The relationship between self-oriented perfectionism and exercise participation: based on the dualistic model of passion.

Background: During the critical formative years of college, active participation in sports not only helps to alleviate stress, but also promotes the development of healthy habits. Although the multifaceted benefits of exercise have been widely recognized, there is a relative dearth of research on the relationship between personality traits, particularly college students' self-oriented perfectionism (SOP), and exercise participation. Methods: A questionnaire survey of 374 college students was conducted using the snowball sampling method. SPSS 26.0 and Mplus 8.3 were employed in this study to analyze the correlations between the variables, and on this basis, the effect of SOP on exercise participation was examined. The study also used 5,000 bootstrap samples and a 95% bias-corrected confidence interval to test the significance of the mediating effects. Results: Correlation analysis showed that SOP was positively correlated with exercise participation. Harmonious passion and obsessive passion were positively correlated with SOP, and exercise participation. Further, the results of structural equation analysis revealed that SOP increased exercise participation. Harmonious passion and obsessive passion positively mediated the effect between SOP and exercise participation, respectively. Conclusion: This study provides new perspectives to better understand college students' exercise participation, emphasizing the importance of SOP and its influence on exercise participation through harmonious and obsessive passions. These findings have important implications for the development of effective exercise promotion strategies.

Risks of passive use of social network sites in youth athletes: a moderated mediation analysis.

Background: With the popularity of social media platforms, the use of social networks challenges the well-being and mental health of athletes. Motivation: Despite ongoing scholarly discussions about the effects of passive use of social network sites, few studies have examined the relationship between the passive use of social network sites and mental health in young athletes from a social comparison perspective. Hypothesis: To address this research gap, we draw on the social comparison and developmental systems theories to explore the mediating effect of upward social comparison on passive social network site use and mental health, as well as the moderating effects of positive psychological capital. Methods: We analyzed data about 350 young athletes from professional Chinese sports universities. Results: As predicted, passive use of social network sites by young athletes increased anxiety (ß = 0.26, p < 0.001) and decreased subjective well-being (ß = -0.35, p < 0.001). Upward social comparisons had positive (ß = 0.22, p < 0.001) and negative (ß = -0.34, p < 0.001) mediating effects in passive social network site use and anxiety/subjective well-being. Positive psychological capital played a moderating effect between upward social comparison and anxiety (ß = -0.28, p < 0.001), and subjective well-being (ß = 0.24, p < 0.001); the moderated mediation effect was also supported. Conclusion: Our study informs the current research by highlighting the importance of upward social comparison as a critical mechanism and positive psychological capital as a boundary condition. We suggest actively maintaining and enhancing positive psychological capital to mitigate the adverse effects of upward social comparison.

Mechanistic study of PDIA1-catalyzed TFF3 dimerization during sepsis.

AIMS: Trefoil factor 3 (TFF3) is a gut mucosal protective molecule that is secreted by intestinal goblet cells. The dimeric structure of TFF3 enables it to function in intestinal mucosal repair and to maintain its own stability. Protein disulfide isomerase a1 (PDIA1) can directly catalyze the formation, isomerization and reduction of disulfide bonds in proteins and may play an important role in the formation of TFF3 dimer. In this study, we focused on the specific molecular mechanism of TFF3 dimerization by PDIA1 and the changes during sepsis. METHODS: We examined the changes of PDIA1 and TFF3 in sepsis rats and cell models and used a variety of experimental techniques to investigate the specific molecular mechanism of PDIA1-catalyzed TFF3 dimerization. KEY FINDINGS: We found that PDIA1 can directly catalyze the dimerization of TFF3. Our MD model proposed that two TFF3 monomers form hydrogen bonds with the region b' of PDIA1 through two stepwise reactions. Furthermore, we propose that the Cys24-Cys27 active site at the region a' of PDIA1 mediates disulfide bond formation between the Cys79 residues of each of the two TFF3 monomers via deprotonation and nucleophilic attack. During sepsis, PDIA1 is downregulated and the excessive release of nitric oxide (NO) promoted PDIA1 nitrosylation. This modification reduced PDIA1 activity, which resulted in the corresponding decrease of TFF3 dimerization and compromised TFF3 dimer function. SIGNIFICANCE: Our study revealed a novel mechanism for the inhibition of intestinal mucosal repair during sepsis and revealed novel targets for the prevention and treatment of sepsis.

The role of PDIA3 in myogenesis during muscle regeneration.

Beta 3 (ß3) integrin plays an important role in the initiation of myogenesis in adult muscle. Protein disulfide isomerases (PDIs) can activate ß3 integrin in various cells to promote cell migration, adhesion and fusion. However, the effect of PDIs on myogenesis during muscle regeneration has not been elucidated. Here, we report that PDIA3 expression is induced in regenerating myofibers. The inhibition of PDIA3 in muscle injuries in mice disrupts myoblast differentiation, impairs muscle regeneration, and ultimately aggravates muscle damage. Moreover, PDIA3 expression is upregulated and observed on the cell surfaces of myoblasts during differentiation and fusion. The inhibition of extracellular PDIA3 with an anti-PDIA3 monoclonal antibody attenuates ß3 integrin/AKT/mTOR signal activity, inhibits myoblast differentiation, and blocks the fusion of myoblasts. Thus, PDIA3 may be a mediator of myoblast differentiation and fusion during muscle regeneration.