耐药性颞叶癫痫脑组织中UL16结合蛋白2（ULBP2蛋白）和隆文菌素A（STRN）的表达及临床意义
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摘要
目的:观察ULBP2 (UL16结合蛋白2)和隆文菌素A (STRN)在耐药性颞叶癫痫患者脑组织中的表达,探讨其在耐药性颞叶癫痫发病中的意义。
资料和方法:试验组42例均为临床确诊的耐药性癫痫患者,发作类型符合1981年国际抗癫痫联盟(ILAE)有关癫痫发作分类的标准。其中男26例,女16例,年龄15～56岁,平均26.18±9.60(x±s)岁;病程3～30年,平均为12.88±6.49( x±s)年;发作类型中部分继发全身强直、阵挛或强直-阵挛性发作23例,复杂部分性发作6例,有多种发作类型(单纯部分性、强直性或强直-阵挛性发作)13例。术后获颞叶标本34例,海马标本8例。
对照组共有20例,全部为在我院或第三军医大学新桥医院神经外科行手术减压或清创患者的颞叶和海马脑组织,12例颞叶,8例海马。其中男7例,女5例,年龄16-44岁,平均23.05±9.17岁(X+SD)。
结果:
1.基因芯片结果
耐药性癫痫组脑组织ULBP2蛋白的基因表达上调,与正常对照组间比较有明显差异(Ratio=4.180)。
耐药性癫痫组脑组织STRN蛋白的基因表达下调,与正常对照组间比较有明显差异(Ratio=0.384)。
2.免疫组化
ULBP2主要在神经元和神经胶质细胞的胞膜表达,阴性对照表达极少或无表达。耐药性癫痫颞叶脑组织的A值(AOD值)值为0.0518±0.0232 (x±s),对照组为0.0206±0.0011(x±s),两组方差不起,校正后t’检验结果显示两组间差异有统计学意义(t’=4.969,p<0.05)。耐药性癫痫组海马的AOD值为0.0509±0.0048(x±s),对照组为0.0198±0.0114( x±s),两组间有显著差异(t=2.528, p<0.05)。
STRN正常主要在神经元和神经胶质细胞的胞浆表达,实验组表达极少或无表达。耐药性癫痫颞叶脑组织的A值(AOD值)值为0.3108±0.1087 (x±s),对照组为0.4210±0.1238(x±s),两组方差不起,校正后t’检验结果显示两组间差异有统计学意义(t’=4.858,p<0.05)。耐药性癫痫组海马的AOD值为0.2706±0.0038(x±s),对照组为0.3952±0.0107( x±s),两组间有显著差异(t=2.416, p<0.05)。
3.免疫荧光
在对照组ULBP2蛋白表达极少,而在实验组中ULBP2基因的蛋白表达产物比对照组相同部位的脑组织中表达明显增加。
在对照组STRN蛋白表达明显,而在实验组中STRN蛋白表达产物比对照组相同部位的脑组织中表达明显减少。
4.免疫印记法
ULBP2蛋白条带在对照组明显减弱,反映出实验组中ULBP2基因的蛋白表达产物比对照组相同部位的脑组织中表达明显增加。耐药性癫痫颞叶脑组织灰度值0.9804±0.1401,对照组灰度值0.5914±0.2197,两组间差异有统计学意义(t=2.7633,p<0.05)。耐药性癫痫海马脑组织灰度值0.9832±0.1508,对照组灰度值0.5866±0.1974,两组间差异有统计学意义(t=2.7838,p<0.05)。
STRN蛋白条带在实验组明显减少,反映出实验组中STRN基因的蛋白表达产物比对照组相同部位的脑组织中表达明显减少。耐药性癫痫颞叶脑组织灰度值0.3318±0.1101,对照组灰度值0.5846±0.1024,两组间差异有统计学意义(t=2.6613,p<0.05)。耐药性癫痫海马脑组织灰度值0.2786±0.0308,对照组灰度值0.5686±0.1214,两组间差异有统计学意义(t=2.6808,p<0.05)。
结论:
耐药性颞叶癫痫患者颞叶脑组织中ULBP2基因及蛋白产物表达增高可能与耐药性颞叶癫痫发病中的免疫异常机制有重要关联,甚至可能是关键因素。高表达的ULBP2可通过与NK细胞、T细胞、活性巨噬细胞、CD8细胞表面的NKG.2D受体特异性结合,引起复杂的系列免疫反应,并导致许多自身免疫抗体的大量产生和灭活减少,从而诱发癫痫或是使癫痫发作加重难以控制。它很可能为耐药性颞叶癫痫的免疫治疗提供新的靶点。
耐药性颞叶癫痫患者颞叶脑组织中STRN表达明显降低及其引发的雌激素信号转导和内源性一氧化氮合成减弱在耐药性颞叶癫痫发病中可能有重要作用。
Objective: To study the expression of genes and protein of UL16 binding protein 2 and STRN in the brain tissue of patients with drug-refractory epilepsy , and to explore the possible role in drug-refractory epilepsy and the clinical value.
