Objective To investigate the cognitive dificiency characteristics and the neuro electrophysiological mechanism of sleep disordered breathing(SDB) in school-age children.Methods20 cases of SDB children and 20 cases of normal group at 6-8 years old participated in the continue performance test(CPT-AX).The amplitude and latency of N2,P3 of event related potentials(ERPs) were measured and analysed at Fz leads,and the behavioral results were recorded at the same time.ResultsThere were no significant differences between SDB group and normal group in behavioral correct number (36.10±4.69 vs 35.05±3.49),the reaction time ((523.77±68.73)ms vs (496.59±78.65)ms) and false alarm number (1.0 (0.25,3.75) vs 0.5 (0.00,3.00))(all P>0.05).The SDB group showed significant increase in Go-P3 amplitudes compared with the normal group((10.25±6.46)μV vs (6.56±4.63)μV,P<0.05).The Go-P3 latency in SDB group was significantly prolonged than that in the normal group((438.80±59.72)ms vs (406±36.30)ms,P<0.05),and the Nogo-N2 amplitude in SDB group significantly decreased compared with the normal group ((-12.46±4.75)μV vs (-15.50±3.82)μV,P<0.05).ConclusionThe children aged 6 to 8 years old with sleep disordered breathing consume more resources and time to complete the attention process,like a compensatory response.And during the monitoring process there is a resource shortage that results in obvious defect in process of inhibition.

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.