磁刺激对星形胶质细胞迁移的影响及机制研究
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摘要
第一部分不同强度磁刺激对星形胶质细胞迁移的影响及机制研究
实验一：不同强度磁刺激对星形胶质细胞迁移的影响
[摘要]目的研究不同强度磁刺激对星形胶质细胞迁移作用的量效关系。方法24只Sprague-Dawley大鼠按刺激强度被随机分为对照组(刺激强度：0Tesla)、0.76T组(刺激强度0.76Tesla)、1.52T组(刺激强度：1.52Tesla)、1.9T组(刺激强度：1.9Tesla),4组的刺激频率为1Hz,刺激量为30脉冲,均采用溴乙锭(EB)注射入脊髓左侧背索复制局灶性的脊髓损伤模型。刺激14天后,处死大鼠,Western-Blot检测GFAP、MAP-2,采用图像分析系统观察GFAP、Brdu和MAP-2的免疫组化表达及脊髓损伤空洞体积的变化。结果随着磁刺激强度的增加,在14天时空洞的体积逐渐缩小,组间差异具有显著性差异(P＜0.05)。在空洞缩小的区域中,可以观察到GFAP的阳性表达,而无Brdu、MAP-2的阳性表达。随着磁刺激强度的增加,GFAP的阳性表达显著增强(P<0.05)。Western-Blot显示：随着磁刺激强度的增加,GFAP的光密度值相应增加,而MAP-2的光密度值没有明显变化,与组化的变化趋势一致。结论刺激频率为1Hz,刺激强度不大于1.9Tesla的条件下,磁刺激可促进星形胶质细胞的迁移,随着刺激强度的增强,星形胶质细胞迁移的能力亦增强。
实验二：不同强度磁刺激对星形胶质细胞迁移作用的机制研究
[摘要]目的研究不同剂量ERK抑制剂U0126对1Hz磁刺激促进星形胶质细胞迁移作用的影响,以探讨不同强度磁刺激促进星形胶质细胞迁移作用和ERK信号通路的关系,并选择U0126合适的阻滞剂量。方法24只Sprague-Dawley大鼠按U0126剂量被随机分为对照组(Omg/kg U0126, n=6)、低剂量组(0.1mg/kgU0126,n=6)、中剂量组(0.2mg/kg U0126, n= 6)、高剂量组(0.4mg/kg U0126,n=6),4组的刺激参数都为频率1Hz,强度1.52Tesla,刺激量为30脉冲；均采用溴乙锭(EB)注射入脊髓左侧背索复制局灶性的脊髓损伤模型。刺激14天后,处死大鼠,Western-Blot检测GFAP、ERK1/2和MAP-2,采用图像分析系统观察GFAP、ERK1/2和MAP-2的免疫组化表达及脊髓损伤空洞体积的变化。结果随着U0126剂量的增加,在14天时空洞的体积逐渐增大,GFAP和ERK1／2的阳性表达逐渐减弱,与对照组相比具有显著性差异(P<0.05)；并且,GFAP和ERK1／2的阳性表达呈相同的趋势；U0126中剂量组和高剂量组作用则无明显差异(P>0.05)；而病灶区域MAP-2呈阴性表达。Western-Blot显示：随着U0126剂量的增加,ERK1／2逐渐被抑制,0.2mg/kg和0.4mg/kgU0126都可完全抑制ERK1／2的表达,随着ERK逐渐被抑制,GFAP的表达亦逐渐减弱。结论不同剂量的U0126可抑制1Hz磁刺激引起的星形胶质细胞的迁移,0.2mg/kg是较合适的剂量；1.52Tesla,1Hz磁刺激引起的星形胶质细胞迁移与ERK信号通路有关。
第二部分不同频率磁刺激对星形胶质细胞迁移的影响及机制研究
实验一：不同频率磁刺激对星形胶质细胞迁移的影响
[摘要]目的研究不同频率磁刺激对星形胶质细胞迁移作用的量效关系。方法30只Sprague-Dawley大鼠按刺激频率被随机分为对照组(刺激频率：0Hz,强度：1.52Tesla)、1Hz组(刺激频率：1Hz,强度：1.52Tesla)、5Hz组(刺激频率：5Hz,强度：1.52Tesla)、10Hz组(刺激频率：10Hz,强度：1.52Tesla)和20Hz组(刺激频率：20Hz,强度：1.52Tesla),5组的刺激量均为30个脉冲,采用溴乙锭(EB)注射入脊髓左侧背索复制局灶性的脊髓损伤模型。刺激14天后,处死大鼠,Western-Blot检测GFAP、MAP-2,采用图像分析系统观察GFAP、Brdu和MAP-2的表达及脊髓损伤区空洞体积的变化。结果随着磁刺激频率的增加,在第14天时空洞的体积逐渐缩小,组间差异具有显著性差异(P<0.05)。在空洞缩小的区域中,可以观察到GFAP的阳性表达,而无Brdu和MAP-2的阳性表达。随着磁刺激频率的增加,GFAP的阳性表达亦显著增强(P＜0.05)。Western-Blot显示：随着磁刺激频率的增加,GFAP的光密度值相应增加,而MAP-2的光密度值没有明显变化,与组化变化趋势一致。结论刺激强度为1.52 Tesla,刺激频率不大于20Hz的条件下,磁刺激可促进星形胶质细胞的迁移,并随着刺激频率的提高,星形胶质细胞迁移的能力亦增强。
实验二：不同频率磁刺激对星形胶质细胞迁移作用的机制研究
[摘要]目的研究不同频率磁刺激促进星形胶质细胞迁移过程中ERK1／2所起的作用,以探讨不同频率磁刺激促进星形胶质细胞迁移作用的机制,并选择U0126合适的阻滞剂量。方法24只Sprague-Dawley大鼠按U0126剂量被随机分为对照组(0mg/kg U0126, n= 6)、低剂量组(0.1mg/kg U0126, n=6)、中剂量组(0.2mg/kg U0126, n=6)、高剂量组(0.4mg/kg U0126, n=6)，4组的磁刺激参数均为频率10Hz、强度1.52 Tesla,刺激量30脉冲,均采用溴乙锭(EB)注射入脊髓左侧背索复制局灶性的脊髓损伤模型。刺激14天后,处死大鼠,Western-Blot检测3FAP、ERK1/2和MAP-2,采用图像分析系统观察GFAP、ERK1/2和MAP-2的表达及脊髓损伤空洞体积的变化。结果随着U0126剂量的增加,在第14天时空洞的体积逐渐增大,GFAP和ERK1／2的阳性表达逐渐减弱,与对照组相比具有显著性差异(P<0.05),U0126中剂量组和高剂量组的作用相似无明显差异(P>0.05)。而病灶区域MAP-2呈阴性表达。Western-Blot显示：随着U0126剂量的增加,ERK1／2逐渐被抑制,0.2mg/kg和0.4mg/kgU0126都可完全抑制ERK1／2的表达,随着ERK逐渐被抑制,GFAP的表达亦逐渐减弱。结论不同剂量的U0126可抑制10Hz磁刺激引起的星形胶质细胞的迁移,0.2mg/kg是较合适的剂量；1.52 Tesla,10Hz磁刺激引起的星形胶质细胞迁移与ERK信号通路有关；
Part I:Effects of magnetic stimulation with different intensities on astrocytes migration and underlying mechanism
Exp I:Effects of magnetic stimulation with different intensities on astrocytes migration
[Abstract] Objective To investigate the effects of magnetic stimulation with different intensities on astrocytes migration.Methods Twenty-four adult healthy Sprague-Dawley rats were selected and injected with 0.5μl of 1% ethidium bromide (EB) in PBS into the dorsal spinal cord funiculus of the left side at T10-11 level to make located spinal cord injury models and were randomly divided into four groups.The rats of four groups were exposed to pulsed magnetic stimulation(1Hz,30 pulses) at the following intensities respectively:0 Tesla(control group),0.76 Tesla (Group 0.76T),1.52 Tesla(Group 1.52T),1.9 Tesla(Group 1.9T). On the day 14 after stimulation, the rats were sacrificed and the expressions of glial fibrillary acidic protein(GFAP),5-Bromo-2'-deoxyuridine (Brdu), microtubule associated protein-2 (MAP-2) and the volume of the holes of injuried area of spinal cord were detected with immunohistochemistry and Western-Blot technique. Quantitative analysis of the expression of GFAP, Brdu and MAP-2 were performed with the image analysis system.Results With the increase of magnetic stimulation intensity, the volume of the holes of injuried area of spinal cord discrease at day 14. In the reduced area of the holes,the expressions of GFAP could be seen,while Brdu and MAP-2 could not be seen. Significant differences were revealed in the expressions of GFAP among the four groups, which were significantly higher in magnetic stimulation groups than that in control group (P< 0.05). Conclusion Under the condition of 1Hz, no larger than 1.9Tesla magnetic stimulation, magnetic stimulation promote astrocytes to migrate. After magnetic stimulation, astrocytes migrate into the injuried spinal cord holes. the ability of astrocytes migration increase with the increase of magnetic stimulation intensities.
ExpⅡ:The mechanism of different intensities magnetic stimulation promoting astrocytes migration.
[Abstract] Objective To investigate effects of ERK inhibitor U0126 of different dose on the ability of 1Hz magnetic stimulation promoting astrocytes migration, then to select suitable dose of U0126, and study the mechanism of different intensity magnetic stimulation promoting astrocytes migration. Methods 24 adult healthy Sprague-Dawley rats were selected to inject 0.5ml of 1% ethidium bromide (EB) in PBS into the dorsal spinal cord funiculus on the left side at the T10-11 level to make located spinal cord injury models and be randomly devided into four groups.The four groups were exposed to magnetic stimulation(1Hz,1.52Tesla, 30pulses) at the following dose respectively:Omg/kg U0126 (control group), 0.1mg/kg U0126(low-dose group),0.2mg/kg U0126(middle-dose group),0.4mg/kg U0126(high-dose group). On the day 14 after stimulation, the rats were killed and the expression of glial fibrillary acidic protein(GFAP),microtubule associated protein-2 (MAP-2), extracellular signal-regulated kinase1/2 (ERK1/2) and the volume of holes were detected with immunohistochemistry and Western-Blot technique. Quantitative analysis of the expression of GFAP, MAP-2 and ERK1/2 were performed with the image analysis system.Results With the increase of U0126 dose,the volume of holes increased on day 14. In the lesion area, the positive expression of GFAP and ERK1/2 could be seen and had identical change tendency,while MAP-2 could not be seen. Significant difference was revealed in the expression of GFAP and ERK1/2 among the four groups, it was significantly lower in the U0126 groups than that in the control group (P< 0.05). while the middle-dose group had similar effect with the high-dose group (P> 0.05).Conclusion U0126 of different dose all could inhibit astrocytes migration that 1Hz,1.52Tesla magnetic stimulation caused,and 0.2mg/kg was the suitable dose.What's more, the effect of 1 Hz,1.52 Tesla magnetic stimulation promoting astrocytes to migrate is relevant to ERK pathway.
Part II:Effects of magnetic stimulation with different frequencies on astrocytes migration and underlying mechanism
Exp I:Effects of magnetic stimulation with different frequencies on astrocytes migration
[Abstract] Objective To investigate the action tendency of magnetic stimulation with different frequencies on astrocytes migration. Methods Thirty adult healthy Sprague-Dawley rats were selected and injected with 0.5μl of 1% ethidium bromide (EB) in PBS into the dorsal spinal cord funiculus of the left side at T10-11 level to make located spinal cord injury models and were randomly divided into five groups.The rats of five groups were exposed to pulsed magnetic stimulation (1.52Tesla,30 pulses) at the following frequencies respectively:0Hz(control group, 1Hz(Group 1HzT),5Hz(Group 5Hz),10Hz(Group 10Hz) and 20Hz(20Hz Group). On the day 14 after stimulation, the rats were sacrificed and the expressions of glial fibrillary acidic protein(GFAP),5-Bromo-2'-deoxyuridine(Brdu), microtubule associated protein-2 (MAP-2) and the volume of the holes of injuried area of spinal cord were detected with immunohistochemistry and Western-Blot technique. Quantitative analysis of the expression of GFAP, Brdu and MAP-2 were performed with the image analysis system. Results With the increase of magnetic stimulation frequency, the volume of the holes of injuried area of spinal cord discrease at day 14. In the reduced area of the holes, the positeve expressions of GFAP could be seen, while Brdu and MAP-2 could not be seen. Significant differences were revealed in the expressions of GFAP among the five groups, which were significantly higher in magnetic stimulation groups than that in control group (P< 0.05). Conclusion Under the condition of 1.52 Tesla, no larger than 20Hz magnetic stimulation, Magnetic stimulation promote astrocytes to migrate. After magnetic stimulation, astrocytes migrate into the injuried spinal cord holes. the ability of astrocytes migration increase with the increase of magnetic stimulation frequencies.
Exp II:The mechanism of different frequencies magnetic stimulation promoting astrocytes migration.
[Abstract] Objective To investigate the effects of ERK inhibitor U0126 of different doses on the ability of lOHz magnetic stimulation promoting astrocyte migration, then to select suitable dose of U0126, and study the mechanism of different frequencies magnetic stimulation promoting astrocyte migration. Methods Twenty-four adult healthy Sprague-Dawley rats were selected to inject 0.5ml of 1% ethidium bromide (EB) in PBS into spinal cord dorsal funiculus on the left side at T10-11 level to make located spinal cord injury models and randomly divided into four groups.The four groups were exposed to magnetic stimulation (10Hz,1.52Tesla, 30 pulses) at the following doses respectively:Omg/kg U0126(control group), 0.1mg/kg U0126(low-dose group),0.2mg/kg U0126 (middle-dose group),0.4mg/kg U0126(high-dose group). On the 14 after stimulation, the rats were sacrificed and the expression of glial fibrillary acidic protein(GFAP), microtubule associated protein-2 (MAP-2), extracellular signal-regulated kinasel/2 (ERK1/2) and the volume of spinal cord injuried holes were detected with immunohistochemistry and Western-Blot technique. Quantitative analysis of the expression of GFAP, MAP-2 and ERK1/2 were performed with the image analysis system. Results With the increase of U0126 dose, the volume of spinal cord injuried hole increase on 14(P< 0.05). In the lesion area, the positive expression of GFAP and ERK1/2 could be seen and had identical change tendency,while MAP2 could not be found. Significant difference was revealed in the expression of GFAP and ERK1/2 among the four groups, and it was significantly lower in U0126 groups than that in control group (P< 0.05). while the middle-dose group had similar effect with the high-dose group (P> 0.05) Conclusion U0126 of different dose all could inhibit astrocytes migration that 1.52Tesla,10Hz magnetic stimulation caused, and 0.2mg/kg was the suitable dose. What's more, the effect of 1.52Tesla,10Hz magnetic stimulation promoting astrocytes migrate is relevant to ERK pathway.