Materials and Methods: The 42 cases with refractory epilepsy included in this study were obtained from the files of the Departments of Neurosurgery of the following hospitals: the First Affiliated Hospital of Chongqing Univerisyt of Medical Sciences, Beijing Tiantan Hospital, Xuanwu Hospital of the Capital University of Medical Sciences, and Xinqiao Hospital of the Third Military Medical Univeristy. All the patients involved in our study group underwent the surgical resection of temporal lobe tissue. Before surgery, informed consents were obtained for the use of human brain tissues for research, and the study was approved by the local Ethic Committee. Two neuropathologists reviewed all the cases independently. The diagnosis of seizure type was confirmed according to the 1981 International Classification of Epileptic Seizures of the International League Against Epilepsy.
The 20 controls were obtained from the files of the neurosurgery department of the first affiliated hospital of Chongqing University of Medical Sciences. These samples were comprised of temporal neocortical tissues adjacent of the lesion. All patients were diagnosed by pathological tests to have been suffered brain trauma. the two neurophthologists both reviewed these cases to confirm that they had no history of seizures or other neurological disorders as controls.
Gene-chip, immunohistochemistry, immunofluorescence and Western blotting were used to test expression of ULBP2 protein and STRN protein in the surgically removed brain tissue of patients with drug-refractory epilepsy from the brain bank of our department(n=42), and the results were compared with that of normal controls (n=20)。The Computer Graphic Analysis System is used to test the average optical density (AOD) which is expressed as mean±SD( x±s)and tested via t-test. P value less than 0.05 as the level of significance.
Results
1.Gene chip: There was significant difference between the control group and the pharmacoresistance group (Ratio=4.180). The expression of SCN8A gene was shown to be increased in the brain tissues of the pharmacoresistance epilepsy group. There was significant difference between the control group and the pharmacoresistance group (Ratio=0.384). The expression of STRN gene was shown to be decreased in the brain tissues of the pharmacoresistance epilepsy group.
2. Immunohistochemistry : In human temporal cortex of patients with epilepsy, ULBP2 immunoreactivity was consistently observed in all cases and was confined mainly to neurons and glial cells, whereas faint immunoreactivity was apparent in the control brain tissues. Four visual field images were obtained randomly in every section by TC-FY-2050 pathology system acquisi-tioned image and were automatically analyzed by Motic Med 6.0 CMIAS pathology image analysis system. AOD value in epileptic temporal cortex tissue tissues was determined 0.0518±0.0232 ( x±s), and 0.0206±0.0011 ( x±s) in the control. AOD value in hippocampus of pharmacoresistance epilepsy group was determined 0.0509±0.0048( x±s), and 0.0198±0.0114 ( x±s) in the control. ANOVA analysis shows significantly up-regulated ULBP2 in epileptic tissue than the control (P<0.05).
