ABSTRACT
Objective@#To explore the roles of self efficacy and smoking rationalization tendency in the relationship between college students physical activity and smoking cessation beliefs, in order to provide a basis for the positive effects of college students physical activity on smoking cessation beliefs.@*Methods@#From May 6 to 23 in 2023, 3 048 students from 10 colleges in Jiangxi Province were recruited and surveyed using the Physical Activity Participation Scale, the Smoking Cessation Self efficacy Scale, the Smoking Rationalization Tendency Scale and the Smoking Cessation Belief Scale. The Harman one way test was adopted for common method bias test. Bias correction was unfolded by Bootstrap method, and 95% confidence intervals of parameter estimates were analyzed using repeated sampling 5 000 times.@*Results@#The results of the sequential mediation model analysis showed that physical activity was positively associated with college students beliefs about smoking cessation ( β =0.17), and physical activity, self efficacy and smoking rationalization tendency were positively associated with each other ( β =0.41, 0.08, 0.19) ( P <0.05). Both self efficacy and smoking rationalization tendency positively predicted smoking cessation beliefs ( β =0.19, 0.17, P <0.01). Self efficacy and smoking rationalization tendency mediated the relationship between physical activity and smoking cessation beliefs, with a mediating effect value of 0.09, accounting for 62.82% of the total effect value (0.15).@*Conclusions@#Self efficacy and smoking rationalization tendency have a serial mediating effect between physical activity and smoking cessation beliefs among college students. Interventions should be actively used to enhance college students beliefs about smoking cessation, promote smoking cessation behaviors.
ABSTRACT
The differentiation fate of bone marrow mesenchymal stem cells (BMSCs) affects the progression of steroid-induced osteonecrosis of the femoral head (SONFH). We find that lncRNA DGCR5 encodes a 102-amino acid polypeptide, RIP (Rac1 inactivated peptide), which promotes the adipogenic differentiation of BMSCs and aggravates the progression of SONFH. RIP, instead of lncRNA DGCR5, binds to the N-terminal motif of RAC1, and inactivates the RAC1/PAK1 cascade, resulting in decreased Ser675 phosphorylation of ß-catenin. Ultimately, the nuclear localization of ß-catenin decreases, and the differentiation balance of BMSCs tilts toward the adipogenesis lineage. In the femoral head of rats, overexpression of RIP causes trabecular bone disorder and adipocyte accumulation, which can be rescued by overexpressing RAC1. This finding expands the regulatory role of lncRNAs in BMSCs and suggests RIP as a potential therapeutic target.