实验一：不同强度磁刺激对星形胶质细胞迁移的影响
[摘要]目的研究不同强度磁刺激对星形胶质细胞迁移作用的量效关系。方法24只Sprague-Dawley大鼠按刺激强度被随机分为对照组(刺激强度：0Tesla)、0.76T组(刺激强度0.76Tesla)、1.52T组(刺激强度：1.52Tesla)、1.9T组(刺激强度：1.9Tesla),4组的刺激频率为1Hz,刺激量为30脉冲,均采用溴乙锭(EB)注射入脊髓左侧背索复制局灶性的脊髓损伤模型。刺激14天后,处死大鼠,Western-Blot检测GFAP、MAP-2,采用图像分析系统观察GFAP、Brdu和MAP-2的免疫组化表达及脊髓损伤空洞体积的变化。结果随着磁刺激强度的增加,在14天时空洞的体积逐渐缩小,组间差异具有显著性差异(P＜0.05)。在空洞缩小的区域中,可以观察到GFAP的阳性表达,而无Brdu、MAP-2的阳性表达。随着磁刺激强度的增加,GFAP的阳性表达显著增强(P<0.05)。Western-Blot显示：随着磁刺激强度的增加,GFAP的光密度值相应增加,而MAP-2的光密度值没有明显变化,与组化的变化趋势一致。结论刺激频率为1Hz,刺激强度不大于1.9Tesla的条件下,磁刺激可促进星形胶质细胞的迁移,随着刺激强度的增强,星形胶质细胞迁移的能力亦增强。
实验二：不同强度磁刺激对星形胶质细胞迁移作用的机制研究
[摘要]目的研究不同剂量ERK抑制剂U0126对1Hz磁刺激促进星形胶质细胞迁移作用的影响,以探讨不同强度磁刺激促进星形胶质细胞迁移作用和ERK信号通路的关系,并选择U0126合适的阻滞剂量。方法24只Sprague-Dawley大鼠按U0126剂量被随机分为对照组(Omg/kg U0126, n=6)、低剂量组(0.1mg/kgU0126,n=6)、中剂量组(0.2mg/kg U0126, n= 6)、高剂量组(0.4mg/kg U0126,n=6),4组的刺激参数都为频率1Hz,强度1.52Tesla,刺激量为30脉冲；均采用溴乙锭(EB)注射入脊髓左侧背索复制局灶性的脊髓损伤模型。刺激14天后,处死大鼠,Western-Blot检测GFAP、ERK1/2和MAP-2,采用图像分析系统观察GFAP、ERK1/2和MAP-2的免疫组化表达及脊髓损伤空洞体积的变化。结果随着U0126剂量的增加,在14天时空洞的体积逐渐增大,GFAP和ERK1／2的阳性表达逐渐减弱,与对照组相比具有显著性差异(P<0.05)；并且,GFAP和ERK1／2的阳性表达呈相同的趋势；U0126中剂量组和高剂量组作用则无明显差异(P>0.05)；而病灶区域MAP-2呈阴性表达。Western-Blot显示：随着U0126剂量的增加,ERK1／2逐渐被抑制,0.2mg/kg和0.4mg/kgU0126都可完全抑制ERK1／2的表达,随着ERK逐渐被抑制,GFAP的表达亦逐渐减弱。结论不同剂量的U0126可抑制1Hz磁刺激引起的星形胶质细胞的迁移,0.2mg/kg是较合适的剂量；1.52Tesla,1Hz磁刺激引起的星形胶质细胞迁移与ERK信号通路有关。
第二部分不同频率磁刺激对星形胶质细胞迁移的影响及机制研究
实验一：不同频率磁刺激对星形胶质细胞迁移的影响
[摘要]目的研究不同频率磁刺激对星形胶质细胞迁移作用的量效关系。方法30只Sprague-Dawley大鼠按刺激频率被随机分为对照组(刺激频率：0Hz,强度：1.52Tesla)、1Hz组(刺激频率：1Hz,强度：1.52Tesla)、5Hz组(刺激频率：5Hz,强度：1.52Tesla)、10Hz组(刺激频率：10Hz,强度：1.52Tesla)和20Hz组(刺激频率：20Hz,强度：1.52Tesla),5组的刺激量均为30个脉冲,采用溴乙锭(EB)注射入脊髓左侧背索复制局灶性的脊髓损伤模型。刺激14天后,处死大鼠,Western-Blot检测GFAP、MAP-2,采用图像分析系统观察GFAP、Brdu和MAP-2的表达及脊髓损伤区空洞体积的变化。结果随着磁刺激频率的增加,在第14天时空洞的体积逐渐缩小,组间差异具有显著性差异(P<0.05)。在空洞缩小的区域中,可以观察到GFAP的阳性表达,而无Brdu和MAP-2的阳性表达。随着磁刺激频率的增加,GFAP的阳性表达亦显著增强(P＜0.05)。Western-Blot显示：随着磁刺激频率的增加,GFAP的光密度值相应增加,而MAP-2的光密度值没有明显变化,与组化变化趋势一致。结论刺激强度为1.52 Tesla,刺激频率不大于20Hz的条件下,磁刺激可促进星形胶质细胞的迁移,并随着刺激频率的提高,星形胶质细胞迁移的能力亦增强。
实验二：不同频率磁刺激对星形胶质细胞迁移作用的机制研究
[摘要]目的研究不同频率磁刺激促进星形胶质细胞迁移过程中ERK1／2所起的作用,以探讨不同频率磁刺激促进星形胶质细胞迁移作用的机制,并选择U0126合适的阻滞剂量。方法24只Sprague-Dawley大鼠按U0126剂量被随机分为对照组(0mg/kg U0126, n= 6)、低剂量组(0.1mg/kg U0126, n=6)、中剂量组(0.2mg/kg U0126, n=6)、高剂量组(0.4mg/kg U0126, n=6)，4组的磁刺激参数均为频率10Hz、强度1.52 Tesla,刺激量30脉冲,均采用溴乙锭(EB)注射入脊髓左侧背索复制局灶性的脊髓损伤模型。刺激14天后,处死大鼠,Western-Blot检测3FAP、ERK1/2和MAP-2,采用图像分析系统观察GFAP、ERK1/2和MAP-2的表达及脊髓损伤空洞体积的变化。结果随着U0126剂量的增加,在第14天时空洞的体积逐渐增大,GFAP和ERK1／2的阳性表达逐渐减弱,与对照组相比具有显著性差异(P<0.05),U0126中剂量组和高剂量组的作用相似无明显差异(P>0.05)。而病灶区域MAP-2呈阴性表达。Western-Blot显示：随着U0126剂量的增加,ERK1／2逐渐被抑制,0.2mg/kg和0.4mg/kgU0126都可完全抑制ERK1／2的表达,随着ERK逐渐被抑制,GFAP的表达亦逐渐减弱。结论不同剂量的U0126可抑制10Hz磁刺激引起的星形胶质细胞的迁移,0.2mg/kg是较合适的剂量；1.52 Tesla,10Hz磁刺激引起的星形胶质细胞迁移与ERK信号通路有关；
Part I:Effects of magnetic stimulation with different intensities on astrocytes migration and underlying mechanism
Exp I:Effects of magnetic stimulation with different intensities on astrocytes migration
[Abstract] Objective To investigate the effects of magnetic stimulation with different intensities on astrocytes migration.Methods Twenty-four adult healthy Sprague-Dawley rats were selected and injected with 0.5μl of 1% ethidium bromide (EB) in PBS into the dorsal spinal cord funiculus of the left side at T10-11 level to make located spinal cord injury models and were randomly divided into four groups.The rats of four groups were exposed to pulsed magnetic stimulation(1Hz,30 pulses) at the following intensities respectively:0 Tesla(control group),0.76 Tesla (Group 0.76T),1.52 Tesla(Group 1.52T),1.9 Tesla(Group 1.9T). On the day 14 after stimulation, the rats were sacrificed and the expressions of glial fibrillary acidic protein(GFAP),5-Bromo-2'-deoxyuridine (Brdu), microtubule associated protein-2 (MAP-2) and the volume of the holes of injuried area of spinal cord were detected with immunohistochemistry and Western-Blot technique. Quantitative analysis of the expression of GFAP, Brdu and MAP-2 were performed with the image analysis system.Results With the increase of magnetic stimulation intensity, the volume of the holes of injuried area of spinal cord discrease at day 14. In the reduced area of the holes,the expressions of GFAP could be seen,while Brdu and MAP-2 could not be seen. Significant differences were revealed in the expressions of GFAP among the four groups, which were significantly higher in magnetic stimulation groups than that in control group (P< 0.05). Conclusion Under the condition of 1Hz, no larger than 1.9Tesla magnetic stimulation, magnetic stimulation promote astrocytes to migrate. After magnetic stimulation, astrocytes migrate into the injuried spinal cord holes. the ability of astrocytes migration increase with the increase of magnetic stimulation intensities.
ExpⅡ:The mechanism of different intensities magnetic stimulation promoting astrocytes migration.
[Abstract] Objective To investigate effects of ERK inhibitor U0126 of different dose on the ability of 1Hz magnetic stimulation promoting astrocytes migration, then to select suitable dose of U0126, and study the mechanism of different intensity magnetic stimulation promoting astrocytes migration. Methods 24 adult healthy Sprague-Dawley rats were selected to inject 0.5ml of 1% ethidium bromide (EB) in PBS into the dorsal spinal cord funiculus on the left side at the T10-11 level to make located spinal cord injury models and be randomly devided into four groups.The four groups were exposed to magnetic stimulation(1Hz,1.52Tesla, 30pulses) at the following dose respectively:Omg/kg U0126 (control group), 0.1mg/kg U0126(low-dose group),0.2mg/kg U0126(middle-dose group),0.4mg/kg U0126(high-dose group). On the day 14 after stimulation, the rats were killed and the expression of glial fibrillary acidic protein(GFAP),microtubule associated protein-2 (MAP-2), extracellular signal-regulated kinase1/2 (ERK1/2) and the volume of holes were detected with immunohistochemistry and Western-Blot technique. Quantitative analysis of the expression of GFAP, MAP-2 and ERK1/2 were performed with the image analysis system.Results With the increase of U0126 dose,the volume of holes increased on day 14. In the lesion area, the positive expression of GFAP and ERK1/2 could be seen and had identical change tendency,while MAP-2 could not be seen. Significant difference was revealed in the expression of GFAP and ERK1/2 among the four groups, it was significantly lower in the U0126 groups than that in the control group (P< 0.05). while the middle-dose group had similar effect with the high-dose group (P> 0.05).Conclusion U0126 of different dose all could inhibit astrocytes migration that 1Hz,1.52Tesla magnetic stimulation caused,and 0.2mg/kg was the suitable dose.What's more, the effect of 1 Hz,1.52 Tesla magnetic stimulation promoting astrocytes to migrate is relevant to ERK pathway.
Part II:Effects of magnetic stimulation with different frequencies on astrocytes migration and underlying mechanism
Exp I:Effects of magnetic stimulation with different frequencies on astrocytes migration
[Abstract] Objective To investigate the action tendency of magnetic stimulation with different frequencies on astrocytes migration. Methods Thirty adult healthy Sprague-Dawley rats were selected and injected with 0.5μl of 1% ethidium bromide (EB) in PBS into the dorsal spinal cord funiculus of the left side at T10-11 level to make located spinal cord injury models and were randomly divided into five groups.The rats of five groups were exposed to pulsed magnetic stimulation (1.52Tesla,30 pulses) at the following frequencies respectively:0Hz(control group, 1Hz(Group 1HzT),5Hz(Group 5Hz),10Hz(Group 10Hz) and 20Hz(20Hz Group). On the day 14 after stimulation, the rats were sacrificed and the expressions of glial fibrillary acidic protein(GFAP),5-Bromo-2'-deoxyuridine(Brdu), microtubule associated protein-2 (MAP-2) and the volume of the holes of injuried area of spinal cord were detected with immunohistochemistry and Western-Blot technique. Quantitative analysis of the expression of GFAP, Brdu and MAP-2 were performed with the image analysis system. Results With the increase of magnetic stimulation frequency, the volume of the holes of injuried area of spinal cord discrease at day 14. In the reduced area of the holes, the positeve expressions of GFAP could be seen, while Brdu and MAP-2 could not be seen. Significant differences were revealed in the expressions of GFAP among the five groups, which were significantly higher in magnetic stimulation groups than that in control group (P< 0.05). Conclusion Under the condition of 1.52 Tesla, no larger than 20Hz magnetic stimulation, Magnetic stimulation promote astrocytes to migrate. After magnetic stimulation, astrocytes migrate into the injuried spinal cord holes. the ability of astrocytes migration increase with the increase of magnetic stimulation frequencies.
Exp II:The mechanism of different frequencies magnetic stimulation promoting astrocytes migration.
[Abstract] Objective To investigate the effects of ERK inhibitor U0126 of different doses on the ability of lOHz magnetic stimulation promoting astrocyte migration, then to select suitable dose of U0126, and study the mechanism of different frequencies magnetic stimulation promoting astrocyte migration. Methods Twenty-four adult healthy Sprague-Dawley rats were selected to inject 0.5ml of 1% ethidium bromide (EB) in PBS into spinal cord dorsal funiculus on the left side at T10-11 level to make located spinal cord injury models and randomly divided into four groups.The four groups were exposed to magnetic stimulation (10Hz,1.52Tesla, 30 pulses) at the following doses respectively:Omg/kg U0126(control group), 0.1mg/kg U0126(low-dose group),0.2mg/kg U0126 (middle-dose group),0.4mg/kg U0126(high-dose group). On the 14 after stimulation, the rats were sacrificed and the expression of glial fibrillary acidic protein(GFAP), microtubule associated protein-2 (MAP-2), extracellular signal-regulated kinasel/2 (ERK1/2) and the volume of spinal cord injuried holes were detected with immunohistochemistry and Western-Blot technique. Quantitative analysis of the expression of GFAP, MAP-2 and ERK1/2 were performed with the image analysis system. Results With the increase of U0126 dose, the volume of spinal cord injuried hole increase on 14(P< 0.05). In the lesion area, the positive expression of GFAP and ERK1/2 could be seen and had identical change tendency,while MAP2 could not be found. Significant difference was revealed in the expression of GFAP and ERK1/2 among the four groups, and it was significantly lower in U0126 groups than that in control group (P< 0.05). while the middle-dose group had similar effect with the high-dose group (P> 0.05) Conclusion U0126 of different dose all could inhibit astrocytes migration that 1.52Tesla,10Hz magnetic stimulation caused, and 0.2mg/kg was the suitable dose. What's more, the effect of 1.52Tesla,10Hz magnetic stimulation promoting astrocytes migrate is relevant to ERK pathway.
引文
[1]Johansson CB, Momma DL, Clarke M. Idebtification of a neural stem cell in the adult mammalian central nervous system. Cell,1999,96(l):25-34.
[2]Chiasson BJ,Tropepe V,Morshead CM, et al. Adult mammmalian forebrain ependymal and subependymal cells demonstrate proliferative potential, but only subependymal cells have neural stem cell characteristics. J Neurosci, 1999,19(11):4462-71.
[3]Profyris C, Cheema SS, Zang D, et al. Degenerative and regenerative machanisms governing spinal cord injury. Neurobiol Dis,2004,15(3):415-36.
[4]Schnell L, Schwab ME. Sprouting and regeneration of lesioned corticcspinal tract fibe in the adult rat spinal cord. Eur J Neurosci,1993,5(9):1156-71.
[5]Horvat JC. Spinal cord reconstruction and neural transplants. New the rapeutic vectors. Bull Acad Natl Med,1994,178(3):455-63.
[6]Joesten EA, Bar PR, Gispen WH. Directional regrowth of lesioned corticcspinal tract axons in the adult rat spinal cord. Neuroscience,1995,69(2):619-26.
[7]Lu P, JonesL L, Tuszynski MH. BDNF-expressing marrow stromal cells support extensive axonal growth at sites of spinal cord injury.Exp Neurol, 2005,191(2):344-60.
[8]Arthur B,Mary JR,Lynne CW. NGF message and protein distribution in the injured rat spinal cord. Exp Neurol,2004,188(1):115-27.
[9]Qiao L,Vizzard MA. Up-regulation of tyrosine kinase(Trka,Trkb) receptor expression and phosphorylation in lumbosacral dorsal root ganglia after chronic spinal cord(T8-T10)injury.Comp Neurol,2002,449(3):217-30.
[10]Cao X,Tang C,Luo Y. Effect of nerve growth factor on neuronal apoptosis after spinal cord injury in rats.Neurotrauma,2002,5(3):131-5.
[11]Kim DH,Jahng TA. Continuous brain-derived neurotrophic factor(BDNF)infusion after methylprednisolone treatment in severe spinal cord injury.Korean Med Sci,2004,19(1):113-22.
[12]Novikova LN, Kellerth JO. Differential effects of neurotrophins on neuronal survival and axonal regeneration after spinal cord injury in adult rats.Comp Neurol,2002,452(3):255-63.
[13]Skaper SD, Moore SE, Walsh FS. Cell signaling cascades regulating neuronal growth2promoting and inhibitory cues. Prog Neurobio,2001,65:593-608.
[14]Prinjha R, Moore SE, Vinson M, et al. Inhibitor of neurite outgrowth in humans. Nature,2000,403(6768):383-4.
[15]Goldbery JL, Barree BA. Nogo in nerve regeneration. Nature, 2000,403(6768):369-70.
[16]Vikis HG, Li W, He Z, et al. The semaphorin receptor plexin-B1 specifically interacts with active Rac in a ligand-dependent manner. Proc Natl Acad Sci, 2000,97(23):12457-62.
[17]Tatagiba M, Brosamle C, Schwab ME. Regeneration of injured axons in the adult mammalian central nervous system. Neurosurg,1997,40(3):541-7.
[18]Chen MS, Huber AB,Vander Haar ME,et al. Nogo-A is a myelinassociated neurite outgrowth inhibitor and an antigen for monoclonal antibody IN-1. Nature,2000,403(29):434-9.
[19]Schnell L, Schwab ME. Axonal regeneration in the rat spinal cord producted by an antibody against myelin-associated neurite growth inhibitors.Nature, 1990,343(6255):269-72.