In control brain tissues, STRN immunoreactivity was consistently observed in all cases and was confined mainly to neurons and glial cells, whereas faint immunoreactivity was apparent in control brain tissues. Four visual field images were obtained randomly in every section by TC-FY-2050 pathology system acquisi-tioned image and were automatically analyzed by Motic Med 6.0 CMIAS pathology image analysis system. AOD value in epileptic temporal cortex tissue tissues was determined 0.3108±0.1087 ( x±s), and 0.4210±0.1238 ( x±s) in the control. AOD value in hippocampus of pharmacoresistance epilepsy group was determined 0.2706±0.0038 ( x±s), and 0.3952±0.0107 ( x±s) in the control. ANOVA analysis shows significantly down-regulated STRN in epileptic tissue than the control (P<0.05).
3. Immunofluorescence analysis: In the temporal lobe cortex and hippocampus, strong immunoreactivity for the staining of ULBP2 protein was observed. There were more obvious in the pharmacoresistance epilepsy group than in control group.
In the temporal lobe cortex and hippocampus, faint immunoreactivity for the staining of STRN protein was observed. There were less obvious in the pharmacoresistance epilepsy group than in control group.
4. Western blot: Immunoblot was performed with ULBP2 antibody, the protein was detected by immunoblot as a band at 29kDa. Strongly stained bands were present in all samples of epileptic tissue whereas relative faint expression of the ULBP2 was observed in the control group. Another band ofβ-actin as positive control at 42 kDa also was observed correspondently in every channel. The ratio of optical density of ULBP2 andβ-actin was taken as variance calculated between two groups. Optical density value in Epileptic temporal cortex tissue was 0.9804±0.1401 and 0.5914±0.2197 ( x±s) in the control tissue. Optical density value in Epileptic hippocampus tissue was 0.9832±0.1508 and ( x±s)0.5866±0.1974 in the control tissue.The result shows a significant difference between epileptic tissue and the control group (P<0.05) .
Immunoblot was performed with STRN antibody, the protein was detected by immunoblot as a band at 110kDa. faint stained bands were present in all samples of epileptic tissue whereas relative strongly expression of the STRN was observed in the control group. Another band ofβ-actin as positive control at 42 kDa also was observed correspondently in every channel. The ratio of optical density of STRN andβ-actin was taken as variance calculated between two groups. Optical density value in Epileptic temporal cortex tissue was 0.3318±0.1101 and 0.5846±0.1024 ( x±s) in the control tissue. Optical density value in Epileptic hippocampus tissue was 0.2786±0.0308 ( x±s)and 0.5686±0.1214 in the control tissue.The result shows a significant difference between epileptic tissue and the control group (P<0.05) .
Conclusions:
Our work showed that a increase in ULBP2 cDNA and protein level may be involved in the pathophysiology of refractory epilepsy which suggested that the ULBP2 may play a key role in the epilepsy immune disorder,so bring some promising immune targets toward the therapy of refractory epilepsy. Additional studies will be required to elucidate the mechanism by which ULBP2 affects brain function in refractory epilepsy.
Our work also showed that a decrease in STRN cDNA and protein level may be involved in the pathophysiology of refractory epilepsy which suggested that the STRN may be associated with impairment of the brain protection cased by endogenous NO in refractory epilepsy,so bring some promising targets toward the therapy of refractory epilepsy. Additional studies will be required to elucidate the mechanism by which STRN affects brain function in refractory epilepsy.
