosis and non-small cell lung cancer influenced by atorvastatin.

BACKGROUND: Cardiovascular disease and cancer are the main causes of morbidity and mortality worldwide. Studies have shown that these two diseases may have some common risk factors. Atorvastatin is mainly used for the treatment of atherosclerosis in clinic. A large number of studies show that atorvastatin may produce anti-tumor activities. This study aimed to predict the common targets of atorvastatin against atherosclerosis and non-small cell lung cancer (NSCLC) based on network pharmacology. METHODS: The target genes of atherosclerosis and NSCLC were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. The disease-target-component model map and the core network were obtained using Cytoscape 3.7.1. The MTS and wound healing assay were used to detect the effect of atorvastatin on cell viability and migration of A549 cells. The expression of potential common target genes of atorvastatin against atherosclerosis and NSCLC were confirmed in A549 cells and lung cancer tissues of patients. RESULTS: We identified 15 identical pathogenic genes, and four of which (MMP9, MMP12, CD36, and FABP4) were considered as the key target genes of atorvastatin in anti-atherosclerosis and NSCLC. The MTS and wound healing assays revealed that atorvastatin decreased A549 cells migration significantly. Atorvastatin markedly decreased the expression of MMP9, MMP12, CD36, and FABP4 in A549 cells and patients were treated with atorvastatin. CONCLUSIONS: This study demonstrated 15 common pathogenic genes in both atherosclerosis and NSCLC. And verified that MMP 9, MMP 12, CD 36 and FABP 4 might be the common target genes of atorvastatin in anti-atherosclerosis and NSCLC.

The novel small molecule BH3 mimetic nobiletin synergizes with vorinostat to induce apoptosis and autophagy in small cell lung cancer.

Small cell lung cancer (SCLC) is a highly lethal subtype of lung cancer with few therapeutic options; therefore, the identification of new targets and drugs with potent combination therapy is desirable. We previously screened BH3 mimetics from a natural product library, and in this study, we validated nobiletin as a BH3 mimetic. Specifically, we observed its combination potential and mechanism with vorinostat in SCLC in vitro and in vivo. The results showed that combination treatment with nobiletin and vorinostat reduced the proliferation of SCLC H82 cells and increased the levels of apoptotic proteins such as cleaved caspase-9 and cleaved PARP. The combination treatment increased LC3-II expression and induced autophagic cell death. In addition, this treatment significantly inhibited H82 cell xenograft SCLC tumor growth in nude mice. The combination treatment with nobiletin and vorinostat efficiently increased autophagy by inhibiting the PI3K-AKT-mTOR pathway and promoting dissociation of the BCL-2 and Beclin 1 complex, increasing the level of isolated Beclin 1 to stimulate autophagy. Molecular docking and surface plasmon resonance analysis showed that nobiletin stably bound to the BCL-2, BCL-XL and MCL-1 proteins with high affinity in a concentration-dependent manner. These results suggest that nobiletin is a BH3-only protein mimetic. Furthermore, the combination of nobiletin with vorinostat increased histone H3K9 and H3K27 acetylation levels in SCLC mouse tumor tissue and enhanced the expression of the BH3-only proteins BIM and BID. We conclude that nobiletin is a novel natural BH3 mimetic that can cooperate with vorinostat to induce apoptosis and autophagy in SCLC.

Starch phosphorylase 2 is essential for cellular carbohydrate partitioning in maize.

Carbohydrate partitioning is essential for plant growth and development, and its hindrance will result in excess accumulation of carbohydrates in source tissues. Most of the related mutants in maize (Zea mays L.) display impaired whole-plant sucrose transport, but other mechanisms affecting carbohydrate partitioning have seldom been reported. Here, we characterized chlorotic leaf3 (chl3), a recessive mutation causing leaf chlorosis with starch accumulation excessively in bundle sheath chloroplasts, suggesting that chl3 is defective in carbohydrate partitioning. Positional cloning revealed that the chl3 phenotype results from a frameshift mutation in ZmPHOH, which encodes starch phosphorylase 2. Two mutants in ZmPHOH exhibited the same phenotype as chl3, and both alleles failed to complement the chl3 mutant phenotype in an allelism test. Inactivation of ZmPHOH in chl3 leaves reduced the efficiency of transitory starch conversion, resulting in increased leaf starch contents and altered carbohydrate metabolism patterns. RNA-seq revealed the transcriptional downregulation of genes related to photosynthesis and carbohydrate metabolism in chl3 leaves compared to the wild type. Our results demonstrate that transitory starch remobilization is very important for cellular carbohydrate partitioning in maize, in which ZmPHOH plays an indispensable role.

The Relationship between Effort-Reward Imbalance for Learning and Academic Burnout in Junior High School: A Moderated Mediation Model.

Although effort-reward imbalance has been proven to affect academic burnout, how effort-reward imbalance affects academic burnout remains unclear. This study, from the perspective of learning satisfaction and resilience, investigates how effort-reward imbalance affects academic burnout and reveals the influence of effort-reward imbalance on academic burnout. A sample of 755 junior high school students was assessed using the Revised Effort-Reward Imbalance for Learning Scale, Revised Learning Satisfaction Scale, Academic Burnout Scale, and Resilience Scale. Junior high school students' effort-reward imbalance rates for learning, learning satisfaction, and academic burnout were all significantly correlated with each other; learning satisfaction mediated the relationship between them. Learning satisfaction mediated the relationship between junior high school students' effort-reward imbalance rate for learning and academic burnout, and resilience negatively moderated the path from junior high school students' effort-reward imbalance rate from learning to learning satisfaction. The results suggest that improving students' resilience can effectively decrease the negative effects of effort-reward imbalance.