1.Clinical Controlled Trial of Lumbar Intervertebral Disc Herniation Treated by Leverage Replacement Manipulation
Lijiang LV ; Xianglong YUAN ; Fangjun WANG
Journal of Zhejiang Chinese Medical University 2006;0(04):-
[Objective]Observe the clinical effect of leverage replacement manipulation on lumbar intervertebral disc herniation.[Method]299 hospitalized patients were divided into two groups.153 cases were in trial group and 146 patients were in controlled group.Trial group accepted constant traction and leverage replacement manipulation.While the controlled group accepted the same traction and muscular massage.[Result]In trial group,90 patients were cured,57 improved and 6 no improvement.The total effective rate was 96.08%;in controlled group,21 were cured,75 cases improved,and 50 no improvement.The total effective rate was 65.75%.The effect of trial group was better than the controlled group(P
2.The effect of SiRNA -Oct4 expression on HCC cell line HepG2
Wenbo ZHOU ; Fangjun YUAN ; Can ZOU ; Zhengpeng ZHU ; Jianbo MA ; Zongqing DAI ; Youshun ZHANG
Chinese Journal of General Surgery 2011;26(6):467-469
Objective To investigate the expression of Oct4 in liver cancer, and the interrelation of the Oct4 and Wnt/β-catenin genes in hepatocellular carcinoma( HCC) cell line HepG2. Methods RTPCR technique was used to detect the expression of Oct4 and β-Catenin in HCC specimens; RNAi was used to knock-down the expression of Oct4 in HepG2, and the change of Wnt/β-catenin related genes were detected by Real time-PCR. Results In HCC specimens, the expression of Oct4 and β-Catenin in tumor and cirrhotic liver tissues were stronger than normal liver tissues. In SiRNA Oct4 HepG2 cells, the expression of Oct4 was downregulated, and β-catenin as well as Wnt10b were in a positive correlation with Oct4, TCF3 was in negative correlation with Oct4. Clone formation and move ability of the HepG2 were downregulated. Conclusions The expression of Oct4 was higher in tumor tissues than in normal liver tissues. Silencing Oct4 by SiRNA-0ct4 in HepG2 resulted in decreased ability of clone formation and cell movement.