资料和方法:试验组42例均为临床确诊的耐药性癫痫患者,发作类型符合1981年国际抗癫痫联盟(ILAE)有关癫痫发作分类的标准。其中男26例,女16例,年龄15～56岁,平均26.18±9.60(x±s)岁;病程3～30年,平均为12.88±6.49( x±s)年;发作类型中部分继发全身强直、阵挛或强直-阵挛性发作23例,复杂部分性发作6例,有多种发作类型(单纯部分性、强直性或强直-阵挛性发作)13例。术后获颞叶标本34例,海马标本8例。
对照组共有20例,全部为在我院或第三军医大学新桥医院神经外科行手术减压或清创患者的颞叶和海马脑组织,12例颞叶,8例海马。其中男7例,女5例,年龄16-44岁,平均23.05±9.17岁(X+SD)。
结果:
1.基因芯片结果
耐药性癫痫组脑组织ULBP2蛋白的基因表达上调,与正常对照组间比较有明显差异(Ratio=4.180)。
耐药性癫痫组脑组织STRN蛋白的基因表达下调,与正常对照组间比较有明显差异(Ratio=0.384)。
2.免疫组化
ULBP2主要在神经元和神经胶质细胞的胞膜表达,阴性对照表达极少或无表达。耐药性癫痫颞叶脑组织的A值(AOD值)值为0.0518±0.0232 (x±s),对照组为0.0206±0.0011(x±s),两组方差不起,校正后t’检验结果显示两组间差异有统计学意义(t’=4.969,p<0.05)。耐药性癫痫组海马的AOD值为0.0509±0.0048(x±s),对照组为0.0198±0.0114( x±s),两组间有显著差异(t=2.528, p<0.05)。
STRN正常主要在神经元和神经胶质细胞的胞浆表达,实验组表达极少或无表达。耐药性癫痫颞叶脑组织的A值(AOD值)值为0.3108±0.1087 (x±s),对照组为0.4210±0.1238(x±s),两组方差不起,校正后t’检验结果显示两组间差异有统计学意义(t’=4.858,p<0.05)。耐药性癫痫组海马的AOD值为0.2706±0.0038(x±s),对照组为0.3952±0.0107( x±s),两组间有显著差异(t=2.416, p<0.05)。
3.免疫荧光
在对照组ULBP2蛋白表达极少,而在实验组中ULBP2基因的蛋白表达产物比对照组相同部位的脑组织中表达明显增加。
在对照组STRN蛋白表达明显,而在实验组中STRN蛋白表达产物比对照组相同部位的脑组织中表达明显减少。
4.免疫印记法
ULBP2蛋白条带在对照组明显减弱,反映出实验组中ULBP2基因的蛋白表达产物比对照组相同部位的脑组织中表达明显增加。耐药性癫痫颞叶脑组织灰度值0.9804±0.1401,对照组灰度值0.5914±0.2197,两组间差异有统计学意义(t=2.7633,p<0.05)。耐药性癫痫海马脑组织灰度值0.9832±0.1508,对照组灰度值0.5866±0.1974,两组间差异有统计学意义(t=2.7838,p<0.05)。
STRN蛋白条带在实验组明显减少,反映出实验组中STRN基因的蛋白表达产物比对照组相同部位的脑组织中表达明显减少。耐药性癫痫颞叶脑组织灰度值0.3318±0.1101,对照组灰度值0.5846±0.1024,两组间差异有统计学意义(t=2.6613,p<0.05)。耐药性癫痫海马脑组织灰度值0.2786±0.0308,对照组灰度值0.5686±0.1214,两组间差异有统计学意义(t=2.6808,p<0.05)。
结论:
耐药性颞叶癫痫患者颞叶脑组织中ULBP2基因及蛋白产物表达增高可能与耐药性颞叶癫痫发病中的免疫异常机制有重要关联,甚至可能是关键因素。高表达的ULBP2可通过与NK细胞、T细胞、活性巨噬细胞、CD8细胞表面的NKG.2D受体特异性结合,引起复杂的系列免疫反应,并导致许多自身免疫抗体的大量产生和灭活减少,从而诱发癫痫或是使癫痫发作加重难以控制。它很可能为耐药性颞叶癫痫的免疫治疗提供新的靶点。
耐药性颞叶癫痫患者颞叶脑组织中STRN表达明显降低及其引发的雌激素信号转导和内源性一氧化氮合成减弱在耐药性颞叶癫痫发病中可能有重要作用。
Objective: To study the expression of genes and protein of UL16 binding protein 2 and STRN in the brain tissue of patients with drug-refractory epilepsy , and to explore the possible role in drug-refractory epilepsy and the clinical value.