[20]Hagino S, Iseki K, Mori T, et al. Slit and glypican-1 mRNAs are coexpressed in the reactive astrocytes of the injuried adult brain. Glia,2003,42(2):130-8.
[21]Lin L,Rao Y, Isacson O. Nestrin-1 and slit-2 regulate and disrect neurite growth of ventral midbrain dopaminergic neurons. Mol Cell Neurosci,2005,28(3):547-55.
[22]Li GL,Farooque M,Olsson Y,et al. Change of Fas and Fas ligand immunoreactivity after compression trauma to rat spinal cord. Acta Neuropathal(Berl),2000,100(1):75-81.
[23]Emery E, Aldana P,Bunge MB, et al. Apoptosis after traumatic human spinal cord injury. J Neurosurg,1998,89(6):911-20.
[24]Van De Craen M,Van Loo,Pype S,et al. Identification of a new caspase homologue:caspase 14.Cell Death Differ,1998,5(10):838-46.
[25]Zoltan NO,Stanley JK. Checkpoints of dueling diermers foil death wishes.Cell,1994,79(2):189-92.
[26]Nakahara S, Yone K, Sakou T, et al. Induction of apoptosis signal regulating kinase1(ASK1) after spinal cord injury in rats:possible invovle of ASK1-JNK and P38 pathways in neuronal apoptosis.Neuropathol Exp Neurol,1999.58(3):442-50.
[27]马传学,杨青.脊髓损伤的治疗进展[J].江苏药学与临床研究,2006,14(1)：15-16。
[28]Fehlings MQTator CH. The effect of direct current field polarity on Recovery after acute experimental spinal cord injury.Brain Res,1992,579 (1):32-42.
[29]沈宁江,朱家恺.电刺激与周围神经再生.中华显微外科杂志,1992,15(3)：184-186。
[30]Borgens RB,Blighr AR,Murphy DJ,et al. Transected dorsal column axons within the guinea pig spinal cord regenerate in the presence of an applied electic fields.J Comp Neurol,1986,250(2):168-80.
[31]Strautman AF,Cork RJ,Robinson KR,et al. The distribution of free calcium in transected spinal axons and its modulation by appliedelectrical fields.J Neuro sci,1990,10(11):3564-75.
[32]郭家松,曾园山,陈玉玲,等.督脉电针治疗大鼠全横断性脊髓损伤的实验研究.中国针灸,2003,23(6)：351-354。
[33]Kusano K, Enomoto M, Hirai T,et al. Transplanted neural progenitor cells expressing mutant NT3 promote myelination and partial hindlimb recovery in the chronic phase after spinal cord injury. Biochem Biophys Res Commun. 2010,393(4):812-7.
[34]Caprani A,Richert A,Guglielmi JP,et al. Preliminary study of pulsed-electromagnetic fields effects on endothelial (HUVEC) cell secretions-modulation of the thrombo-hemorrhagic balance.Electromagn Biol Med.2008,27(4):386-92.
[35]Qu X, Wen J, Zhang J,et al. Development and application of extremely low frequency multi-waveform electromagnetic field generator. Sheng Wu Yi Xue Gong Cheng Xue Za Zhi,2009,26(1):173-76.
[36]Zyss T.Magnetotherapy. Neuro Endocrinol Lett,2008,29 Suppl 1:161-201.
[37]Todd G, Flavel SC, Ridding MC. Priming theta-burst repetitive transcranial magnetic stimulation with low-and high-frequency stimulation. Exp Brain Res. 2009,195(2):307-15.
[38]Ross ML, Koren SA, Persinger MA. Physiologically patterned weak magnetic fields applied over left frontal lobe increase acceptance of false statements as true. Electromagn Biol Med.2008,27(4):365-71.
[39]Macias MY,Battocletti JH,Sutton CH, et al. Directed and enhanced neurite growth with pulsed magnetic field stimulation. Bioelectromagnetics, 2000,21(4):272-7.
[1]Silver J, Miller JH. Regeneration beyond the glial scar.Nat Rev Neurosci,2004,5(2):146-56.
[2]Talbott JF, Loy DN, Liu Y,et al. Endogenous Nkx2.2+/Olig2+ oligodendrocyte precursor cells fail to remyelinate the demyelinated adult rat spinal cord in the absence of astrocytes. Exp Neurol,2005,192(1):11-24.
[3]White RE, McTigue DM, Jakeman LB. Regional heterogeneity in astrocyte responses following contusive spinal cord injury in mice. J Comp Neurol. 2010,518(8):1370-90.
[4]Pekny M, Nilsson M. Astrocyte activation and reactive gliosis. Glia 2005,50(4):427-34.
[5]Silver J, Miller JH. Regeneration beyond the glial scar. Neurosci. 2004,5:146-56.
[6]A.T. Barker, I.L. Freeston, R. Jalinous, et al. Magnetic stimulation of the human brain and peripheral nervous system-an introduction and the results of an initial clinical evaluation. Neurosurgery,1987,20:100-9.
[7]J.C. Rothwell, P.D. Thompson, B.L. Day, et al.Stimulation of the human motor cortex through the scalp. Exp. Physiol.1991,76:159-200.
[8]Siebner HR. Treatment of Movement Disorders. In:Hallett M, Chokroverty S (eds) Magnetic stimulation in clinical neurophysiology.2005,2nd edn. Elsevier, Philadelphia.
[9]Dutta SK, Ghosh B, Blackman CF. Radiofrequency radiationinduced calcium ion efflux enhancement from human and other neuroblastoma cells in culture. Bioelectromagnetics,1989,10:197-202.
[10]Goodman R, Henderson AS. Exposure of salivary gland cells to low-frequency electromagnetic fields alters polypeptide synthesis. Proc Natl Acad Sci USA 1988,85:3928-32.
[11]Goodman EM, Greenebaum B, Marron MT. Effects of electromagnetic fields
on molecules and cells. Int Rev Cytol,1995.158:279-337.
[12]Fujiki M, Steward O. High frequency transcranial magnetic stimulation mimics the effects of ECS in upregulating astroglial gene expression in the murine CNS. Molecular Brain Res,1996,44:301-8.
[13]Philip Chan,Lawrence Feng,Yuen Lee, et al.Effects of pulsed magnetic stimulation on GFAP levels in cultured astrocytes. Journal of Neuroscience Research,1999,55:238-44.
[14]孙永安,赵合庆,张志琳,等.长程经颅磁刺激对脑梗死大鼠皮质脑源性神经营养因子表达及神经功能恢复的影响.中华物理医学与康复杂志,2005,27：712-716。
[15]Fang Z, Duthoit N, Wicher G,et al. Intracellular calcium-binding protein S100A4 influences injury-induced migration of white matter astrocytes.Acta Neuropathol,2006,111:213-9.
[16]卢培刚,冯华,王宪荣,等.高压氧预处理对大鼠脊髓损伤后和巢蛋白表达的影响.中华神经外科疾病研究杂志,2008,7(2)：149-153。
[17]肖锋,季玉红,孙琳琳,等.细胞周期蛋白依赖性蛋白激酶11在大鼠脊髓横断性损伤后的表达变化.解剖学报,2008,39(1)：1-6。
[18]李幼忱,李志成,刘杰,等.大鼠皮肤创伤愈合瘢痕的三维重建和体积定量.中国体视学与图像分析,2007,12：1-5。
[19]Malhotra S, Shnitka T, Elabrink J. Reactive astrocytes:A review. Cytobios, 1990,61:133-60.
[20]Sofroniew MV, Vinters HV. Astrocytes:biology and pathology. Acta Neuropathol.2010,119(1):7-35.
[21]Hinkle D. Baldwin S, Schef S, et al. GFAP and S100 gene expression in the codex and hippocampusin response to mild comical contusion. J Ncurotrauma,1997,14:729-38.
[22]Lim JH, Gibbons HM, O'Carroll SJ, et al. Extracellular signal-regulated kinase involvement in human astrocyte migration. Brain Res, 2007,1164:1-13.
[23]Kurtis I, Songwan Jin, Kazunori Uchida, et al. Greatly impaired migration of implanted aquaporin-4-deficient astroglial cells in mouse brain toward a site of injury. FASEB J,2007,21:108-16.
[24]Kimura-Kuroda J, Teng X, Komuta Y, et al.An in vitro model of the inhibition of axon growth in the lesion scar formed after central nervous system injury. Mol Cell Neurosci.2010,43(2):177-87.
[25]Frontczak-Baniewicz M, Struzynska L, Andrychowski J, et al.Ultrastructural and immunochemical studies of glial scar formation in diabetic rats. Acta Neurochir Suppl.2010;106:251-5.
[26]Zhu WZ, Ni JX, Tang Q, Study on the effect of cluster needling of scalp acupuncture on the plasticity protein MAP-2 in rats with focal cerebral infarction. Zhongguo Zhen Jiu,2010,30(1):46-50.
[27]Kinugasa-Taniguchi Y, Tomimatsu T, Mimura K, et al.Human C-reactive protein enhances vulnerability of immature rats to hypoxic-ischemic brain damage:a preliminary study. Reprod Sci,17(5):419-25.
[28]Lin Q, Hai J, Yao LY, et al.Neuroprotective effects of NSTyr on cognitive function and neuronal plasticity in rats of chronic cerebral hypoperfusion. Brain Res.2010,1325:183-90.
[29]Sun M, Zhao Y, Gu Y, et al.Neuroprotective actions of aminoguanidine involve reduced the activation of calpain and caspase-3 in a rat model of stroke. Neurochem Int,56(4):634-41.
[30]Ma D, Chow S, Obrocka M,et al. Induction of microtubule associated protein 1B expression in Schwann cells during nerve regeneration. Brain Res,1999, 823:141-153.
[31]Blomgren K, McRae A, Elmered A, et al. The calpain proteolytic system in neonatal hypoxic-ischemia. Ann N Y Acad Sci,1997,825:104-19.
[32]Talmor D, Applebaum A, Rudich A, et al. Activation of mitogen-activated protein kinases in human heart during cardiopulmonary bypass. Circ Res, 2000,86:1004-7.
[33]Tokita-Ishikawa Y, Wakusawa R, Abe T.Evaluation of Retinal Degeneration in P27KIP1 Null Mouse. Adv Exp Med Biol.2010;664:467-71.
[34]Hemmer E, Kohl Y, Colquhoun V, et al. Probing cytotoxicity of gadolinium hydroxide nanostructures. J Phys Chem B,2010,114(12):4358-65.
[35]Morales-Avila E, Ferro-Flores G, Vallarino-Kelly T, et al. Radiosensitization of murine normoblasts in vivo by bromodeoxyuridine to the genotoxicity and cytotoxicity of the bone-seeking radiopharmaceutical 153Sm-EDTMP. Radiat Res.2010,173(3):386-91.
[36]Erguven M, Yazihan N, Aktas E, et al. Carvedilol in glioma treatment alone and with imatinib in vitro. Int J Oncol.2010,36(4):857-66.
[37]Smith JM, Hechtman A, Swann J. Fluctuations in cellular proliferation across the light/dark cycle in the subgranular zone of the dentate gyrus in the adult male Syrian hamster. Neurosci Lett.2010,12;473(3):192-5.
[38]Cho SR, Kim YR, Kang HS, et al. Functional recovery after the transplantation of neurally differentiated mesenchymal stem cells derived from bone barrow in a rat model of spinal cord injury. Cell Transplant. 2009;18(12):1359-68.
[39]Blakemore WF.Ethidium bromide induced demyelination in the spinal cord of the cat. Neuropathol Appl Neurobiol,1982,8:365-75.
[40]Faber-Elman A, Solomon A, Abraham JA,et al. Involvement of wound-associated factors in rat brain astrocyte migratory response to axonal injury:in vitro simulation. J Clin Invest,1996:162-71.
[41]Fushimi S, Shirabe T.The reaction of glial progenitor cells in remyelination following ethidium bromide-induced demyelination in the mouse spinal cord. Neuropathology,2002:233-42.
[1]李哲,方征宇,黄晓琳.不同强度磁刺激对星形胶质细胞迁移的影响及其机制研究.中华物理医学与康复杂志,2010,32(4)：249-252。
[2]Hamidi M, Slagter HA, Tononi G,et al. Brain responses evoked by high-frequency repetitive TMS:An ERP study. Brain Stimulat. 2010,3(1):2-17.
[3]Salvador R, Miranda PC. Transcranial magnetic stimulation of small animals: a modeling study of the influence of coil geometry, size and orientation. Conf Proc IEEE Eng Med Biol Soc.2009,2009:674-7.
[4]Hindy NC, Hamilton R, Houghtling AS, et al.Computer-mouse tracking reveals TMS disruptions of prefrontal function during semantic retrieval. J Neurophysiol.2009,102(6):3405-13.
[5]Ahmed Z, Wieraszko A. The influence of pulsed magnetic fields (PMFs) on nonsynaptic potentials recorded from the central and peripheral nervous systems in vitro. Bioelectromagnetics.2009,30(8):621-30.
[6]Wieraszko A, Ahmed Z. Axonal release of glutamate analog, d-2,3-3H-Aspartic acid and 1-14C-proline from segments of sciatic nerve following electrical and magnetic stimulation. Neurosci Lett. 2009,458(1):19-22.
[7]Chaudhry K, Rogers R, Guo M, et al. Matrix metalloproteinase-9 (MMP-9) expression and extracellular signal-regulated kinase 1 and 2 (ERK1/2) activation in exercise-reduced neuronal apoptosis after stroke. Neurosci Lett. 2010,474(2):109-14.
[8]Armstead WM, Kiessling JW, Bdeir K, et al. Adrenomedullin prevents sex-dependent impairment of autoregulation during hypotension after piglet brain injury through inhibition of ERK MAPK upregulation. J Neurotrauma. 2010,27(2):391-402.
[9]Xie KM, Hou XF, Li MQ, et al. NME1 at the human maternal-fetal interface downregulates titin expression and invasiveness of trophoblast cells via MAPK pathway in early pregnancy. Reproduction.2010,139(4):799-808.
[10]Menakongka A, Suthiphongchai T. Involvement of PI3K and ERK1/2 pathways in hepatocyte growth factor-induced cholangiocarcinoma cell invasion. World J Gastroenterol.2010,16(6):713-22.
[11]Newton R, King EM, Gong W, et al. MEK modulates force fluctuation-induced relengthening of canine tracheal smooth muscle. Glucocorticoids inhibit IL-1beta-induced GM-CSF expression at multiple levels:roles for the ERK pathway and repression by MKP-1. Biochem J. 2010,427(1):113-24.
[12]Fang Z, Duthoit N, Wicher G,et al. Intracellular calcium-binding protein S100A4 influences injury-induced migration of white matter astrocytes.Acta Neuropathol,2006,111:213-9.
[13]李哲,方征宇,黄晓琳.不同剂量U0126抑制低频磁刺激引起的星形胶质细胞迁移的实验研究.中国康复医学杂志,2010,25(3)：195-199。
[14]Santamaria PG, Nebreda AR. Deconstructing ERK signaling in tumorigenesis. Mol Cell.2010,38(1):3-5.
[15]Fang H, Zhang LF, Meng FT, et al. Acute hypoxia promote the phosphorylation of tau via ERK pathway. Neurosci Lett.2010,474(3):173-7.
[16]LoRusso PM, Krishnamurthi SS, Rinehart JJ, et al. Phase I pharmacokinetic and pharmacodynamic study of the oral MAPK/ERK kinase inhibitor PD-0325901 in patients with advanced cancers. Clin Cancer Res. 2010,16(6):1924-37.
[17]Lu Z, Zreiqat H. Beta-tricalcium phosphate exerts osteoconductivity through alpha2betal integrin and down-stream MAPK/ERK signaling pathway. Biochem Biophys Res Commun.2010,394(2):323-9.
[18]Lee EG, Yun HJ, Lee SI, et al. Ethyl Acetate Fraction from Cudrania Tricuspidata Inhibits IL-1 beta-Stimulated Osteoclast Differentiation through Downregulation of MAPKs, c-Fos and NFATc1. Korean J Intern Med. 2010,25(1):93-100.
[19]Shiflett MW, Brown RA, Balleine BW. Acquisition and performance of goal-directed instrumental actions depends on ERK signaling in distinct regions of dorsal striatum in rats. J Neurosci.2010 Feb 24;30(8):2951-9.
[20]Pearson G, Robinson F, Beers Gibson T, et al. Mitogen-activated protein (MAP) kinase pathways:regulation and physiological functions[J]. Endocr Rev,2001,22(2):153-83.
[21]Favata, M.F., et al. Identfication of a novel inhibitor of mitogen-activated protein kinase kinase[J]. J. Biol. Chem.1998,273:18623-32.
