Objective To study the efficacy of microvascular decompression in treating cranial nerve diseases. Methods 156 patients were treated with microvaseular decompression,of whom 119 were with trigeminal neuralgia,34 with hemifacial spasm and three with glossopharyngeal neuralgia.Rusults The overall effective rate was 96.8%(151/156) and the corresponding effective rate for the above three conditions were 94.2%,97.1% and 66.7%. Conlusions Mierovaseular decompression iS an effective treatment for cranial nerve diseases.

Objective To observe the dynamic changes of Notch1 protein expression in the subventricular zone (SVZ) after traumatic cerebral injury (TBI) in rats,and to explore the correlation between Notch signaling pathway and neural stem cells (NSCs) proliferation after TBI.Methods Ninety-six SD rats were randomly divided into sham-operated group (only opening the scalp and shall window,n=16),control group (without any treatment,n=16) and experimental group (establishing medium-sized TBI models with Feeney's free fall method,n=64);rats in the experimental group were divided into 4 sub groups according to the execution times (one,three,7 and 14 d after TBI,n=16).Immunofluorescence staining was performed to detect the Notchl/nestin labeled cell expressions in SVZ of rats,and Notch1 protein expression was detected by Western blotting.Results Immunofluorescence results showed that the Notch1/nestin double staining positive cells in the right SVZ brain tissues of the experimental group on the first day of TBI had peak level,which was 2-3 times of the control group;and then,it gradually declined and basically returned to normal on 144 day of TBI;the differences between the 4 subgroups were statistically different (P＜0.05).The positive cell counts in the subgroups of first,third,and 74 d after TBI were statistically different as compared with those in the control group and sham operated group (P＜0.05).Western blotting results indicated that there was no significant difference in the Notch1 protein expression between control group and sham operated group;Notch1 protein expression in SVZ of the experimental group had peak level on the first day of TBI,gradual decline was noted after that,and normal level was noted on the 14th d of TBI.Conclusion TBI can activate the Notch1 protein expression,which induces the opening of Notch signaling pathway so as to affect the regulation of NSCs proliferation.

Objective To investigate the potential pathogenesis of Focal cortical dysplasia (FCD), we performed cDNA microarray analysis to obtain gene expression profile of FCD. Methods Three FCD samples and three normal controls were enrolled. Total RNA of the brain tissues were extracted. The difference gene expressions between FCD group and control group was detected using Affymetrix gene chip. The up and down-regulated genes were confirmed by Real-time PCR. Further, the related signal pathways involved in the pathogenic mechanisms of FCD were predicted by bioinformatics. Result In FCD, two up-regulated genes C21orF2 and AU152162 and 5 down-regulated genes ENPP2, ANLN, IP6K3, UGT8, and AZGP were found. Compared the FCD samples with the normal controls , there were significantly different in all down-regulated genes (P < 0.05), while the up-regulated genes were not (P > 0.05). Using bioinformatics analysis, the ENPP2 , UGT8 , and AZGP1 protein which located in the cell membrane or secreted into the extracellular matrix may be involved in the formation of the myelin sheath and the development of the nervous system by the lipid metabolism and LPA signaling pathway. Conclusion ENPP2, UGT8 and AZGP1 may be involved in pathogenesis of FCD through the process of myelin sheath formation and LPA signal pathway , which warrants further study to know their roles in the pathogenesis of FCD.