Materials and Methods: The 42 cases with refractory epilepsy included in this study were obtained from the files of the Departments of Neurosurgery of the following hospitals: the First Affiliated Hospital of Chongqing Univerisyt of Medical Sciences, Beijing Tiantan Hospital, Xuanwu Hospital of the Capital University of Medical Sciences, and Xinqiao Hospital of the Third Military Medical Univeristy. All the patients involved in our study group underwent the surgical resection of temporal lobe tissue. Before surgery, informed consents were obtained for the use of human brain tissues for research, and the study was approved by the local Ethic Committee. Two neuropathologists reviewed all the cases independently. The diagnosis of seizure type was confirmed according to the 1981 International Classification of Epileptic Seizures of the International League Against Epilepsy.
The 20 controls were obtained from the files of the neurosurgery department of the first affiliated hospital of Chongqing University of Medical Sciences. These samples were comprised of temporal neocortical tissues adjacent of the lesion. All patients were diagnosed by pathological tests to have been suffered brain trauma. the two neurophthologists both reviewed these cases to confirm that they had no history of seizures or other neurological disorders as controls.
Gene-chip, immunohistochemistry, immunofluorescence and Western blotting were used to test expression of ULBP2 protein and STRN protein in the surgically removed brain tissue of patients with drug-refractory epilepsy from the brain bank of our department(n=42), and the results were compared with that of normal controls (n=20)。The Computer Graphic Analysis System is used to test the average optical density (AOD) which is expressed as mean±SD( x±s)and tested via t-test. P value less than 0.05 as the level of significance.
Results
1.Gene chip: There was significant difference between the control group and the pharmacoresistance group (Ratio=4.180). The expression of SCN8A gene was shown to be increased in the brain tissues of the pharmacoresistance epilepsy group. There was significant difference between the control group and the pharmacoresistance group (Ratio=0.384). The expression of STRN gene was shown to be decreased in the brain tissues of the pharmacoresistance epilepsy group.
2. Immunohistochemistry : In human temporal cortex of patients with epilepsy, ULBP2 immunoreactivity was consistently observed in all cases and was confined mainly to neurons and glial cells, whereas faint immunoreactivity was apparent in the control brain tissues. Four visual field images were obtained randomly in every section by TC-FY-2050 pathology system acquisi-tioned image and were automatically analyzed by Motic Med 6.0 CMIAS pathology image analysis system. AOD value in epileptic temporal cortex tissue tissues was determined 0.0518±0.0232 ( x±s), and 0.0206±0.0011 ( x±s) in the control. AOD value in hippocampus of pharmacoresistance epilepsy group was determined 0.0509±0.0048( x±s), and 0.0198±0.0114 ( x±s) in the control. ANOVA analysis shows significantly up-regulated ULBP2 in epileptic tissue than the control (P<0.05).
In control brain tissues, STRN immunoreactivity was consistently observed in all cases and was confined mainly to neurons and glial cells, whereas faint immunoreactivity was apparent in control brain tissues. Four visual field images were obtained randomly in every section by TC-FY-2050 pathology system acquisi-tioned image and were automatically analyzed by Motic Med 6.0 CMIAS pathology image analysis system. AOD value in epileptic temporal cortex tissue tissues was determined 0.3108±0.1087 ( x±s), and 0.4210±0.1238 ( x±s) in the control. AOD value in hippocampus of pharmacoresistance epilepsy group was determined 0.2706±0.0038 ( x±s), and 0.3952±0.0107 ( x±s) in the control. ANOVA analysis shows significantly down-regulated STRN in epileptic tissue than the control (P<0.05).
3. Immunofluorescence analysis: In the temporal lobe cortex and hippocampus, strong immunoreactivity for the staining of ULBP2 protein was observed. There were more obvious in the pharmacoresistance epilepsy group than in control group.
In the temporal lobe cortex and hippocampus, faint immunoreactivity for the staining of STRN protein was observed. There were less obvious in the pharmacoresistance epilepsy group than in control group.
