Stroke is a common clinical disease,if without timely effective treatment after the onset will not only affect the health of patients,but also cause a variety of sequelae,and spasticity is a higher incidence of stroke after the sequelae.Patients with spasticity will not only cause joint contracture,damage to skin defense function and cause body pain,but also increase the morbidity of stroke,seriously affecting the health of patients.Therefore,to strengthen the clinical treatment of spasticity is key measures to accelerate the process of stroke rehabilitation.This study reviews the progress of drug therapy,physiotherapy and surgical treatment in the treatment of spasticity at home and abroad,and provides the basis for clinical treatment.

ObjectiveTo observe the effect of comprehensive therapy on forearm extensor myotenositis.Methods72 cases were divided into two groups: a control group of 36 cases who were given routine treatment,and an experiment group of 36 cases who were given thermotherapy,computerized medium-frequency electrotherapy,physiotherapy,and ADL instruction,etc.After two courses,a simple grading score(for forearms) was used to assess the effect.ResultsOf the control group,22 cases were cured,10 remarkably effective,4 effective;of the experiment,30 cured,4 remarkably effective,2 effective(u=2.04, P<0.05).The difference of average score for forearms before and after the treatment were(6.58±3.17) points for the control and(8.19±3.55) for the experiment(t=2.03,P<0.05).The average days of cure were(5.60±2.54) d for the experiment group,shorter than those for the control(7.00±2.27) d(t=2.05,P<0.05).ConclusionComprehensive therapy is effective on forearm extensor myotenositis.

ObjectiveTo observe effect of combined treatment for piriformis syndrome and analyze its cause, pathoge nesis, pathology and recovery mechanism.Methods73 piriformis syndrome cases were divided randomly into two groups. The control gro up (35 cases) was given routine treatment, but the treatment group (38 cases) ad ded with thermal therapy, computerized medium frequency electrotherapy, manual t herapy, etc. After two courses, therapeutic effects were observed and assessed w ith standards for hip joint function.Results Of the control group,14 cases were cured,9 effectual,9 effective, and 3 ineffecti ve; of the experiment group, 23 cured,9 effectual, 5 effective, and 1 ineffecti ve. By statistical analysis, the therapeutic effect in the treatment group is su perior to those in the control group (P<0.05). Hip joint fu nction is assessed by scores as: the median point before and after the treatment for the control group is 18.00,the experiment group is 27.50, with statistical ly significance difference (P<0.01).The average cure time f or the experiment group is 11.04±5.10 days, fewer than that for the control gro up (14.79±5.79 days)(P<0.05).Conclusions Comb ined treatment used for piriformis syndrome can produce remarkable therapeutic e ffect, and various types of therapies can play such coordinate roles as promotin g blood circulation, repercussion, anti-inflammation, analgesia, relaxing adhes ion and softening scar.

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.