[22]Talmor D, Applebaum A, Rudich A, et al. Activation of mitogen-activated protein kinases in human heart during cardiopulmonary bypass [J]. Circ Res, 2000,86:1004-7.
[1]Berardelli A, Inghilleri M, Rothwell JC, et al. Facilitation of muscle evoked responses after repetitive cortical stimulation in man. Exp Brain Res 1998,122:79-84.
[2]Chen R, Classen J, Gerloff C, et al. Depression of motor cortex excitability by low-frequency transcranial magnetic stimulation. Neurology,1997,48:1398-403.
[3]Pascual-Leone A, Tormos JM, Keenan J, et al. Study and modulation of human cortical excitability with transcranial magnetic stimulation. J Clin Neurophysiol, 1998,15:333-43.
[4]Fang Z, Duthoit N, Wicher G,et al. Intracellular calcium-binding protein S100A4 influences injury-induced migration of white matter astrocytes.Acta Neuropathol,2006,111:213-9.
[5]李哲方征宇黄晓琳.不同强度磁刺激对星形胶质细胞迁移的影响及其机制研究.中华物理医学与康复杂志,2010,32(4)：249-252
[6]Marie-Anne Vanderhasselt, Rudi De Raedt, Lemke Leyman, et al. Acute effects of repetitive transcranial magneticstimulation on attentional control are related to antidepressant outcomes. J Psychiatry Neurosci,2009,34(2):119-26.
[7]Mobascher A, Arends M, Eschweiler GW, et al. Biological correlates of prefrontal activating and temporoparietal inhibiting treatment with repetitive transcranial magnetic stimulation (rTMS). Fortschr Neurol Psychiatr.2009,77(8):432-43.
[8]Verges S, Maffiuletti NA, Kerherve H, et al. Comparison of electrical and magnetic stimulations to assess quadriceps muscle function. J Appl Physiol. 2009,106(2):701-10.
[9]Dimitrijevic A, Lolli B, Michalewski HJ, et al. Intensity changes in a continuous tone:auditory cortical potentials comparison with frequency changes. Clin Neurophysiol.2009,120(2):374-83.
[10]Se Hee Jung, Jae Eun Shin, Yong-Seol Jeong, et al. Changes in motor cortical excitability induced by high-frequency repetitive transcranial magnetic stimulation of different stimulation durations. Clinical Neurophysiology, 2008,119:71-9
[1]Fang Z, Duthoit N, Wicher G,et al. Intracellular calcium-binding protein S100A4 influences injury-induced migration of white matter astrocytes.Acta Neuropathol,2006,111:213-9.
[2]李哲,方征宇,黄晓琳.不同剂量U0126抑制高频磁刺激引起的星形胶质细胞迁移.中国康复,2010,25(2)：86-89。
[3]李哲方征宇黄晓琳.不同强度磁刺激对星形胶质细胞迁移的影响及其机制研究.中华物理医学与康复杂志,2010,32(4)：249-252。
[4]李哲方征宇黄晓琳.不同剂量U0126抑制低频磁刺激引起的星形胶质细胞迁移的实验研究.中国康复医学杂志,2010,25(3)：195-199。
[1]Qu X, Wen J, Zhang J,et al. Development and application of extremely low frequency multi-waveform electromagnetic field generator. Sheng Wu Yi Xue Gong Cheng Xue Za Zhi,2009,26:173-6.
[2]Zyss T.Magnetotherapy. Neuro Endocrinol Lett,2008,29 Suppl 1:161-201.
[3]Barker AT.An Introduction to the Basic Principles of Magnetic Nerve Stimulation. Journal of Clinical Neurophysiology,1991,8(1):26-37.
[4]Ueno Shoogo.Biomagnetic approaches to studying the brain.IEEE Engineering in Medic Biology,1999,18(3):108-20.
[5]王洪磁刺激设计及感应电场检测的研究：硕士学位论文重庆：重庆大学,2003。
[6]郑建斌,霍小林,吴昌哲等.经颅磁刺激系统各主要参数实现的量化设计.中国临床康复,2004,8(34)：7655-7。
[7]陈昭燃,张蔚婷,韩济生.经颅磁刺激：生理、心理、脑成像及其临床应用.生理科学进展,2004,35(2)：102-106。
[8]Polsen MJR, Freeston JL. Stimulation of nerve trunk with time varying magnetic field. Med Biol Eng Comput,1982,20:243-7.
[9]Barker AT, Jalinous R, Freeston IL. Non-invasive Stimulation of the Human Motor Cortex. Lancet,1985,1:1106-7.
[10]Barker AT, Freeston IL,Jalinous R,et al. Magnetic Stimulation of the Human Brain. J Physiol(Lond),1985,3:369-74.
[11]蓝青,郭铁成.经颅磁刺激研究中风的新进展.中国康复,1997,12(2)：88-89。
[12]高志强.经颅磁刺激运动诱发电位.中华神经精神科杂志,1990,123(5)：309-11。
[13]Amassian V, Cadwell J,Ceacco RQ,et al.Focal Cerveral and Peripheral Nerve Stimulation in Man with the Magnetic Coil. J Physiol(Lond),1987,24:390-5.
[14]Cohen LG, Bradley J, Roth JN,et al. Efffects of Coil Design on Delivery of Focal MagneticStimulation:Technical Considerations.Electroencephalography and Clinical Neurophsiology,1990,75:350-7.
[15]Ueno S, Tashiro T, Harada K.Localize Stimulation of the Human Brain and Spinal Cord by a pair of Opposing Pulsed Magnetic Fields. J Appl Phys,1990,66:5838-40.
[16]程艮.经颅磁刺激在精神科的应用.国外医学精神病学分册,2003,30(1)：8-10.
[17]Takata S, Ikata T. Differences in energy metabolism and neuromuscular transmission between 30-Hz and 100-Hz stimulation in rat skeletal muscle. Arch Phys Med Rehabil.2001,82(5):666-70.
[18]Todd G, Flavel SC, Ridding MC. Priming theta-burst repetitive transcranial magnetic stimulation with low-and high-frequency stimulation. Exp Brain Res.2009,195:307-15.
[19]Ross ML, Koren SA, Persinger MA. Physiologically patterned weak magnetic fields applied over left frontal lobe increase acceptance of false statements as true. Electromagn Biol Med.2008,27:365-71.
[20]胡永善,白玉龙,林伟平,等.经颅磁刺激促进周围神经再生的实验研究.中华物理医学与康复杂志,2003,25：267-69.
[21]Bervar M. Effect of weak, interrupted sinusoidal low frequency magnetic field on neural regeneration in rats:functional evaluation. Bioelectromagnetics 2005,26:351-6.
[22]Battocletti JH, Macias MY, Pintar FA,et al. A box coil for the stimulation of biological tissue and cells in vitro and in vivo by pulsed magnetic fields.IEEE Trans Biomed Eng,2000,47:402-8.
[23]Macias MY,Battocletti JH,Sutton CH, et al. Directed and enhanced neurite growth with pulsed magnetic field stimulation. Bioelectromagnetics, 2000,21:272-86.
[24]Mert T, Gunay I, Gocmen C,et al. Regenerative effects of pulsed magnetic field on injured peripheral nerves.Altern Ther Health Med,2006,12:42-9.
[25]De Pedro JA,Perez-Caballer AJ, Dominguez J,et al. Pulsed electromagnetic fields induce peripheral nerve regeneration and endplate enzymatic changes. Bioelectromagnetic,2005,26:20-7.
[26]Byers JM, Clark KF, Thompson GC. Effect of pulsed electromagnetic stimulation on facial nerve regeneration. Arch Otolaryngol Head Neck Surg,1998,124:383-9.
[27]Rusovan A, Kanje M, Mild KH. The stimulatory effect of magnetic fields on regeneration of the rat sciatic nerve is frequency dependent. Exp Neurol, 1992,117:81-4.
[28]Rusovan A, Kanje M. Stimulation of regeneration of the rat sciatic nerve by 50 Hz sinusoidal magnetic fields. Exp Neurol,1991,112:312-316. 2005,115:881-92.
[29]李新志,郭风劲,陈安民,等.磁刺激对脊髓损伤后神经再生的影响.中国康复,2001,16：129-131。
[30]许涛,郭风劲,郭铁成,等.磁刺激对损伤大鼠脊髓组织巢蛋白表达的影响.中华物理医学与康复杂志,2005,27：720-723。
[31]刘传玉,梅元武,张小乔.经颅磁刺激对局灶性脑缺血大鼠梗死周边区GAP243和Syp表达的影响.卒中与神经疾病,2006,13：15-8。
[32]Sun LY, Hsieh DK, Yu DC,et al. Effect of pulsed electromagnetic field on the proliferation and differentiation potential of human bone marrow mesenchymal stem cells.Bioelectromagnetics,2009,30:251-60.
[33]赵合庆,刘晶,余锋,等.经颅磁刺激对短暂性大脑中动脉闭塞大鼠突触素表达和超微结构改变的影响.中华脑血管病杂志,2008,1：25-27。
[34]许涛,郭风劲,郭铁成,等.磁刺激对大鼠离体神经干细胞生长和分化的影响.中华物理医学与康复杂志,2005,27：129-132。
[35]许涛,饶耀剑,郭风劲,等.磁刺激对大鼠神经干细胞CD K5基因表达的影响.中国康复,2006,21：294-296。
[36]郭风劲,李新志,许涛,等.磁刺激对脊髓神经组织损伤的早期保护作用.中国康复,2001,16：4-6。
[37]Grassi C,Ascenzo M,Torsello A,et al. Effects of 50 Hz electromagnetic fields on voltage-gated Ca2+ channels and their role in modulation of neuroendocrine cell proliferation and death. Cell Calcium,2004,35:307-15.
[38]Rusovan A, Kanje M.D600, a Ca2+ antagonist, prevents stimulation of nerve regeneration by magnetic fields. Neuroreport,1992,3:813-4.
[39]Yue L,Xiao-Lin H,Tao S. The effects of chronic repetitive transcranial magnetic stimulation on glutamate and gamma-aminobutyric acid in rat brain.Brain Res,2009,19:423-31.
[40]许涛,郭风劲,李新志,等.磁刺激对脊髓损伤组织c-fos基因表达的影响.中华物理医学与康复杂志,2003,25：3-6。
[41]董巧云, 顾平,王全懂,等.经颅磁刺激对帕金森病小鼠黑质区多巴胺能神经元及脑源性神经营养因子表达的影响.第二军医大学学报,2008,3：46-49。
[42]孙永安,赵合庆,张志琳,等.长程经颅磁刺激对脑梗死大鼠皮质脑源性神经营养因子表达及神经功能恢复的影响.中华物理医学与康复杂志,2005,27：712-716。
[43]张小乔,梅元武,刘传玉,等.经颅磁刺激对脑梗死大鼠神经功能恢复与皮层BDNF表达的影响.卒中与神经疾病,2006,13：259-261。
[44]张小乔,梅元武,刘传玉.经颅磁刺激对脑梗死大鼠皮质c2Fos和BDNF表达的影响.中华物理医学与康复杂志,2006,28：86-89。
[45]李新志,郭风劲,许涛,等.磁刺激和碱性成纤维细胞生长因子对脊髓损伤后神经再生的影响.中华创伤杂志,2004,20：491-492。
[46]郭风劲,李新志,许 涛,等.磁刺激和碱性成纤维细胞生长因子对脊髓损伤早期的保护作用.脊柱外科杂志,2004,2：345-348。
[47]Chan P,Eng LF,Lin VW. Effects of pulsed magnetic stimulation on GFAP levels in cultured astrocytes. J Neurosci Res,1999,55:238-244.
[48]宋毅军,田心.低频经颅磁刺激对颞叶癫痫大鼠颞叶和海马细胞凋亡的影响.中国神经科学杂志,2004,：14-17。
[49]Yao C, Mi Y, Hu X, et al. Experiment and mechanism research of SKOV3 cancer cell apoptosis induced by nanosecond pulsed electric field.Conf Proc IEEE Enq Med Biol Soc,2008,2008:1044-7.
[1]Johansson CB, Momma DL, Clarke M. Idebtification of a neural stem cell in the adult mammalian central nervous system. Cell,1999,96:25-34.
[2]Chiasson BJ, Tropepe V, Morshead CM, et al. Adult mammmalian forebrain ependymal and subependymal cells demonstrate proliferative potential, but only subependymal cells have neural stem cell charicteristics. J Neurosci, 1999,19:4462-71.
[3]Shibuya S, Miyamoto O, Auer RN, et al. Embryonic intermediate filament, nestin, expression following traumatic spinal cord injury in adult rats. Neuroscience,2002,114:905-16.
[4]Yamamoto S, Yamamoto N, Kitamura T,et al. Proliferation of parenchymal neural progenitors in response to injury in the adult rat spinal cord. Exp Neurol,2001,172:115-27.
[5]张辉,尹宗生,张胜权等.成体小鼠脊髓实质神经干细胞的分离培养及其多能性的鉴定.中华创伤杂志。2006,22(7)：527-530。
[6]Pfeifer K, Vroemen M, Blesch A, et al. Adult neural progenitor cells provide a permisssive guiding substrate for corticospinal axon growth following spinal cord injury. Eur J Neurosci,2004,20:1695-704.
[7]Vroemen M, Aigner L, Weikler J,et al. Adult neural progenitor cell grafts survive after acute spinal cord injury and integrate along axonal pathways. Eur J Neurosci,2003,18,743-51.
[8]Profyris C, Cheema SS, Zang D, et al. Degenerative and regenerative machanisms governing spinal cord injury. Neurobiol Dis,2004, 15(3):415-36.
[9]Schnell L, Schwab ME. Sprouting and regeneration of lesioned corticcspinal tract fibe in the adult rat spinal cord. Eur J Neurosci,1993,5(9):1156-71.
[10]Horvat JC. Spinal cord reconstruction and neural transplants. New the rapeutic vectors. Bull Acad Natl Med,1994,178(3):455-63.
[11]Joesten EA, Bar PR, Gispen WH. Directional regrowth of lesioned corticcspinal tract axons in the adult rat spinal cord. Neuroscience,1995, 69(2):619-26.
[12]Lu P, JonesL L, Tuszynski MH. BDNF-expressing marrow stromal cells support extensive axonal growth at sites of spinal cord injury.Exp Neurol, 2005,191(2):344-60.
[13]Arthur B, Mary JR, Lynne CW. NGF message and protein distribution in the injured rat spinal cord. Exp Neurol,2004,188(1):115-27.
[14]Qiao L,Vizzard MA. Up-regulation of tyrosine kinase(Trka,Trkb) receptor expression and phosphorylation in lumbosacral dorsal root ganglia after chronic spinal cord(T8-T10)injury.Comp Neurol,2002,449(3):217-30.
[15]Cao X, Tang C, LuoY. Effect of nerve growth factor on neuronal apoptosis after spinal cord injury in rats. Neurotrauma,2002,5(3):131-5.
[16]Kim DH, Jahng TA.Continuous brain-derived neurotrophic factor(BDNF) infusion after methylprednisolone treatment in severe spinal cord injury. Korean Med Sci,2004,19(1):113-22.
[17]Novikova LN, Kellerth JO. Differential effects of neurotrophins on neuronal survival and axonal regeneration after spinal cord injury in adult rats.Comp Neurol,2002,452(3):255-63.
[18]Skaper SD, Moore SE, Walsh FS. Cell signaling cascades regulating neuronal growth promoting and inhibitory cues. Prog Neurobio,2001, 65:593-608.
[19]Suenaga T, Satoh T, Somboonthum P, et al. Myelin-associated glycoprotein mediates membrane fusion and entry of neurotropic herpesviruses. Proc Natl Acad Sci U S A.2010,107(2):866-71.
[20]Broggini T, Nitsch R, Savaskan NE. Plasticity-related gene 5 (PRG5) induces filopodia and neurite growth and impedes lysophosphatidic acid-and nogo-A-mediated axonal retraction. Mol Biol Cell,21(4):521-37.
[21]Prinjha R, Moore SE, Vinson M, et al. Inhibitor of neurite outgrowth in
humans. Nature,2000,403:383-4.
[22]Goldbery JL, Barree BA. Nogo in nerve regeneration. Nature,2000,403:369-70.
[23]Pasterkamp RJ, Giger RJ, Ruitenberg MJ,et al. Expression of the gene encoding the chemorepellent semaphorin Ⅲ is induced in the fibroblast component of neural scar tissue formed following injuries of adult but not neonatal CNS. Mol Cell Neurosci.1999,13(2):143-66.