4. Western blot: Immunoblot was performed with ULBP2 antibody, the protein was detected by immunoblot as a band at 29kDa. Strongly stained bands were present in all samples of epileptic tissue whereas relative faint expression of the ULBP2 was observed in the control group. Another band ofβ-actin as positive control at 42 kDa also was observed correspondently in every channel. The ratio of optical density of ULBP2 andβ-actin was taken as variance calculated between two groups. Optical density value in Epileptic temporal cortex tissue was 0.9804±0.1401 and 0.5914±0.2197 ( x±s) in the control tissue. Optical density value in Epileptic hippocampus tissue was 0.9832±0.1508 and ( x±s)0.5866±0.1974 in the control tissue.The result shows a significant difference between epileptic tissue and the control group (P<0.05) .
Immunoblot was performed with STRN antibody, the protein was detected by immunoblot as a band at 110kDa. faint stained bands were present in all samples of epileptic tissue whereas relative strongly expression of the STRN was observed in the control group. Another band ofβ-actin as positive control at 42 kDa also was observed correspondently in every channel. The ratio of optical density of STRN andβ-actin was taken as variance calculated between two groups. Optical density value in Epileptic temporal cortex tissue was 0.3318±0.1101 and 0.5846±0.1024 ( x±s) in the control tissue. Optical density value in Epileptic hippocampus tissue was 0.2786±0.0308 ( x±s)and 0.5686±0.1214 in the control tissue.The result shows a significant difference between epileptic tissue and the control group (P<0.05) .
Conclusions:
Our work showed that a increase in ULBP2 cDNA and protein level may be involved in the pathophysiology of refractory epilepsy which suggested that the ULBP2 may play a key role in the epilepsy immune disorder,so bring some promising immune targets toward the therapy of refractory epilepsy. Additional studies will be required to elucidate the mechanism by which ULBP2 affects brain function in refractory epilepsy.
Our work also showed that a decrease in STRN cDNA and protein level may be involved in the pathophysiology of refractory epilepsy which suggested that the STRN may be associated with impairment of the brain protection cased by endogenous NO in refractory epilepsy,so bring some promising targets toward the therapy of refractory epilepsy. Additional studies will be required to elucidate the mechanism by which STRN affects brain function in refractory epilepsy.
引文
[1] Sutherland CL, Chalupny NJ, Schooley K et al. UL16-binding proteins, novel MHC class I-related proteins, bind to NKG2D and activate multiple signaling pathways in primary NK cells[J]. J Immunol. 2002 Jan 15;168(2):671-9.
[2] Rolle A, Mousavi-Jazi M, Eriksson M et al. Effects of human cytomegalovirus infection on ligands for the activating NKG2D receptor of NK cells: up-regulation of UL16-binding protein (ULBP)1 and ULBP2 is counteracted by the viral UL16 protein[J]. J Immunol. 2003 Jul 15;171(2):902-8.
[3] Borchers MT,Harris NL,Wesselkamper SC et al. The NKG2D-activating receptor mediates pulmonary clearance of Pseudomonas aeruginosa[J]. Infect Immun. 2006 May;74(5):2578-86.
[4] Von Strandmann EP, Hansen HP, Reiners KS et al. A novel bispecific protein (ULBP2-BB4) targeting the NKG2D receptor on natural killer (NK) cells and CD138 activates NK cells and has potent antitumor activity against human multiple myeloma in vitro and in vivo[J]. Blood. 2006 Mar 1;107(5):1955-62.
[5] Vankayalapati R, Garg A, Porgador A et al. Role of NK cell-activating receptors and their ligands in the lysis of mononuclear phagocytes infected with an intracellular bacterium [J]. J Immunol. 2005 Oct 1;175(7):4611-7.
[6] Sutherland CL, Rabinovich B, Chalupny NJ et al. ULBPs, human ligands of the NKG2D receptor, stimulate tumor immunity with enhancement by IL-15 [J]. Blood. 2006 Aug 15;108(4):1313-9.
[7] Eisele G, Wischhusen J, Mittelbronn M et al.TGF-beta and metalloproteinases differentially suppress NKG2D ligand surface expression on malignant glioma cells[J]. Brain.2006 Sep;129(Pt 9):2416-25.
