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1.
Chinese Journal of School Health ; (12): 496-498, 2019.
Article in Chinese | WPRIM | ID: wpr-818805

ABSTRACT

Objective@#To explore the characteristics of Auditory Brainstem Response (ABR) in children with ASD, and analyze their relation with the core symptoms of ASD.@*Methods@#Ninty children aged 2-6 with ASD were recruited from Harbin in this study. The data of ABR was collected by using BAEP, and the association among children’s absolute latency and interpeak latency of ABR, core symptoms of ASD children’s behavior and clinical manifestation was analyzed.@*Results@#Compared with the normal average value, children with ASD had longer the absolute latency of wave Ⅰ,Ⅲ,Ⅴ in bilateral ears, which were (1.51±0.20)(3.83±0.34)(5.63±0.23)ms, (1.54±0.16) (3.78±0.23) (5.63±0.22)ms, respectively(P<0.05). Some children’s interpeak latency of Ⅰ-Ⅲ, Ⅲ-Ⅴ, Ⅰ-Ⅴ were longer than normal values. Children younger than 3 years old showed prolonged peak intervals of Ⅰ-Ⅲ and Ⅰ-Ⅴ than children in 3-7 years old. The study has also showed that there was positive correlation between the absolute latency of waveⅠin left ear and the social function defect(r=0.45, P<0.05); there was positive correlation between the latency of wave Ⅴin right ear or the latency of waveⅠin left ear or the Ⅰ-Ⅲ peakinterval and nonverbal communication ability dysfunction(r=0.35, 0.39, 0.34, P<0.05); there was positive correlation between the Ⅰ-Ⅲ peak interval and the repeated stereotyped symptoms(r=0.39, 0.35, P<0.05).@*Conclusion@#Children with ASD have abnormal auditory behavior. The absolute latency and interpeak latency of ABR is correlated to some parts of core symptoms of ASD.

2.
Journal of Peking University(Health Sciences) ; (6): 937-947, 2017.
Article in Chinese | WPRIM | ID: wpr-664789

ABSTRACT

Objective:Vacuolar ATPase (V-ATPase) was found within the membranes and internal organelles of a vast array of eukaryotic cells,and was related to various kinds of highly metastatic tumors.LASS2/TMSG1 gene was a novel tumor metastasis suppressor gene cloned from human prostate cancer cell line PC-3M in 1999 by our laboratory.It was found out that protein encoded by LASS2/TMSG1 could interact with the c subunit of V-ATPase (ATP6V0C).In this study,To use RNA interference to suppress the expression of ATP6V0C and try to further investigate the molecular mechanism of ATP6V0C in tumor metastasis and its relationship with LASS2/TMSG1 gene.Methods and Results:The expression level of ATP6V0C mRNA and protein in high metastatic potential prostate cancer cell lines (PC-3M-1E8 and PC-3M) was significantly higher than that in low metastatic potential prostate cancer cell lines (PC-3M-2B4 and PC-3),the expression level in PC-3M-1E8 being the highest.Follow-up tests selected PC-3M-1E8 cells for gene silencing.The expression and secretion of MMP-2 and the expression of MMP-9 in ATP6V0C siRNA transfected PC-3M-1E8 cells displayed no obvious change,but the activity of secreted MMP-9 was abated noticeably compared with the controls (P < 0.05).Extracellular hydrogen ion concentration and V-ATPase activity in interference group were both reduced significantly compared with the controls (P < 0.05).The migration and invasion capacity of ATP6V0C siRNA interfered cells in vitro were diminished significantly compared with the controls (P < 0.05).Furthermore,a dramatic reduction of LASS2/TMSG1 mRNA and protein level after transfection of siRNA in PC-3M-1 E8 cells was discovered (P < 0.05).Confocal immunofluorescence showed a vast co-localization of ATP6V0C protein and LASS2/TMSG1 protein in plasma and membrane.The co-localization signals of control group were much stronger than those of interference group.Conclusion:Specific siRNA silencing of ATP6V0C gene inhibits the invasion of human prostate cancer cells in vitro by mechanism of inhibiting V-ATPase activity and then reducing the extracellular hydrogen ion concentration,inhibiting MMP-9 activation and affecting ECM degradation and reconstruction.Meanwhile,ATP6V0C and LASS2/TMSG1 have interaction and it is likely that ATP6V0C functions as a feedback regulator of LASS2/TMSG1.

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