[24]Kawasaki T, Kitsukawa T, Bekku Y, et al. A requirement for neuropilin-1 in embryonic vessel formation. Development.1999,126(21):4895-902.
[25]Soker S, Miao HQ, Nomi M, et al. VEGF165 mediates formation of complexes containing VEGFR-2 and neuropilin-1 that enhance VEGF165-receptor binding. J Cell Biochem.2002;85(2):357-68.
[26]Kolodkin AL, Levengood DV, Rowe EG, et al. Neuropilin is a semaphorin Ⅲ receptor. Cell.1997,90(4):753-62.
[27]Vikis HG, Li W, He Z, et al. The semaphoring receptor plex-in-B1 specifically interacts with active Rac in a ligand2dependent manner. Proc Natl Acad Sci,2000,97:12457-62.
[28]Tatagiba M, Brosamle C, Schwab ME. Regeneration of injured axons in the adult mammalian central nervous system. Neurosurg,1997,40(3):541-7.
[29]Chen MS, Huber AB, van der Haar ME, et al. Nogo-A is a myelinassociated neurite outgrowth inhibitor and an antigen for monoclonal antibody IN-1. Nature,2000,403(29):434-9.
[30]Schnell L, Schwab ME. Axonal regeneration in the rat spinal cord producted by an antibody against myelinassociated neurite growth inhibition. Neuron,1990,343:269-70.
[31]肖卫东,易成腊,陈安民等.成年大鼠SCI后神经生长导向因子Netrin和Slit的表达及定位.中国脊柱脊髓杂志,2006,16(11)：843-846
[32]闵敏,丁新生,田向阳,等.神经生长导向因子slitmRNA在人胚胎脊髓的原位杂交定位.江苏医药杂志2001,30(5)：337-338.
[33]刘宏志,李佐文,杨永利.脊髓损伤大鼠组织形态学变化与不同时点的Netrin-1表达.中国临床康复,2005,9(14)：98-99.
[34]Hagino S, Iseki K, Mori T, et al. Slit and glypican-1 mRNAs are coexpressed in the reactive astrocytes of the injuried adult brain. Glia,2003,42(2): 130-138.
[35]Lin L,Rao Y, Isacson O. Nestrin-1 and slit-2 regulate and disrect neurite growth of ventral midbrain dopaminergic neurons. Mol Cell Neurosci, 2005,28(3):547-55.
[36]Li GL, Farooque M, Olsson Y, et al. Change of Fas and Fas ligand immunoreactivity after compression trauma to rat spinal cord. Acta Neuropathal(Berl),2000,100(1):75-81.
[37]Emery E, Aldana P,Bunge MB, et al. Apoptosis after traumatic human spinal cord injury. J Neurosurg,1998,89(4):911-20.
[38]Van De Craen M, Van Loo, Pype S, et al. Identification of a new caspase homologue:caspase-14.Cell Death Differ,1998,5(10):838-46.
[39]李军利,陈平.转录因子活化蛋白-2α对人脐静脉内皮细胞ECV304细胞凋亡和半胱氨酸天冬氨酸蛋白酶-3活化的影响.中华结核和呼吸杂志,2009,32(12)：931-934。
[40]李立萍,张建新,李兰芳.L-精氨酸通过抑制凋亡途径对脂多糖导致的急性肺损伤的作用.中国药理学与毒理学杂志,2009,23(6)：417-422。
[41]沈彤,马秦,叶良平,等.三氯乙烯诱导人表皮角质形成细胞凋亡的实验研究.中华医学杂志,2009,89(44)：3101-3105
[42]傅强,侯铁胜,鲁凯伍等.大鼠脊髓急性损伤后神经细胞凋亡及相关基因表达.中国脊柱脊髓杂志,2001,11(2)：92-94。
[43]Zoltan NO, Stanley JK. Checkpoints of dueling dimers foil death wishes.Cell,1999,79(2):189-92.
[44]Buganim Y, Solomon H, Rais Y, et al. p53 Regulates the Ras circuit to inhibit the expression of a cancer-related gene signature by various molecular pathways. Cancer Res.2010,70(6):2274-84.
[45]Tsiambas E, Kravvaritis C, Tsounis D, et al. Correlation between different p53 expression patterns and chromosome 17 imbalances in pancreatic ductal adenocarcinoma based on tissue microarray analysis. J BUON.2010 15(1):94-100.
[46]Maringer K, Elliott G. Recruitment of herpes simplex virus type 1 immediate-early protein ICPO to the virus particle. J Virol.2010, 84(9):4682-96.
[47]Nakahara S, Yone K, Sakou T, et al. Induction of apoptosis signal regulating kinase1(ASK1) after spinal cord injury in rats possible invovle of ASK1-JNK and P38 pathways in neuronal apoptosis.Neuropathol Exp Neurol,1999.58 (3):442-50.
[48]马传学,杨青.脊髓损伤的治疗进展[J].江苏药学与临床研究,2006,14(1)：15-16。
[49]Fehlings MG,Tator CH.The effect of direct current field polarity on Recovery after acute experimental spinal cord injury.Brain Res,1992,579:32-3.
[50]沈宁江,朱家恺.电刺激与周围神经再生.中华显微外科杂志,1992,15：184-186。
[51]Borgens RB,Blighr AR,Murphy DJ,etal. Transected dorsal colum2naxons within the guinea pig spinal cord regenerate in the presence of An applied electic fields.J Comp Neurol,1986,250:168-80.
[52]Strautman AF,Cork RJ,Robinson KR,etal.The distribution of free calcium in transected spinal axons and its modulation by appliedelectrical fields. J Neuro sci,1990,10:3564-75.
[53]郭家松,曾园山,陈玉玲,等.督脉电针治疗大鼠全横断性脊髓损伤的实验研究.中国针灸,2003,23(6)：351-4。
[54]陈雅云,曾园山,陈玉玲,等.电针在脊髓损伤修复中的应用基础研究概况.针刺研究,2005,3(2)：120-4。
[55]Shapiro,Borgens RB,Pascuzzi R,etal. Oscillating field stimulation for complete spinal cord injury in humans:a phase 1 trial.J Neurosurg Spine,2005,2(1): 3-10.
[56]徐帆,陈建敏,张 晓.细胞移植治疗脊髓损伤的研究进展.四川生理科学杂志2006,28(3)：123-126。
[57]谢兴文,施 杞.嗅鞘细胞移植治疗脊髓损伤的进展.第二军医大学学报,2005,26(10)：1181-1183。
[58]冯世庆周先虎孔晓红等.自体激活雪旺细胞移植治疗急性脊髓损伤的实验研究.中华骨科杂志2006,26(8)：553-557。
[59]褚尤彪 罗卓荆 宫伟等.嗅鞘细胞对脊髓源性神经干细胞分化的影响.中华创伤杂志,2006,22(2)：136-139。
[60]冯大雄,宋跃明.生物多聚合物与脊髓损伤后再生.国际骨科学杂志,2006,27(1)： 55-59。
[61]侯天勇,伍亚民,陈恒胜.神经干细胞假体移植促进脊髓损伤后功能恢复的实验研究.中华物理医学与康复杂志,2005,28(6)：368-372。
[62]吴军, 孙天胜, 王献章等.神经营养素-3基因修饰嗅鞘细胞移植对急性脊髓损伤作用的实验研究.中国脊柱脊髓杂志,2006,16(2)：147-151。
[63]尹国栋,汤逊,林月秋等.人胚胎嗅鞘细胞与神经干细胞联合移植修复大鼠脊髓全横断损伤的研究.中国康复医学杂志,2006,21(8)：680-682。
[64]张强,邹德威.脑源性神经营养因子转基因细胞移植和神经节苷脂对大鼠脊髓损伤N-甲基-D-天门冬氨酸受体的影响.中华创伤骨科杂志,2006,8(2)：162-164。
[65]程朝辉郑启新.神经组织工程修复脊髓损伤的研究进展.国际生物医学工程杂志,2006,29(5)：280-285。
[1]王传英,肖宛平,李庆波.脊髓损伤的治疗及康复进展.神经损伤与功能重建,2006,1(4)：245-246。
[2]杨迎暴,朴英杰.脊髓损伤模型的建立及其评价标准.中华创伤杂志,2002,18(3)：187-189.
[3]Allen AR. Surgery of experimental lessions of spinal cord equivalent to crush injury of fracture dislocation. Preliminary Report. JAMA,1911,57:878-80.
[4]Kaptanoglu E, Tuncel M, Palaoglu S, et al. Comparison of the effects of malatonin and methylprednisolone in experimental spinal cord injury. J Neurosurg,2000,93(1 Suppl):S77-S84.
[5]Falconer JC, Narayana PA, Bhattacharjee M, et al.Characterization of experimental spinal cord injury model using waveform and morphometric analysis. Spine,1996,21:104-12.
[6]Khan T, Havey RM, Sayers ST,et al.Animal models of spinal cord contusion injuries. Lab Anim Sci,1999,49:161-72.
[7]张磊,梅元武.不同途径给予神经生长因子对大鼠脊髓损伤后的影响.中风与神经疾病杂志,2006,23(1)：55-57。
[8]张国庆,燕景锋,刘世勤.BDNF基因修饰神经干细胞移植对大鼠脊髓损伤后神经细胞凋亡的影响.山东医药,2006,46(14)：22-23。
[9]钱 军,孙正义,马延超等.大鼠脊髓损伤后M A P 2的表达及与运动功能恢复的相关性.西安交通大学学报(医学版),2006,27(5)：489-492。
[10]陈君.大鼠胚胎神经干细胞异体移植对脊髓损伤的修复.河北医药,2006,28(10)：904-905。
[11]陈庆山,陈欣,杨磊等.大鼠自体嗅成鞘细胞移植治疗脊髓损伤的实验研究.解剖学报,2005,36(5)：477-480。
[12]王 民,王栋琪,宋焕瑾.脊髓损伤后大鼠后肢运动功能恢复不同评分标准的比较.西安交通大学学报(医学版),27(3)：243-244。
[13]冯世庆,周先虎,孔晓红等.自体激活雪旺细胞移植治疗急性脊髓损伤 的实验研究.中华骨科杂志,2006,26(8)：553-557。
[14]陈钢,梁群,陈安民等.二甲胺四环素对大鼠脊髓损伤后iNOS表达及细胞凋亡的影响.中国现代医学杂志,2006,16(8)：1177-1180。
[15]孟步亮,尹 昭,李 明.脊髓半横断损伤后腹角神经元神经生长因子、脑源性神经营养因子、神经营养因子3和神经营养因子4表达的变化.解剖学杂志,2006,29(2)：221。
[16]王革生,张庆俊,韩忠朝.人脐带间充质干细胞对大鼠脊髓损伤神经功能恢复的评价.中华神经外科杂志,2006,22(1)：19-22。
[17]侯天勇,伍亚民,李 强等.大鼠脊髓半切块状缺损模型的建立及科学性评估.创伤外科杂志,2006,8(4)：362-365。
[18]蔡中续,李玉华,祁磊,等.嗅粘膜源性嗅鞘细胞移植联合NGF对脊髓损伤的修复.山东大学学报.医学版,2007,45(5)：470-473,477。
[19]魏开斌,刘爱华,杨宪勇,等.嗅球组织块和细胞悬液移植对脊髓损伤的修复.中华实验外科杂志,2005,22(3)：359-360。
[20]孙永明,郑祖根,董启榕,等.周围神经移植联合神经营养因子治疗损伤脊髓的实验研究.江苏医药,2003,29(8)：578-580。
[21]Kim D. Anderson, Ardi Gunawan, Oswald Steward. Spinal pathways involved in the control of forelimb motor function in rats. Experimental Neurology,2007,206:318-9.
[22]尹国栋,汤逊,林月秋等.人胚胎嗅鞘细胞与神经干细胞联合移植修复大鼠脊髓全横断损伤的研究.中国康复医学杂志,2006,21(8)：680-682
[23]Sara J. Taylor, Shelly E. Sakiyama-Elbert. Effect of controlled delivery of neurotrophin-3 from fibrin on spinal cord injury in a long term model. Journal of Controlled Release,2006,116:204-10。
[24]刘 雷,唐康来,杨 柳等.碱性成纤维细胞生长因子对牵张性脊髓损伤后ChAT表达的影响.第三军医大学学报,2006,28(14)：1493-4。
[25]赵宁辉,李云霞,黄晓玮等.脊髓损伤后醛缩酶A和M型乳酸脱氢酶表达的变化.中华创伤杂志,2006,22(7)：523-524。
[26]Maiko Okada, Osamu Miyamoto, Sei Shibuya, et al. Expression and role of type I collagen in a rat spinal cord contusion injury model, Neuroscience Research,2007,58:371-2。
[27]张峡,王正国,朱佩芳.脊髓腹侧压迫损伤后MP、Iloprost和Riluzole对BCL-2表达的影响.中国脊柱脊髓杂志,2001,11(5)：282-284。
[28]Watson BD, Prado R, Dietrich WD, et al. Protochemically induced spinal cord injury in the rat. Brain Res,1986,367:296-300.
[29]Cameron T, Prado R, Watson BD, et al. Protochemically induced cystic lesion in the rat spinal cord.Ⅰ.Behavioral and morphological analysis. Exp Neurol,1990,109:214-23.
[30]von Euler M, Seiger A, Sundstrom E. Clip compression injury in the spinal cord:a correlative study of neurological and morphological alterations. Exp Neurol,1997,145:502-10.
[31]Baffour R, Achanta K, Kaufman J,et al. Synergistic effect of basic fibroblast growth factor and methyprednisolone on neurological function after experimental spinal cord injury. J Neurosurg,1995,83:105-10.
[32]Blakemore WF.Ethidium bromide induced demyelination in the spinal cord of the cat. Neuropathol Appl Neurobiol,1982,8:365-75.
[33]Faber-ElmanA,SolomonA,AbrahamJA,etal.Involvement of wound-associated factors in rat brain astrocyte migratory response to axonal injury:in vitro simulation. J Clin Invest,1996:162-71.
[34]Fushimi S, Shirabe T.The reaction of glial progenitor cells in remyelination following ethidium bromide-induced demyelination in the mouse spinal cord. Neuropathology,2002:233-42.
[35]Christian Broamle, Andrea B. Huber. Cracking the black box-and putting it back together again:Animal models of pinal cord injury. DrugDiscoveryToday:DiseaseModel,2006,3(4):341-42.
[36]Dimou,L.etal. Nogo-A-deficient mice reveal strain-dependentdifferences in axonal regeneration. J. Neurosci.2006,26,5591-603.
[37]Basso, D.M. et al. Basso Mouse Scale for locomotion detectsdifferences in recovery after spinal cord injury in five common mousestrains. J. Neurotrauma,2006,23,635-59.
[38]伍亚民,王正国,朱佩芳,等.脊髓缺血损伤模型及行为学的实验研究.中华创伤杂志,2000,16：538-540。
[2]Chiasson BJ,Tropepe V,Morshead CM, et al. Adult mammmalian forebrain ependymal and subependymal cells demonstrate proliferative potential, but only subependymal cells have neural stem cell characteristics. J Neurosci, 1999,19(11):4462-71.
[3]Profyris C, Cheema SS, Zang D, et al. Degenerative and regenerative machanisms governing spinal cord injury. Neurobiol Dis,2004,15(3):415-36.
[4]Schnell L, Schwab ME. Sprouting and regeneration of lesioned corticcspinal tract fibe in the adult rat spinal cord. Eur J Neurosci,1993,5(9):1156-71.
[5]Horvat JC. Spinal cord reconstruction and neural transplants. New the rapeutic vectors. Bull Acad Natl Med,1994,178(3):455-63.
[6]Joesten EA, Bar PR, Gispen WH. Directional regrowth of lesioned corticcspinal tract axons in the adult rat spinal cord. Neuroscience,1995,69(2):619-26.
[7]Lu P, JonesL L, Tuszynski MH. BDNF-expressing marrow stromal cells support extensive axonal growth at sites of spinal cord injury.Exp Neurol, 2005,191(2):344-60.
[8]Arthur B,Mary JR,Lynne CW. NGF message and protein distribution in the injured rat spinal cord. Exp Neurol,2004,188(1):115-27.
[9]Qiao L,Vizzard MA. Up-regulation of tyrosine kinase(Trka,Trkb) receptor expression and phosphorylation in lumbosacral dorsal root ganglia after chronic spinal cord(T8-T10)injury.Comp Neurol,2002,449(3):217-30.
[10]Cao X,Tang C,Luo Y. Effect of nerve growth factor on neuronal apoptosis after spinal cord injury in rats.Neurotrauma,2002,5(3):131-5.