[8] Maasho K, Opoku-Anane J, Marusina AI et al. NKG2D is a costimulatory receptor for human naive CD8+ T cells[J]. Immunol. 2005 Apr 15;174(8):4480-4.
[9] Mitchell GW, Williams GS, Bosch EP, et al. ClassⅡantigen expression in peripheral neuropathies[J]. J Neurol Sci, 1991;102:170.
[10] Levite M,Mishina M,Watanabe M,et al.Autoimmune in Epilepsy Nat Immunol[J]. J Neurol Sci,2002,3:500-505.
[11] Mokran V , Simko M , Nyulassy S. Seizures and immune disordersJ[J] . B ratisl Lek L isty ,1997 ,98 (4) :229.
[12]晏勇.癫痫的免疫学异常.见:吴逊,主编.癫痫和发作性疾病.北京:人民军医出版社,2001.
[13] Mokran V , Simko M , Nyulassy S. Seizures and immune disorders [J]. B ratisl Lek L isty ,1997 ,98 (4) :229.
[14] Chapman J ,Cohen2Armon M , Shoenfeld Y ,et al. Antipholipid antibodies permeabilize depolarize brain synaptoneurosomes [J] .L upus ,1999 ,8 (2) :127
[15] Tang FR, Chia SC, Zhang S. Glutamate receptor 1-immunopositive neurons in the gliotic CA1 area of the mouse hippocampus after pilocarpine-induced status epilepticus[J].Eur J Neurosci. 2005 May;21(9):2361-74.
[16] Takahashi Y, Mori H, Mishina M, et al.Autoantibodies andcell-mediated autoimmunity to NMDA-type GluRepsilon2 in patients with Rasmussen's encephalitis and chronic progressive epilepsia partialis continua[J]. Epilepsia.2005;46 Suppl 5:152-8.
[17] Xu X, Sun R, Jin R,et al. The effect of the ketogenic diet on hippocampal GluR5 and Glu6 mRNA expression and Q/R site editing in the kainate-induced epilepsy model.Epilepsy Behav[J]. 2008 Oct;13(3):445-8.
[18] Krestel HE, Shimshek DR, Jensen V,et al A genetic switch for epilepsy in adult mice[J].J Neurosci. 2004 Nov 17;24(46):10568-78.
[19]姚君茹,潘强,吕束清,等.癫痫夫鼠海马结构谷氨酸和nNOS神经元的动态变化.解剖学杂志,2004,27:505 506.
[20] Takahashi Y, Mori H, Mishina M,et al. Autoantibodies to NMDA receptor in patients with chronic forms of epilepsia partialis continua.Neurology[J]. 2003 Oct 14;61(7):891-6.
[21] Pehola J.Autoantibodies to glutamic acid decarboxylase in patients with therapy-resistant epilepsy[J].Neurology.2000,55:46-50,
[22] McKnight K, Jiang Y, Hart Y. Serum antibodies in epilepsy and seizure-associated disorders[J].Neurology. 2005 Dec 13;65(11):1730-6.
[23] Proia RL. Gangliosides help stabilize the brain[J].Nat Genet. 2004 Nov;36(11):1147-8.
[24] Yamamoto HA, Mohanan PV. Ganglioside GT1B and melatonin inhibit brain mitochondrial DNA damage and seizures induced by kainic acid in mice[J].Brain Res. 2003 Feb 21;964(1):100-6.
[25] Okada K, Yamashita U, Tsuji S, et al, et al. Ameliorative effect of pioglitazone on seizure responses in genetically epilepsy-susceptible EL mice[J]. Brain Res. 2006 Aug 2;1102(1):175-8.
[26]曾常茜.消炎痛对癫痫保护作用的免疫学研究J .中国神经免疫学和神经病学杂志,2002 ,9 (3) :135.
[27]刘保群.免疫调节剂辅助治疗癫痫J .中国神经免疫学和神经病学杂志,2002 ,9 (3) :141.
