Why Cannot I Stop Phubbing? Boredom Proneness and Phubbing: A Multiple Mediation Model.

Background: With the popularity of smartphone and their increasingly rich functions, people's attachment to their phones is increasing. While people enjoy the convenience that smartphone bring (eg, accessing information and socializing), it also leads to problematic smartphone use (eg, phubbing). Previous research has shown that boredom proneness can trigger phubbing. However, the underlying psychological mechanisms are not yet clear. Methods: To address this research gap, we surveyed 556 Chinese college students (Mage = 18.89 years, SD = 1.18) during the COVID-19 pandemic and all participants completed a self-report questionnaire. Drawing the Interaction of Person-Affect-Cognition-Execution model (I-PACE) for addictive behaviors, this study developed and examined a multiple mediation model incorporating boredom proneness, loneliness, fear of missing out (FoMO), and phubbing. Results: (1) Boredom proneness could positively predict phubbing; (2) loneliness and FoMO mediated the relationship between boredom proneness and phubbing, respectively; and (3) loneliness and FoMO sequentially mediated the relationship between boredom proneness and phubbing. Conclusion: These findings are not only valuable for understanding the underlying mechanisms linking boredom proneness and phubbing, but also suggest that three types of interventions could be effectively used to decrease the risk of phubbing among college students, namely, reducing boredom proneness, relieving loneliness, and decreasing FoMO.

Why mobile social media-related fear of missing out promotes depressive symptoms? the roles of phubbing and social exclusion.

BACKGROUND: With the popularity of mobile socialization, people have become more closely connected with their phones. While people enjoy the convenience that phones bring (e.g., accessing information and socializing), they also feel anxious about missing out on certain information. Previous researches have shown that fear of missing out (FoMO) can trigger depressive symptoms, however, the underlying psychological mechanisms are not yet clear. In addition, limited research has explored this issue in the context of mobile social media. METHODS: To address this research gap, we surveyed 486 Chinese college students (278 males and 208 females, mean age = 19.95 years, SD = 1.14) and all participants completed a self-report questionnaire including mobile social media-related FoMO scale, phubbing scale, social exclusion scale, and the patient health questionnaire-9. The data were analyzed by SPSS24.0 and the Process macro and developed a mediating and moderating model incorporating phubbing and social exclusion. RESULTS: The results showed that (1) mobile social media-related FoMO (MSM-related FoMO) can significantly and positively predict depressive symptoms among college students; (2) phubbing partially mediates the relationship between MSM-related FoMO and depressive symptoms; (3) the direct predictive effect of MSM-related FoMO on depressive symptoms is moderated by social exclusion. CONCLUSION: These findings are not only valuable for understanding the underlying mechanisms linking MSM-related FoMO and depressive symptoms, but also contribute to the development of psychological intervention programs (e.g., interventions based on social exclusion or phubbing) aiming at reducing college students' depressive symptoms.

Propofol inhibits cell apoptosis and inflammatory response in ox-LDL-induced human umbilical vein endothelial cells through the modulation of the circ_0003645/miR-149-3p/TRAF7 axis.

BACKGROUND: Propofol is an anesthetic agent and can impede the progression of human diseases. Circular RNA (circRNA) circ_0003645 has been identified to promote the development of atherosclerosis (AS). This study aimed at the functional mechanism of propofol and circ_0003645 in AS. METHODS: AS cell model was established by treatment of oxidized low-density lipoprotein (ox-LDL) in human umbilical vein endothelial cells (HUVECs). Cell viability or apoptosis detection was performed by Cell Counting Kit-8 (CCK-8) assay and flow cytometry. Circ_0003645, microRNA-149-3p (miR-149-3p) and tumor necrosis factor receptor-associated factor 7 (TRAF7) levels were determined by the quantitative real-time polymerase chain reaction (qRT-PCR). Inflammatory cytokines were examined using enzyme-linked immunosorbent assay (ELISA). Protein analysis was conducted by western blot. The interaction of miR-149-3p and circ_0003645 or TRAF7 was analyzed using dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. RESULTS: Treatment of ox-LDL inhibited cell viability and enhanced apoptosis in HUVECs to establish the AS cell model. Propofol protected against cell viability inhibition and apoptosis promotion in AS cell model. Circ_0003645 expression was downregulated by propofol in AS cell model. Propofol alleviated cell apoptosis and inflammation by decreasing the circ_0003645 level. Circ_0003645 targeted miR-149-3p, and circ_0003645/miR-149-3p axis was involved in the functional regulation of propofol. TRAF7 was the target of miR-149-3p. Inhibition of miR-149-3p affected the function of propofol by upregulating the TRAF7 expression. Circ_0003645 sponged miR-149-3p to induce the upregulation of TRAF7 following propofol treatment. CONCLUSION: It has been suggested that propofol acted as an inhibitor against the ox-LDL-induced cell injury by the circ_0003645/miR-149-3p/TRAF7 axis.