[11]Kim DH,Jahng TA. Continuous brain-derived neurotrophic factor(BDNF)infusion after methylprednisolone treatment in severe spinal cord injury.Korean Med Sci,2004,19(1):113-22.
[12]Novikova LN, Kellerth JO. Differential effects of neurotrophins on neuronal survival and axonal regeneration after spinal cord injury in adult rats.Comp Neurol,2002,452(3):255-63.
[13]Skaper SD, Moore SE, Walsh FS. Cell signaling cascades regulating neuronal growth2promoting and inhibitory cues. Prog Neurobio,2001,65:593-608.
[14]Prinjha R, Moore SE, Vinson M, et al. Inhibitor of neurite outgrowth in humans. Nature,2000,403(6768):383-4.
[15]Goldbery JL, Barree BA. Nogo in nerve regeneration. Nature, 2000,403(6768):369-70.
[16]Vikis HG, Li W, He Z, et al. The semaphorin receptor plexin-B1 specifically interacts with active Rac in a ligand-dependent manner. Proc Natl Acad Sci, 2000,97(23):12457-62.
[17]Tatagiba M, Brosamle C, Schwab ME. Regeneration of injured axons in the adult mammalian central nervous system. Neurosurg,1997,40(3):541-7.
[18]Chen MS, Huber AB,Vander Haar ME,et al. Nogo-A is a myelinassociated neurite outgrowth inhibitor and an antigen for monoclonal antibody IN-1. Nature,2000,403(29):434-9.
[19]Schnell L, Schwab ME. Axonal regeneration in the rat spinal cord producted by an antibody against myelin-associated neurite growth inhibitors.Nature, 1990,343(6255):269-72.
[20]Hagino S, Iseki K, Mori T, et al. Slit and glypican-1 mRNAs are coexpressed in the reactive astrocytes of the injuried adult brain. Glia,2003,42(2):130-8.
[21]Lin L,Rao Y, Isacson O. Nestrin-1 and slit-2 regulate and disrect neurite growth of ventral midbrain dopaminergic neurons. Mol Cell Neurosci,2005,28(3):547-55.
[22]Li GL,Farooque M,Olsson Y,et al. Change of Fas and Fas ligand immunoreactivity after compression trauma to rat spinal cord. Acta Neuropathal(Berl),2000,100(1):75-81.
[23]Emery E, Aldana P,Bunge MB, et al. Apoptosis after traumatic human spinal cord injury. J Neurosurg,1998,89(6):911-20.
[24]Van De Craen M,Van Loo,Pype S,et al. Identification of a new caspase homologue:caspase 14.Cell Death Differ,1998,5(10):838-46.
[25]Zoltan NO,Stanley JK. Checkpoints of dueling diermers foil death wishes.Cell,1994,79(2):189-92.
[26]Nakahara S, Yone K, Sakou T, et al. Induction of apoptosis signal regulating kinase1(ASK1) after spinal cord injury in rats:possible invovle of ASK1-JNK and P38 pathways in neuronal apoptosis.Neuropathol Exp Neurol,1999.58(3):442-50.
[27]马传学,杨青.脊髓损伤的治疗进展[J].江苏药学与临床研究,2006,14(1)：15-16。
[28]Fehlings MQTator CH. The effect of direct current field polarity on Recovery after acute experimental spinal cord injury.Brain Res,1992,579 (1):32-42.
[29]沈宁江,朱家恺.电刺激与周围神经再生.中华显微外科杂志,1992,15(3)：184-186。
[30]Borgens RB,Blighr AR,Murphy DJ,et al. Transected dorsal column axons within the guinea pig spinal cord regenerate in the presence of an applied electic fields.J Comp Neurol,1986,250(2):168-80.
[31]Strautman AF,Cork RJ,Robinson KR,et al. The distribution of free calcium in transected spinal axons and its modulation by appliedelectrical fields.J Neuro sci,1990,10(11):3564-75.
[32]郭家松,曾园山,陈玉玲,等.督脉电针治疗大鼠全横断性脊髓损伤的实验研究.中国针灸,2003,23(6)：351-354。
[33]Kusano K, Enomoto M, Hirai T,et al. Transplanted neural progenitor cells expressing mutant NT3 promote myelination and partial hindlimb recovery in the chronic phase after spinal cord injury. Biochem Biophys Res Commun. 2010,393(4):812-7.
[34]Caprani A,Richert A,Guglielmi JP,et al. Preliminary study of pulsed-electromagnetic fields effects on endothelial (HUVEC) cell secretions-modulation of the thrombo-hemorrhagic balance.Electromagn Biol Med.2008,27(4):386-92.
[35]Qu X, Wen J, Zhang J,et al. Development and application of extremely low frequency multi-waveform electromagnetic field generator. Sheng Wu Yi Xue Gong Cheng Xue Za Zhi,2009,26(1):173-76.
[36]Zyss T.Magnetotherapy. Neuro Endocrinol Lett,2008,29 Suppl 1:161-201.
[37]Todd G, Flavel SC, Ridding MC. Priming theta-burst repetitive transcranial magnetic stimulation with low-and high-frequency stimulation. Exp Brain Res. 2009,195(2):307-15.
[38]Ross ML, Koren SA, Persinger MA. Physiologically patterned weak magnetic fields applied over left frontal lobe increase acceptance of false statements as true. Electromagn Biol Med.2008,27(4):365-71.
[39]Macias MY,Battocletti JH,Sutton CH, et al. Directed and enhanced neurite growth with pulsed magnetic field stimulation. Bioelectromagnetics, 2000,21(4):272-7.
[1]Silver J, Miller JH. Regeneration beyond the glial scar.Nat Rev Neurosci,2004,5(2):146-56.
[2]Talbott JF, Loy DN, Liu Y,et al. Endogenous Nkx2.2+/Olig2+ oligodendrocyte precursor cells fail to remyelinate the demyelinated adult rat spinal cord in the absence of astrocytes. Exp Neurol,2005,192(1):11-24.
[3]White RE, McTigue DM, Jakeman LB. Regional heterogeneity in astrocyte responses following contusive spinal cord injury in mice. J Comp Neurol. 2010,518(8):1370-90.
[4]Pekny M, Nilsson M. Astrocyte activation and reactive gliosis. Glia 2005,50(4):427-34.
[5]Silver J, Miller JH. Regeneration beyond the glial scar. Neurosci. 2004,5:146-56.
[6]A.T. Barker, I.L. Freeston, R. Jalinous, et al. Magnetic stimulation of the human brain and peripheral nervous system-an introduction and the results of an initial clinical evaluation. Neurosurgery,1987,20:100-9.
[7]J.C. Rothwell, P.D. Thompson, B.L. Day, et al.Stimulation of the human motor cortex through the scalp. Exp. Physiol.1991,76:159-200.
[8]Siebner HR. Treatment of Movement Disorders. In:Hallett M, Chokroverty S (eds) Magnetic stimulation in clinical neurophysiology.2005,2nd edn. Elsevier, Philadelphia.
[9]Dutta SK, Ghosh B, Blackman CF. Radiofrequency radiationinduced calcium ion efflux enhancement from human and other neuroblastoma cells in culture. Bioelectromagnetics,1989,10:197-202.
[10]Goodman R, Henderson AS. Exposure of salivary gland cells to low-frequency electromagnetic fields alters polypeptide synthesis. Proc Natl Acad Sci USA 1988,85:3928-32.
[11]Goodman EM, Greenebaum B, Marron MT. Effects of electromagnetic fields
on molecules and cells. Int Rev Cytol,1995.158:279-337.
[12]Fujiki M, Steward O. High frequency transcranial magnetic stimulation mimics the effects of ECS in upregulating astroglial gene expression in the murine CNS. Molecular Brain Res,1996,44:301-8.
[13]Philip Chan,Lawrence Feng,Yuen Lee, et al.Effects of pulsed magnetic stimulation on GFAP levels in cultured astrocytes. Journal of Neuroscience Research,1999,55:238-44.
[14]孙永安,赵合庆,张志琳,等.长程经颅磁刺激对脑梗死大鼠皮质脑源性神经营养因子表达及神经功能恢复的影响.中华物理医学与康复杂志,2005,27：712-716。
[15]Fang Z, Duthoit N, Wicher G,et al. Intracellular calcium-binding protein S100A4 influences injury-induced migration of white matter astrocytes.Acta Neuropathol,2006,111:213-9.
[16]卢培刚,冯华,王宪荣,等.高压氧预处理对大鼠脊髓损伤后和巢蛋白表达的影响.中华神经外科疾病研究杂志,2008,7(2)：149-153。
[17]肖锋,季玉红,孙琳琳,等.细胞周期蛋白依赖性蛋白激酶11在大鼠脊髓横断性损伤后的表达变化.解剖学报,2008,39(1)：1-6。
[18]李幼忱,李志成,刘杰,等.大鼠皮肤创伤愈合瘢痕的三维重建和体积定量.中国体视学与图像分析,2007,12：1-5。
[19]Malhotra S, Shnitka T, Elabrink J. Reactive astrocytes:A review. Cytobios, 1990,61:133-60.
[20]Sofroniew MV, Vinters HV. Astrocytes:biology and pathology. Acta Neuropathol.2010,119(1):7-35.
[21]Hinkle D. Baldwin S, Schef S, et al. GFAP and S100 gene expression in the codex and hippocampusin response to mild comical contusion. J Ncurotrauma,1997,14:729-38.
[22]Lim JH, Gibbons HM, O'Carroll SJ, et al. Extracellular signal-regulated kinase involvement in human astrocyte migration. Brain Res, 2007,1164:1-13.
[23]Kurtis I, Songwan Jin, Kazunori Uchida, et al. Greatly impaired migration of implanted aquaporin-4-deficient astroglial cells in mouse brain toward a site of injury. FASEB J,2007,21:108-16.
[24]Kimura-Kuroda J, Teng X, Komuta Y, et al.An in vitro model of the inhibition of axon growth in the lesion scar formed after central nervous system injury. Mol Cell Neurosci.2010,43(2):177-87.
[25]Frontczak-Baniewicz M, Struzynska L, Andrychowski J, et al.Ultrastructural and immunochemical studies of glial scar formation in diabetic rats. Acta Neurochir Suppl.2010;106:251-5.
[26]Zhu WZ, Ni JX, Tang Q, Study on the effect of cluster needling of scalp acupuncture on the plasticity protein MAP-2 in rats with focal cerebral infarction. Zhongguo Zhen Jiu,2010,30(1):46-50.
[27]Kinugasa-Taniguchi Y, Tomimatsu T, Mimura K, et al.Human C-reactive protein enhances vulnerability of immature rats to hypoxic-ischemic brain damage:a preliminary study. Reprod Sci,17(5):419-25.
[28]Lin Q, Hai J, Yao LY, et al.Neuroprotective effects of NSTyr on cognitive function and neuronal plasticity in rats of chronic cerebral hypoperfusion. Brain Res.2010,1325:183-90.
[29]Sun M, Zhao Y, Gu Y, et al.Neuroprotective actions of aminoguanidine involve reduced the activation of calpain and caspase-3 in a rat model of stroke. Neurochem Int,56(4):634-41.
[30]Ma D, Chow S, Obrocka M,et al. Induction of microtubule associated protein 1B expression in Schwann cells during nerve regeneration. Brain Res,1999, 823:141-153.
[31]Blomgren K, McRae A, Elmered A, et al. The calpain proteolytic system in neonatal hypoxic-ischemia. Ann N Y Acad Sci,1997,825:104-19.
[32]Talmor D, Applebaum A, Rudich A, et al. Activation of mitogen-activated protein kinases in human heart during cardiopulmonary bypass. Circ Res, 2000,86:1004-7.
[33]Tokita-Ishikawa Y, Wakusawa R, Abe T.Evaluation of Retinal Degeneration in P27KIP1 Null Mouse. Adv Exp Med Biol.2010;664:467-71.
[34]Hemmer E, Kohl Y, Colquhoun V, et al. Probing cytotoxicity of gadolinium hydroxide nanostructures. J Phys Chem B,2010,114(12):4358-65.
[35]Morales-Avila E, Ferro-Flores G, Vallarino-Kelly T, et al. Radiosensitization of murine normoblasts in vivo by bromodeoxyuridine to the genotoxicity and cytotoxicity of the bone-seeking radiopharmaceutical 153Sm-EDTMP. Radiat Res.2010,173(3):386-91.
[36]Erguven M, Yazihan N, Aktas E, et al. Carvedilol in glioma treatment alone and with imatinib in vitro. Int J Oncol.2010,36(4):857-66.
[37]Smith JM, Hechtman A, Swann J. Fluctuations in cellular proliferation across the light/dark cycle in the subgranular zone of the dentate gyrus in the adult male Syrian hamster. Neurosci Lett.2010,12;473(3):192-5.
[38]Cho SR, Kim YR, Kang HS, et al. Functional recovery after the transplantation of neurally differentiated mesenchymal stem cells derived from bone barrow in a rat model of spinal cord injury. Cell Transplant. 2009;18(12):1359-68.
[39]Blakemore WF.Ethidium bromide induced demyelination in the spinal cord of the cat. Neuropathol Appl Neurobiol,1982,8:365-75.
[40]Faber-Elman A, Solomon A, Abraham JA,et al. Involvement of wound-associated factors in rat brain astrocyte migratory response to axonal injury:in vitro simulation. J Clin Invest,1996:162-71.
[41]Fushimi S, Shirabe T.The reaction of glial progenitor cells in remyelination following ethidium bromide-induced demyelination in the mouse spinal cord. Neuropathology,2002:233-42.
[1]李哲,方征宇,黄晓琳.不同强度磁刺激对星形胶质细胞迁移的影响及其机制研究.中华物理医学与康复杂志,2010,32(4)：249-252。
[2]Hamidi M, Slagter HA, Tononi G,et al. Brain responses evoked by high-frequency repetitive TMS:An ERP study. Brain Stimulat. 2010,3(1):2-17.
[3]Salvador R, Miranda PC. Transcranial magnetic stimulation of small animals: a modeling study of the influence of coil geometry, size and orientation. Conf Proc IEEE Eng Med Biol Soc.2009,2009:674-7.
[4]Hindy NC, Hamilton R, Houghtling AS, et al.Computer-mouse tracking reveals TMS disruptions of prefrontal function during semantic retrieval. J Neurophysiol.2009,102(6):3405-13.
[5]Ahmed Z, Wieraszko A. The influence of pulsed magnetic fields (PMFs) on nonsynaptic potentials recorded from the central and peripheral nervous systems in vitro. Bioelectromagnetics.2009,30(8):621-30.
[6]Wieraszko A, Ahmed Z. Axonal release of glutamate analog, d-2,3-3H-Aspartic acid and 1-14C-proline from segments of sciatic nerve following electrical and magnetic stimulation. Neurosci Lett. 2009,458(1):19-22.
[7]Chaudhry K, Rogers R, Guo M, et al. Matrix metalloproteinase-9 (MMP-9) expression and extracellular signal-regulated kinase 1 and 2 (ERK1/2) activation in exercise-reduced neuronal apoptosis after stroke. Neurosci Lett. 2010,474(2):109-14.
[8]Armstead WM, Kiessling JW, Bdeir K, et al. Adrenomedullin prevents sex-dependent impairment of autoregulation during hypotension after piglet brain injury through inhibition of ERK MAPK upregulation. J Neurotrauma. 2010,27(2):391-402.
[9]Xie KM, Hou XF, Li MQ, et al. NME1 at the human maternal-fetal interface downregulates titin expression and invasiveness of trophoblast cells via MAPK pathway in early pregnancy. Reproduction.2010,139(4):799-808.
[10]Menakongka A, Suthiphongchai T. Involvement of PI3K and ERK1/2 pathways in hepatocyte growth factor-induced cholangiocarcinoma cell invasion. World J Gastroenterol.2010,16(6):713-22.
[11]Newton R, King EM, Gong W, et al. MEK modulates force fluctuation-induced relengthening of canine tracheal smooth muscle. Glucocorticoids inhibit IL-1beta-induced GM-CSF expression at multiple levels:roles for the ERK pathway and repression by MKP-1. Biochem J. 2010,427(1):113-24.
[12]Fang Z, Duthoit N, Wicher G,et al. Intracellular calcium-binding protein S100A4 influences injury-induced migration of white matter astrocytes.Acta Neuropathol,2006,111:213-9.
[13]李哲,方征宇,黄晓琳.不同剂量U0126抑制低频磁刺激引起的星形胶质细胞迁移的实验研究.中国康复医学杂志,2010,25(3)：195-199。
[14]Santamaria PG, Nebreda AR. Deconstructing ERK signaling in tumorigenesis. Mol Cell.2010,38(1):3-5.
