Objective:To observe any effect of electroacupuncture on the expression of L1 cell adhesion molecule (L1CAM) in mice modeling Alzheimer′s disease (AD) and also any effect on learning and memory.Methods:Thirty male APP/PS1 mice were randomly divided into a model group, an electroacupuncture (EA) group, and a no acupuncture (NA) group, each of 10. All the animals were modeled as AD. Ten C57BL/6 mice served as a control group. The mice in the EA and NA groups were given continuous 50Hz EA at a current intensity of 1mA at and near the Baihui (GV20) and Shenshu (BL23) acupoints, respectively, once a day for 14 days, while the other two groups were not given any EA. The mice in the model and control groups continued to be routinely fed without any special treatment such as electroacupuncture. After the intervention, any behavioral changes were evaluated by using a Morris Water Maze, and the expression of L1CAM, PTEN and p53 protein in the hippocampus of each group was detected using western blotting.Results:Compared with the control group, the escape latency in positioning navigation experiments was significantly longer in the model group on the first 5 days of Morris Water Maze testing. Compared with the model group, the escape latency was significantly shorter in the EA group on days 2 to 5 of the Morris Water Maze testing, and the expression of L1CAM had increased significantly in the electroacupuncture group compared with the model group while PTEN and p53 expression had decreased significantly. The average escape latency of the NA group was significantly longer than that of the model group on days 2 to 5 of the Morris Water Maze testing. The average L1CAM expression in the NA group had decreased significantly, and the expression of PTEN and p53 protein had increased significantly more than in the EA group. The escape latency was negatively correlated with L1CAM expression but positively correlated with p53 protein and PTEN expression.Conclusion:L1CAM is involved in learning and memory processes, at least in mice. Electroacupuncture can improve the learning and memory of mice modeling Alzheimer′s, which may be due to its promoting the expression of L1CAM and inhibiting the expression of PTEN and p53.

Objective To observe the effects of X-blance therapy with uninjured side ear acupoint press in hospitalized patients with unilateral radicular sciatica. Methods A total of 73 patients were randomly divided into experimental group (37 cases) and control group (36 cases) according to the sequence of hospitalization. Both groups were given the conventional treatment and nursing care. Besides of this, the experimental group received X-blance therapy with uninjured side ear acupoint Press. Visual analogue scale ( VAS) and Chinese version of oswestry disability index ( CODI ) were compared between the two groups before and after the treatment. Results The VAS, CODI and the 3 coarse scores of every demension of CODI ( pain, single function and comprehensive function) were respectively (2. 53 ± 2. 37), (19. 63 ± 12. 37), (1. 83 ± 1. 69), (3. 78 ± 3. 24), (3. 22 ± 2. 13) in the experimental group after 3 weeks intervention, and (3. 70 ± 2. 59), (27. 93 ± 15. 88), (2. 70 ± 1. 93), (5. 46 ± 3. 63), (4. 41 ± 2. 76) in the control group, with statistically significant difference (t= -2. 009,-2. 39,-2. 042,-2. 084,-2. 046, respectiuely;P<0. 05). Conclusions X-blance therapy with uninjured side ear acupoint press can effectively reduce pain and improve disability of the patients with radicular sciatica.

Objective To investigate the effect of GTPase activating protein Git2 on metastasis in breast cancer. Methods Git2 gene over?expression was induced by Git2 cDNA, and Git2 gene knockdown was induced by Git2 ShRNA lentivirus in four breast cancer cell lines. Six?week old wide type female mice were also used in this study. The cells were tagged with luciferase and injected into wide type female mice by tail vein or 4th mammary fat pad, respectively, to establish a cancer metastasis model. In vivo real time imaging system and immunohistochemical staining were used to detect the cancer metastasis. Results The relative mRNA expression level of Git2 ( normalized by GAPDH) in the 4T1,4TO7,168FARN and 67NR cells were 0.91 ± 0. 03, 0. 125 ± 0. 06, 0. 131 ± 0. 04 and 0. 92 ± 0. 04, respectively. The expression of EMT marker E?cadherin was inhibited and N?cadherin and vimentin were enhanced when Git2 was over?expressed in 168FARN cells and 4TO7 cells expressing low level of Git2, whereas the expression of E?cadherin was increased and N?cadherin and vimentin were decreased when Git2 was knocked down in 67NR cells and 4T1 cells expressing high level of Git2. Furthermore, over?expression of Git2 promoted 4TO7 cells to progress from micro?metastasis to macro?metastasis. The down?regulation of Git2 pushed 67NR cells to intravasate into blood circulation and suppressed the metastatic ability of 4T1 cells. The number of bioluminescence photos of lung metastatic 4T1?Luc?KD cells was (0.4±0.05) ×106, compared with (3.0±0.04) ×106 in the control 4T1?Luc cells, showing a significant difference (P<0.05). Conclusion Our results indicate that Git2 is involved in breast cancer initiation and metastatic colonization.

Objective To investigate the effect of GTPase activating protein Git2 on metastasis in breast cancer. Methods Git2 gene over?expression was induced by Git2 cDNA, and Git2 gene knockdown was induced by Git2 ShRNA lentivirus in four breast cancer cell lines. Six?week old wide type female mice were also used in this study. The cells were tagged with luciferase and injected into wide type female mice by tail vein or 4th mammary fat pad, respectively, to establish a cancer metastasis model. In vivo real time imaging system and immunohistochemical staining were used to detect the cancer metastasis. Results The relative mRNA expression level of Git2 ( normalized by GAPDH) in the 4T1,4TO7,168FARN and 67NR cells were 0.91 ± 0. 03, 0. 125 ± 0. 06, 0. 131 ± 0. 04 and 0. 92 ± 0. 04, respectively. The expression of EMT marker E?cadherin was inhibited and N?cadherin and vimentin were enhanced when Git2 was over?expressed in 168FARN cells and 4TO7 cells expressing low level of Git2, whereas the expression of E?cadherin was increased and N?cadherin and vimentin were decreased when Git2 was knocked down in 67NR cells and 4T1 cells expressing high level of Git2. Furthermore, over?expression of Git2 promoted 4TO7 cells to progress from micro?metastasis to macro?metastasis. The down?regulation of Git2 pushed 67NR cells to intravasate into blood circulation and suppressed the metastatic ability of 4T1 cells. The number of bioluminescence photos of lung metastatic 4T1?Luc?KD cells was (0.4±0.05) ×106, compared with (3.0±0.04) ×106 in the control 4T1?Luc cells, showing a significant difference (P<0.05). Conclusion Our results indicate that Git2 is involved in breast cancer initiation and metastatic colonization.