Objective: To investigate the mediating effects of resilience and emotion regulation on family cumulative risk and positive coping style among primary and middle school students, so as to provide insights into promoting psychological health among them. Methods: The primary and middle school students from three counties (districts) of Baise City, Guangxi Zhuang Autonomous Region were selected through the stratified cluster random sampling method. Resilience, emotion regulation, family cumulative risk and positive coping style were investigated using the Resilience Scale for Chinese adolescent, Emotion Regulation Questionnaire, Chinese family Assessment Instrument, and Simple Coping Strategies Questionnaire, respectively. Mediating effects of resilience and emotion regulation on family cumulative risk and positive coping style were examined using Process macro program. Results: Totally 1 076 questionnaires were allocated, and 1 006 valid questionnaires were recovered, with an effective rate of 93.49%. There were 515 boys, accounting for 51.19%. The median age was 13 (interquartile range, 1) years. The mean scores of resilience, emotion regulation and positive coping style were (3.36±0.63), (2.26±0.56) and (1.85±0.39) points, respectively. The median family cumulative risk index was 0 (interquartile range, 0). The results of mediating effects showed that family cumulative risk had a direct negative effect on positive coping style (β=-0.037, 95%CI: -0.059 to -0.014, P=0.011), and also had an indirect negative effect on positive coping style through psychological resilience (β=-0.029, 95%CI: -0.041 to -0.017, P=0.006) as a mediator or through psychological resilience and emotion regulation (β=-0.002, 95%CI: -0.004 to -0.001, P=0.001) as a chain mediator. The mediating effect of resilience contributed 44% to the total effect, while the chain mediating effect of resilience and emotion regulation contributed 3%. Conclusion Resilience and emotional regulation serve as negative mediators between family cumulative risk and positive coping style among middle and primary school students.

Objective To evaluate the role of NOX2 in bupivacaine-induced production of reactive oxygen species (ROS) in nerve cells.Methods SH-SY5Y cells were seeded in culture plates and divided into 4 groups (n =11 each) using a random number table:small interfering RNA (siRNA) negative control group (group NC),siRNA negative control plus bupivacaine group (group NC +B),NOX2 siRNA group and NOX2 siRNA plus bupivacaine group (group NOX2 siRNA + B).In NC and NOX2 siRNA groups,the cells were transfected with negative siRNA and NOX2 siRNA,respectively,and then incubated in the culture medium for 24 h.In NC+B and NOX2 siRNA+B groups,cells were transfected with negative siRNA and NOX2 siRNA,respectively,new plates were used,the cells were incubated for 3 h with bupivacaine at the final concentration of 1.5 mmol/L,the culture medium was then replaced,and the cells were incubated until 24 h.The level of intracellular ROS was measured using the fluorogenic probe dihydroethidium,the cell apoptosis was determined by TUNEL,and the expression of activated caspase-3 and caspase-9 was detected using Western blot.Apoptosis rate was calculated.Results Compared with group NC,the level of ROS and apoptosis rate were significantly increased,and the expression of activated caspase-3 and caspase-9 was up-regulated in group NC+B (P＜ 0.05),the level of ROS was significantly increased,and the expression of activated caspase-3 and caspase-9 was up-regulated (P＜0.05),and no significant change was found in apoptosis rate in group NOX2 siRNA+B (P＞0.05),and no significant change was found in the level of ROS or apoptosis rate (P＞0.05),and the expression of activated caspase-3 and caspase-9 was significantly up-regulated in group NOX2 siRNA (P＜ 0.05).Compared with group NC+B,the level of ROS and apoptosis rate were significantly decreased,and the expression of activated caspase-3 and caspase-9 was down-regulated in group NOX2 siRNA+B (P＜0.05).Conclusion NOX2 is involved in the pathophysiological mechanism of bupivacaine-induced burst production of ROS in nerve cells.