[15]Fang H, Zhang LF, Meng FT, et al. Acute hypoxia promote the phosphorylation of tau via ERK pathway. Neurosci Lett.2010,474(3):173-7.
[16]LoRusso PM, Krishnamurthi SS, Rinehart JJ, et al. Phase I pharmacokinetic and pharmacodynamic study of the oral MAPK/ERK kinase inhibitor PD-0325901 in patients with advanced cancers. Clin Cancer Res. 2010,16(6):1924-37.
[17]Lu Z, Zreiqat H. Beta-tricalcium phosphate exerts osteoconductivity through alpha2betal integrin and down-stream MAPK/ERK signaling pathway. Biochem Biophys Res Commun.2010,394(2):323-9.
[18]Lee EG, Yun HJ, Lee SI, et al. Ethyl Acetate Fraction from Cudrania Tricuspidata Inhibits IL-1 beta-Stimulated Osteoclast Differentiation through Downregulation of MAPKs, c-Fos and NFATc1. Korean J Intern Med. 2010,25(1):93-100.
[19]Shiflett MW, Brown RA, Balleine BW. Acquisition and performance of goal-directed instrumental actions depends on ERK signaling in distinct regions of dorsal striatum in rats. J Neurosci.2010 Feb 24;30(8):2951-9.
[20]Pearson G, Robinson F, Beers Gibson T, et al. Mitogen-activated protein (MAP) kinase pathways:regulation and physiological functions[J]. Endocr Rev,2001,22(2):153-83.
[21]Favata, M.F., et al. Identfication of a novel inhibitor of mitogen-activated protein kinase kinase[J]. J. Biol. Chem.1998,273:18623-32.
[22]Talmor D, Applebaum A, Rudich A, et al. Activation of mitogen-activated protein kinases in human heart during cardiopulmonary bypass [J]. Circ Res, 2000,86:1004-7.
[1]Berardelli A, Inghilleri M, Rothwell JC, et al. Facilitation of muscle evoked responses after repetitive cortical stimulation in man. Exp Brain Res 1998,122:79-84.
[2]Chen R, Classen J, Gerloff C, et al. Depression of motor cortex excitability by low-frequency transcranial magnetic stimulation. Neurology,1997,48:1398-403.
[3]Pascual-Leone A, Tormos JM, Keenan J, et al. Study and modulation of human cortical excitability with transcranial magnetic stimulation. J Clin Neurophysiol, 1998,15:333-43.
[4]Fang Z, Duthoit N, Wicher G,et al. Intracellular calcium-binding protein S100A4 influences injury-induced migration of white matter astrocytes.Acta Neuropathol,2006,111:213-9.
[5]李哲方征宇黄晓琳.不同强度磁刺激对星形胶质细胞迁移的影响及其机制研究.中华物理医学与康复杂志,2010,32(4)：249-252
[6]Marie-Anne Vanderhasselt, Rudi De Raedt, Lemke Leyman, et al. Acute effects of repetitive transcranial magneticstimulation on attentional control are related to antidepressant outcomes. J Psychiatry Neurosci,2009,34(2):119-26.
[7]Mobascher A, Arends M, Eschweiler GW, et al. Biological correlates of prefrontal activating and temporoparietal inhibiting treatment with repetitive transcranial magnetic stimulation (rTMS). Fortschr Neurol Psychiatr.2009,77(8):432-43.
[8]Verges S, Maffiuletti NA, Kerherve H, et al. Comparison of electrical and magnetic stimulations to assess quadriceps muscle function. J Appl Physiol. 2009,106(2):701-10.
[9]Dimitrijevic A, Lolli B, Michalewski HJ, et al. Intensity changes in a continuous tone:auditory cortical potentials comparison with frequency changes. Clin Neurophysiol.2009,120(2):374-83.
[10]Se Hee Jung, Jae Eun Shin, Yong-Seol Jeong, et al. Changes in motor cortical excitability induced by high-frequency repetitive transcranial magnetic stimulation of different stimulation durations. Clinical Neurophysiology, 2008,119:71-9
[1]Fang Z, Duthoit N, Wicher G,et al. Intracellular calcium-binding protein S100A4 influences injury-induced migration of white matter astrocytes.Acta Neuropathol,2006,111:213-9.
[2]李哲,方征宇,黄晓琳.不同剂量U0126抑制高频磁刺激引起的星形胶质细胞迁移.中国康复,2010,25(2)：86-89。
[3]李哲方征宇黄晓琳.不同强度磁刺激对星形胶质细胞迁移的影响及其机制研究.中华物理医学与康复杂志,2010,32(4)：249-252。
[4]李哲方征宇黄晓琳.不同剂量U0126抑制低频磁刺激引起的星形胶质细胞迁移的实验研究.中国康复医学杂志,2010,25(3)：195-199。
[1]Qu X, Wen J, Zhang J,et al. Development and application of extremely low frequency multi-waveform electromagnetic field generator. Sheng Wu Yi Xue Gong Cheng Xue Za Zhi,2009,26:173-6.
[2]Zyss T.Magnetotherapy. Neuro Endocrinol Lett,2008,29 Suppl 1:161-201.
[3]Barker AT.An Introduction to the Basic Principles of Magnetic Nerve Stimulation. Journal of Clinical Neurophysiology,1991,8(1):26-37.
[4]Ueno Shoogo.Biomagnetic approaches to studying the brain.IEEE Engineering in Medic Biology,1999,18(3):108-20.
[5]王洪磁刺激设计及感应电场检测的研究：硕士学位论文重庆：重庆大学,2003。
[6]郑建斌,霍小林,吴昌哲等.经颅磁刺激系统各主要参数实现的量化设计.中国临床康复,2004,8(34)：7655-7。
[7]陈昭燃,张蔚婷,韩济生.经颅磁刺激：生理、心理、脑成像及其临床应用.生理科学进展,2004,35(2)：102-106。
[8]Polsen MJR, Freeston JL. Stimulation of nerve trunk with time varying magnetic field. Med Biol Eng Comput,1982,20:243-7.
[9]Barker AT, Jalinous R, Freeston IL. Non-invasive Stimulation of the Human Motor Cortex. Lancet,1985,1:1106-7.
[10]Barker AT, Freeston IL,Jalinous R,et al. Magnetic Stimulation of the Human Brain. J Physiol(Lond),1985,3:369-74.
[11]蓝青,郭铁成.经颅磁刺激研究中风的新进展.中国康复,1997,12(2)：88-89。
[12]高志强.经颅磁刺激运动诱发电位.中华神经精神科杂志,1990,123(5)：309-11。
[13]Amassian V, Cadwell J,Ceacco RQ,et al.Focal Cerveral and Peripheral Nerve Stimulation in Man with the Magnetic Coil. J Physiol(Lond),1987,24:390-5.
[14]Cohen LG, Bradley J, Roth JN,et al. Efffects of Coil Design on Delivery of Focal MagneticStimulation:Technical Considerations.Electroencephalography and Clinical Neurophsiology,1990,75:350-7.
[15]Ueno S, Tashiro T, Harada K.Localize Stimulation of the Human Brain and Spinal Cord by a pair of Opposing Pulsed Magnetic Fields. J Appl Phys,1990,66:5838-40.
[16]程艮.经颅磁刺激在精神科的应用.国外医学精神病学分册,2003,30(1)：8-10.
[17]Takata S, Ikata T. Differences in energy metabolism and neuromuscular transmission between 30-Hz and 100-Hz stimulation in rat skeletal muscle. Arch Phys Med Rehabil.2001,82(5):666-70.
[18]Todd G, Flavel SC, Ridding MC. Priming theta-burst repetitive transcranial magnetic stimulation with low-and high-frequency stimulation. Exp Brain Res.2009,195:307-15.
[19]Ross ML, Koren SA, Persinger MA. Physiologically patterned weak magnetic fields applied over left frontal lobe increase acceptance of false statements as true. Electromagn Biol Med.2008,27:365-71.
[20]胡永善,白玉龙,林伟平,等.经颅磁刺激促进周围神经再生的实验研究.中华物理医学与康复杂志,2003,25：267-69.
[21]Bervar M. Effect of weak, interrupted sinusoidal low frequency magnetic field on neural regeneration in rats:functional evaluation. Bioelectromagnetics 2005,26:351-6.
[22]Battocletti JH, Macias MY, Pintar FA,et al. A box coil for the stimulation of biological tissue and cells in vitro and in vivo by pulsed magnetic fields.IEEE Trans Biomed Eng,2000,47:402-8.
[23]Macias MY,Battocletti JH,Sutton CH, et al. Directed and enhanced neurite growth with pulsed magnetic field stimulation. Bioelectromagnetics, 2000,21:272-86.
[24]Mert T, Gunay I, Gocmen C,et al. Regenerative effects of pulsed magnetic field on injured peripheral nerves.Altern Ther Health Med,2006,12:42-9.
[25]De Pedro JA,Perez-Caballer AJ, Dominguez J,et al. Pulsed electromagnetic fields induce peripheral nerve regeneration and endplate enzymatic changes. Bioelectromagnetic,2005,26:20-7.
[26]Byers JM, Clark KF, Thompson GC. Effect of pulsed electromagnetic stimulation on facial nerve regeneration. Arch Otolaryngol Head Neck Surg,1998,124:383-9.
[27]Rusovan A, Kanje M, Mild KH. The stimulatory effect of magnetic fields on regeneration of the rat sciatic nerve is frequency dependent. Exp Neurol, 1992,117:81-4.
[28]Rusovan A, Kanje M. Stimulation of regeneration of the rat sciatic nerve by 50 Hz sinusoidal magnetic fields. Exp Neurol,1991,112:312-316. 2005,115:881-92.
[29]李新志,郭风劲,陈安民,等.磁刺激对脊髓损伤后神经再生的影响.中国康复,2001,16：129-131。
[30]许涛,郭风劲,郭铁成,等.磁刺激对损伤大鼠脊髓组织巢蛋白表达的影响.中华物理医学与康复杂志,2005,27：720-723。
[31]刘传玉,梅元武,张小乔.经颅磁刺激对局灶性脑缺血大鼠梗死周边区GAP243和Syp表达的影响.卒中与神经疾病,2006,13：15-8。
[32]Sun LY, Hsieh DK, Yu DC,et al. Effect of pulsed electromagnetic field on the proliferation and differentiation potential of human bone marrow mesenchymal stem cells.Bioelectromagnetics,2009,30:251-60.
[33]赵合庆,刘晶,余锋,等.经颅磁刺激对短暂性大脑中动脉闭塞大鼠突触素表达和超微结构改变的影响.中华脑血管病杂志,2008,1：25-27。
[34]许涛,郭风劲,郭铁成,等.磁刺激对大鼠离体神经干细胞生长和分化的影响.中华物理医学与康复杂志,2005,27：129-132。
[35]许涛,饶耀剑,郭风劲,等.磁刺激对大鼠神经干细胞CD K5基因表达的影响.中国康复,2006,21：294-296。
[36]郭风劲,李新志,许涛,等.磁刺激对脊髓神经组织损伤的早期保护作用.中国康复,2001,16：4-6。
[37]Grassi C,Ascenzo M,Torsello A,et al. Effects of 50 Hz electromagnetic fields on voltage-gated Ca2+ channels and their role in modulation of neuroendocrine cell proliferation and death. Cell Calcium,2004,35:307-15.
[38]Rusovan A, Kanje M.D600, a Ca2+ antagonist, prevents stimulation of nerve regeneration by magnetic fields. Neuroreport,1992,3:813-4.
[39]Yue L,Xiao-Lin H,Tao S. The effects of chronic repetitive transcranial magnetic stimulation on glutamate and gamma-aminobutyric acid in rat brain.Brain Res,2009,19:423-31.
[40]许涛,郭风劲,李新志,等.磁刺激对脊髓损伤组织c-fos基因表达的影响.中华物理医学与康复杂志,2003,25：3-6。
[41]董巧云, 顾平,王全懂,等.经颅磁刺激对帕金森病小鼠黑质区多巴胺能神经元及脑源性神经营养因子表达的影响.第二军医大学学报,2008,3：46-49。
[42]孙永安,赵合庆,张志琳,等.长程经颅磁刺激对脑梗死大鼠皮质脑源性神经营养因子表达及神经功能恢复的影响.中华物理医学与康复杂志,2005,27：712-716。
[43]张小乔,梅元武,刘传玉,等.经颅磁刺激对脑梗死大鼠神经功能恢复与皮层BDNF表达的影响.卒中与神经疾病,2006,13：259-261。
[44]张小乔,梅元武,刘传玉.经颅磁刺激对脑梗死大鼠皮质c2Fos和BDNF表达的影响.中华物理医学与康复杂志,2006,28：86-89。
[45]李新志,郭风劲,许涛,等.磁刺激和碱性成纤维细胞生长因子对脊髓损伤后神经再生的影响.中华创伤杂志,2004,20：491-492。
[46]郭风劲,李新志,许 涛,等.磁刺激和碱性成纤维细胞生长因子对脊髓损伤早期的保护作用.脊柱外科杂志,2004,2：345-348。
[47]Chan P,Eng LF,Lin VW. Effects of pulsed magnetic stimulation on GFAP levels in cultured astrocytes. J Neurosci Res,1999,55:238-244.
[48]宋毅军,田心.低频经颅磁刺激对颞叶癫痫大鼠颞叶和海马细胞凋亡的影响.中国神经科学杂志,2004,：14-17。
[49]Yao C, Mi Y, Hu X, et al. Experiment and mechanism research of SKOV3 cancer cell apoptosis induced by nanosecond pulsed electric field.Conf Proc IEEE Enq Med Biol Soc,2008,2008:1044-7.
[1]Johansson CB, Momma DL, Clarke M. Idebtification of a neural stem cell in the adult mammalian central nervous system. Cell,1999,96:25-34.
[2]Chiasson BJ, Tropepe V, Morshead CM, et al. Adult mammmalian forebrain ependymal and subependymal cells demonstrate proliferative potential, but only subependymal cells have neural stem cell charicteristics. J Neurosci, 1999,19:4462-71.
[3]Shibuya S, Miyamoto O, Auer RN, et al. Embryonic intermediate filament, nestin, expression following traumatic spinal cord injury in adult rats. Neuroscience,2002,114:905-16.
[4]Yamamoto S, Yamamoto N, Kitamura T,et al. Proliferation of parenchymal neural progenitors in response to injury in the adult rat spinal cord. Exp Neurol,2001,172:115-27.
[5]张辉,尹宗生,张胜权等.成体小鼠脊髓实质神经干细胞的分离培养及其多能性的鉴定.中华创伤杂志。2006,22(7)：527-530。
[6]Pfeifer K, Vroemen M, Blesch A, et al. Adult neural progenitor cells provide a permisssive guiding substrate for corticospinal axon growth following spinal cord injury. Eur J Neurosci,2004,20:1695-704.
[7]Vroemen M, Aigner L, Weikler J,et al. Adult neural progenitor cell grafts survive after acute spinal cord injury and integrate along axonal pathways. Eur J Neurosci,2003,18,743-51.
[8]Profyris C, Cheema SS, Zang D, et al. Degenerative and regenerative machanisms governing spinal cord injury. Neurobiol Dis,2004, 15(3):415-36.
[9]Schnell L, Schwab ME. Sprouting and regeneration of lesioned corticcspinal tract fibe in the adult rat spinal cord. Eur J Neurosci,1993,5(9):1156-71.
[10]Horvat JC. Spinal cord reconstruction and neural transplants. New the rapeutic vectors. Bull Acad Natl Med,1994,178(3):455-63.
[11]Joesten EA, Bar PR, Gispen WH. Directional regrowth of lesioned corticcspinal tract axons in the adult rat spinal cord. Neuroscience,1995, 69(2):619-26.
[12]Lu P, JonesL L, Tuszynski MH. BDNF-expressing marrow stromal cells support extensive axonal growth at sites of spinal cord injury.Exp Neurol, 2005,191(2):344-60.
[13]Arthur B, Mary JR, Lynne CW. NGF message and protein distribution in the injured rat spinal cord. Exp Neurol,2004,188(1):115-27.
[14]Qiao L,Vizzard MA. Up-regulation of tyrosine kinase(Trka,Trkb) receptor expression and phosphorylation in lumbosacral dorsal root ganglia after chronic spinal cord(T8-T10)injury.Comp Neurol,2002,449(3):217-30.
[15]Cao X, Tang C, LuoY. Effect of nerve growth factor on neuronal apoptosis after spinal cord injury in rats. Neurotrauma,2002,5(3):131-5.
[16]Kim DH, Jahng TA.Continuous brain-derived neurotrophic factor(BDNF) infusion after methylprednisolone treatment in severe spinal cord injury. Korean Med Sci,2004,19(1):113-22.
[17]Novikova LN, Kellerth JO. Differential effects of neurotrophins on neuronal survival and axonal regeneration after spinal cord injury in adult rats.Comp Neurol,2002,452(3):255-63.
[18]Skaper SD, Moore SE, Walsh FS. Cell signaling cascades regulating neuronal growth promoting and inhibitory cues. Prog Neurobio,2001, 65:593-608.
[19]Suenaga T, Satoh T, Somboonthum P, et al. Myelin-associated glycoprotein mediates membrane fusion and entry of neurotropic herpesviruses. Proc Natl Acad Sci U S A.2010,107(2):866-71.
[20]Broggini T, Nitsch R, Savaskan NE. Plasticity-related gene 5 (PRG5) induces filopodia and neurite growth and impedes lysophosphatidic acid-and nogo-A-mediated axonal retraction. Mol Biol Cell,21(4):521-37.
[21]Prinjha R, Moore SE, Vinson M, et al. Inhibitor of neurite outgrowth in
humans. Nature,2000,403:383-4.
[22]Goldbery JL, Barree BA. Nogo in nerve regeneration. Nature,2000,403:369-70.
[23]Pasterkamp RJ, Giger RJ, Ruitenberg MJ,et al. Expression of the gene encoding the chemorepellent semaphorin Ⅲ is induced in the fibroblast component of neural scar tissue formed following injuries of adult but not neonatal CNS. Mol Cell Neurosci.1999,13(2):143-66.
[24]Kawasaki T, Kitsukawa T, Bekku Y, et al. A requirement for neuropilin-1 in embryonic vessel formation. Development.1999,126(21):4895-902.
[25]Soker S, Miao HQ, Nomi M, et al. VEGF165 mediates formation of complexes containing VEGFR-2 and neuropilin-1 that enhance VEGF165-receptor binding. J Cell Biochem.2002;85(2):357-68.
[26]Kolodkin AL, Levengood DV, Rowe EG, et al. Neuropilin is a semaphorin Ⅲ receptor. Cell.1997,90(4):753-62.
[27]Vikis HG, Li W, He Z, et al. The semaphoring receptor plex-in-B1 specifically interacts with active Rac in a ligand2dependent manner. Proc Natl Acad Sci,2000,97:12457-62.
[28]Tatagiba M, Brosamle C, Schwab ME. Regeneration of injured axons in the adult mammalian central nervous system. Neurosurg,1997,40(3):541-7.
[29]Chen MS, Huber AB, van der Haar ME, et al. Nogo-A is a myelinassociated neurite outgrowth inhibitor and an antigen for monoclonal antibody IN-1. Nature,2000,403(29):434-9.
[30]Schnell L, Schwab ME. Axonal regeneration in the rat spinal cord producted by an antibody against myelinassociated neurite growth inhibition. Neuron,1990,343:269-70.
[31]肖卫东,易成腊,陈安民等.成年大鼠SCI后神经生长导向因子Netrin和Slit的表达及定位.中国脊柱脊髓杂志,2006,16(11)：843-846
[32]闵敏,丁新生,田向阳,等.神经生长导向因子slitmRNA在人胚胎脊髓的原位杂交定位.江苏医药杂志2001,30(5)：337-338.
[33]刘宏志,李佐文,杨永利.脊髓损伤大鼠组织形态学变化与不同时点的Netrin-1表达.中国临床康复,2005,9(14)：98-99.
[34]Hagino S, Iseki K, Mori T, et al. Slit and glypican-1 mRNAs are coexpressed in the reactive astrocytes of the injuried adult brain. Glia,2003,42(2): 130-138.
[35]Lin L,Rao Y, Isacson O. Nestrin-1 and slit-2 regulate and disrect neurite growth of ventral midbrain dopaminergic neurons. Mol Cell Neurosci, 2005,28(3):547-55.
[36]Li GL, Farooque M, Olsson Y, et al. Change of Fas and Fas ligand immunoreactivity after compression trauma to rat spinal cord. Acta Neuropathal(Berl),2000,100(1):75-81.
[37]Emery E, Aldana P,Bunge MB, et al. Apoptosis after traumatic human spinal cord injury. J Neurosurg,1998,89(4):911-20.
[38]Van De Craen M, Van Loo, Pype S, et al. Identification of a new caspase homologue:caspase-14.Cell Death Differ,1998,5(10):838-46.
[39]李军利,陈平.转录因子活化蛋白-2α对人脐静脉内皮细胞ECV304细胞凋亡和半胱氨酸天冬氨酸蛋白酶-3活化的影响.中华结核和呼吸杂志,2009,32(12)：931-934。
[40]李立萍,张建新,李兰芳.L-精氨酸通过抑制凋亡途径对脂多糖导致的急性肺损伤的作用.中国药理学与毒理学杂志,2009,23(6)：417-422。
[41]沈彤,马秦,叶良平,等.三氯乙烯诱导人表皮角质形成细胞凋亡的实验研究.中华医学杂志,2009,89(44)：3101-3105
[42]傅强,侯铁胜,鲁凯伍等.大鼠脊髓急性损伤后神经细胞凋亡及相关基因表达.中国脊柱脊髓杂志,2001,11(2)：92-94。
[43]Zoltan NO, Stanley JK. Checkpoints of dueling dimers foil death wishes.Cell,1999,79(2):189-92.
[44]Buganim Y, Solomon H, Rais Y, et al. p53 Regulates the Ras circuit to inhibit the expression of a cancer-related gene signature by various molecular pathways. Cancer Res.2010,70(6):2274-84.
[45]Tsiambas E, Kravvaritis C, Tsounis D, et al. Correlation between different p53 expression patterns and chromosome 17 imbalances in pancreatic ductal adenocarcinoma based on tissue microarray analysis. J BUON.2010 15(1):94-100.
[46]Maringer K, Elliott G. Recruitment of herpes simplex virus type 1 immediate-early protein ICPO to the virus particle. J Virol.2010, 84(9):4682-96.
[47]Nakahara S, Yone K, Sakou T, et al. Induction of apoptosis signal regulating kinase1(ASK1) after spinal cord injury in rats possible invovle of ASK1-JNK and P38 pathways in neuronal apoptosis.Neuropathol Exp Neurol,1999.58 (3):442-50.
[48]马传学,杨青.脊髓损伤的治疗进展[J].江苏药学与临床研究,2006,14(1)：15-16。
[49]Fehlings MG,Tator CH.The effect of direct current field polarity on Recovery after acute experimental spinal cord injury.Brain Res,1992,579:32-3.
[50]沈宁江,朱家恺.电刺激与周围神经再生.中华显微外科杂志,1992,15：184-186。
[51]Borgens RB,Blighr AR,Murphy DJ,etal. Transected dorsal colum2naxons within the guinea pig spinal cord regenerate in the presence of An applied electic fields.J Comp Neurol,1986,250:168-80.
[52]Strautman AF,Cork RJ,Robinson KR,etal.The distribution of free calcium in transected spinal axons and its modulation by appliedelectrical fields. J Neuro sci,1990,10:3564-75.
[53]郭家松,曾园山,陈玉玲,等.督脉电针治疗大鼠全横断性脊髓损伤的实验研究.中国针灸,2003,23(6)：351-4。
[54]陈雅云,曾园山,陈玉玲,等.电针在脊髓损伤修复中的应用基础研究概况.针刺研究,2005,3(2)：120-4。
[55]Shapiro,Borgens RB,Pascuzzi R,etal. Oscillating field stimulation for complete spinal cord injury in humans:a phase 1 trial.J Neurosurg Spine,2005,2(1): 3-10.
[56]徐帆,陈建敏,张 晓.细胞移植治疗脊髓损伤的研究进展.四川生理科学杂志2006,28(3)：123-126。
[57]谢兴文,施 杞.嗅鞘细胞移植治疗脊髓损伤的进展.第二军医大学学报,2005,26(10)：1181-1183。
[58]冯世庆周先虎孔晓红等.自体激活雪旺细胞移植治疗急性脊髓损伤的实验研究.中华骨科杂志2006,26(8)：553-557。
[59]褚尤彪 罗卓荆 宫伟等.嗅鞘细胞对脊髓源性神经干细胞分化的影响.中华创伤杂志,2006,22(2)：136-139。
[60]冯大雄,宋跃明.生物多聚合物与脊髓损伤后再生.国际骨科学杂志,2006,27(1)： 55-59。
[61]侯天勇,伍亚民,陈恒胜.神经干细胞假体移植促进脊髓损伤后功能恢复的实验研究.中华物理医学与康复杂志,2005,28(6)：368-372。
[62]吴军, 孙天胜, 王献章等.神经营养素-3基因修饰嗅鞘细胞移植对急性脊髓损伤作用的实验研究.中国脊柱脊髓杂志,2006,16(2)：147-151。
[63]尹国栋,汤逊,林月秋等.人胚胎嗅鞘细胞与神经干细胞联合移植修复大鼠脊髓全横断损伤的研究.中国康复医学杂志,2006,21(8)：680-682。
[64]张强,邹德威.脑源性神经营养因子转基因细胞移植和神经节苷脂对大鼠脊髓损伤N-甲基-D-天门冬氨酸受体的影响.中华创伤骨科杂志,2006,8(2)：162-164。
[65]程朝辉郑启新.神经组织工程修复脊髓损伤的研究进展.国际生物医学工程杂志,2006,29(5)：280-285。
[1]王传英,肖宛平,李庆波.脊髓损伤的治疗及康复进展.神经损伤与功能重建,2006,1(4)：245-246。
[2]杨迎暴,朴英杰.脊髓损伤模型的建立及其评价标准.中华创伤杂志,2002,18(3)：187-189.
[3]Allen AR. Surgery of experimental lessions of spinal cord equivalent to crush injury of fracture dislocation. Preliminary Report. JAMA,1911,57:878-80.
[4]Kaptanoglu E, Tuncel M, Palaoglu S, et al. Comparison of the effects of malatonin and methylprednisolone in experimental spinal cord injury. J Neurosurg,2000,93(1 Suppl):S77-S84.
[5]Falconer JC, Narayana PA, Bhattacharjee M, et al.Characterization of experimental spinal cord injury model using waveform and morphometric analysis. Spine,1996,21:104-12.
[6]Khan T, Havey RM, Sayers ST,et al.Animal models of spinal cord contusion injuries. Lab Anim Sci,1999,49:161-72.
[7]张磊,梅元武.不同途径给予神经生长因子对大鼠脊髓损伤后的影响.中风与神经疾病杂志,2006,23(1)：55-57。
[8]张国庆,燕景锋,刘世勤.BDNF基因修饰神经干细胞移植对大鼠脊髓损伤后神经细胞凋亡的影响.山东医药,2006,46(14)：22-23。
[9]钱 军,孙正义,马延超等.大鼠脊髓损伤后M A P 2的表达及与运动功能恢复的相关性.西安交通大学学报(医学版),2006,27(5)：489-492。
[10]陈君.大鼠胚胎神经干细胞异体移植对脊髓损伤的修复.河北医药,2006,28(10)：904-905。
[11]陈庆山,陈欣,杨磊等.大鼠自体嗅成鞘细胞移植治疗脊髓损伤的实验研究.解剖学报,2005,36(5)：477-480。
[12]王 民,王栋琪,宋焕瑾.脊髓损伤后大鼠后肢运动功能恢复不同评分标准的比较.西安交通大学学报(医学版),27(3)：243-244。
[13]冯世庆,周先虎,孔晓红等.自体激活雪旺细胞移植治疗急性脊髓损伤 的实验研究.中华骨科杂志,2006,26(8)：553-557。
[14]陈钢,梁群,陈安民等.二甲胺四环素对大鼠脊髓损伤后iNOS表达及细胞凋亡的影响.中国现代医学杂志,2006,16(8)：1177-1180。
[15]孟步亮,尹 昭,李 明.脊髓半横断损伤后腹角神经元神经生长因子、脑源性神经营养因子、神经营养因子3和神经营养因子4表达的变化.解剖学杂志,2006,29(2)：221。
[16]王革生,张庆俊,韩忠朝.人脐带间充质干细胞对大鼠脊髓损伤神经功能恢复的评价.中华神经外科杂志,2006,22(1)：19-22。
[17]侯天勇,伍亚民,李 强等.大鼠脊髓半切块状缺损模型的建立及科学性评估.创伤外科杂志,2006,8(4)：362-365。
[18]蔡中续,李玉华,祁磊,等.嗅粘膜源性嗅鞘细胞移植联合NGF对脊髓损伤的修复.山东大学学报.医学版,2007,45(5)：470-473,477。
[19]魏开斌,刘爱华,杨宪勇,等.嗅球组织块和细胞悬液移植对脊髓损伤的修复.中华实验外科杂志,2005,22(3)：359-360。
[20]孙永明,郑祖根,董启榕,等.周围神经移植联合神经营养因子治疗损伤脊髓的实验研究.江苏医药,2003,29(8)：578-580。
[21]Kim D. Anderson, Ardi Gunawan, Oswald Steward. Spinal pathways involved in the control of forelimb motor function in rats. Experimental Neurology,2007,206:318-9.
[22]尹国栋,汤逊,林月秋等.人胚胎嗅鞘细胞与神经干细胞联合移植修复大鼠脊髓全横断损伤的研究.中国康复医学杂志,2006,21(8)：680-682
[23]Sara J. Taylor, Shelly E. Sakiyama-Elbert. Effect of controlled delivery of neurotrophin-3 from fibrin on spinal cord injury in a long term model. Journal of Controlled Release,2006,116:204-10。
[24]刘 雷,唐康来,杨 柳等.碱性成纤维细胞生长因子对牵张性脊髓损伤后ChAT表达的影响.第三军医大学学报,2006,28(14)：1493-4。
[25]赵宁辉,李云霞,黄晓玮等.脊髓损伤后醛缩酶A和M型乳酸脱氢酶表达的变化.中华创伤杂志,2006,22(7)：523-524。
[26]Maiko Okada, Osamu Miyamoto, Sei Shibuya, et al. Expression and role of type I collagen in a rat spinal cord contusion injury model, Neuroscience Research,2007,58:371-2。
[27]张峡,王正国,朱佩芳.脊髓腹侧压迫损伤后MP、Iloprost和Riluzole对BCL-2表达的影响.中国脊柱脊髓杂志,2001,11(5)：282-284。
[28]Watson BD, Prado R, Dietrich WD, et al. Protochemically induced spinal cord injury in the rat. Brain Res,1986,367:296-300.
[29]Cameron T, Prado R, Watson BD, et al. Protochemically induced cystic lesion in the rat spinal cord.Ⅰ.Behavioral and morphological analysis. Exp Neurol,1990,109:214-23.
[30]von Euler M, Seiger A, Sundstrom E. Clip compression injury in the spinal cord:a correlative study of neurological and morphological alterations. Exp Neurol,1997,145:502-10.
[31]Baffour R, Achanta K, Kaufman J,et al. Synergistic effect of basic fibroblast growth factor and methyprednisolone on neurological function after experimental spinal cord injury. J Neurosurg,1995,83:105-10.
[32]Blakemore WF.Ethidium bromide induced demyelination in the spinal cord of the cat. Neuropathol Appl Neurobiol,1982,8:365-75.
[33]Faber-ElmanA,SolomonA,AbrahamJA,etal.Involvement of wound-associated factors in rat brain astrocyte migratory response to axonal injury:in vitro simulation. J Clin Invest,1996:162-71.
[34]Fushimi S, Shirabe T.The reaction of glial progenitor cells in remyelination following ethidium bromide-induced demyelination in the mouse spinal cord. Neuropathology,2002:233-42.
[35]Christian Broamle, Andrea B. Huber. Cracking the black box-and putting it back together again:Animal models of pinal cord injury. DrugDiscoveryToday:DiseaseModel,2006,3(4):341-42.
[36]Dimou,L.etal. Nogo-A-deficient mice reveal strain-dependentdifferences in axonal regeneration. J. Neurosci.2006,26,5591-603.
[37]Basso, D.M. et al. Basso Mouse Scale for locomotion detectsdifferences in recovery after spinal cord injury in five common mousestrains. J. Neurotrauma,2006,23,635-59.
[38]伍亚民,王正国,朱佩芳,等.脊髓缺血损伤模型及行为学的实验研究.中华创伤杂志,2000,16：538-540。