[28] Bien CG, Granata T, Antozzi C. Pathogenesis, diagnosis and treatment of Rasmussen encephalitis: a European consensus statement[J]. Brain. 2005 Mar;128(Pt 3):454-71.
[29] Dalakas MC. The role of IVIg in the treatment of patients with stiff person syndrome and other neurological diseases associated with anti-GAD antibodies[J]. J Neurol. 2005 May;252 Suppl 1:I19-25.
[30] Zou LP, Zhang WH, Wang HM, et al. Maternal IgG suppresses NMDA-induced spasms in infant rats and inhibits NMDA-mediated neurotoxicity in hippocampal neurons[J]. J Neuroimmunol. 2006 Dec;181(1-2):106-11.
[31] KanwarJR.Anti-inflammatory immunotherapy for multiplesclerosis/experimental autoimmune encephalomyelitis (EAE) disease[J]. Curr Med Chem. 2005;12(25):2947-62.
[32] Cosman DJ, Mullberg CL, Sutherland W, et al. ULBPs, novel MHC class I-related molecules, bind to CMV glycoprotein UL16, and stimulate NK cytotoxicity through the NKG2D receptor. Immunity[J]. 2001;14:123.
[33] Bauer SV, Groh J, Steinle JH, et al. Activation of NK cells and T cells by NKG2D, a receptor for stress-inducible MICA[J]. Science 1999 ;285:727.
[34] Diefenbach AAM, Jamieson SD, Li N, et al. Ligands for the murine NKG2D receptor: expression by tumor cells and activation of NK cells and macrophages. Nat. Immunol. 2000 ;1:119.
[35] Romphruk AV, Romphruk A, Choonhakarn C, et al. Major histocompatibility complex class I chain-related gene A in Thai psoriasis patients: MICA association as a part of human leukocyte antigen-B-Cw haplotypes. Tissue Antigens, 2004, 63(6):547-554.
[36] Okada K, Yamashita U, Tsuji S et al. Ameliorative effect of pioglitazone on seizure responses in genetically epilepsy-susceptible EL mice[J].Brain Res. 2006 Aug 2;1102(1):175-8.
[37] Jamali S, Bartolomei F, Robaglia-Schlupp A et al. Large-scale expression study of human mesial temporal lobe epilepsy: evidence for dysregulation of the neurotransmission and complement systems in the entorhinal cortex[J]. Brain. 2006 Mar;129(Pt 3):625-41.
[38] Di Loreto S, Balestrino M, Pellegrini P. Blockade of N-methyl-D-aspartate receptor prevents hypoxic neuronal death and cytokine releas [J]. Neuroimmunomodulation. 1997 Jul-Aug;4(4):195-9.
[39] Lipton SA. HIV-related neuronal injury. Potential therapeutic intervention with calcium channel antagonists and NMDA antagonists[J]. Mol Neurobiol. 1994 Apr-Jun;8(2-3):181-96.
[40] Hermsen CC, Mommers E, van de Wiel T et al. Convulsions due to increased permeability of the blood-brain barrier in experimental cerebral malaria can be prevented by splenectomy or anti-T cell treatment[J]. J Infect Dis. 1998 Oct;178(4):1225-7.
[41] Ishibashi T, Dakin KA, Stevens B. Astrocytes promote myelination in response to electrical impulses[J].Neuron. 2006 Mar 16;49(6):823-32.
[42] Olah M, Ping G, De Haas AH. Enhanced hippocampal neurogenesis in the absence of microglia T cell interaction and microglia activation in the murine running wheel model[J]. Glia. 2008 Dec 29.
[43] Kurkowska-Jastrzebska I, Joniec I, Zaremba M. Anti-myelin basic protein T cells protect hippocampal neurons against trimethyltin-induced damage[J].Neuroreport. 2007 Mar 26;18(5):425-9.
[44] Dambinova SA.The presence of autoantibodies to N-terminus domain of G1uRI subunit of AMPA receptor in the blood serum of palienls with epiepsy[J].J Neurol Sci,1997,152:93-96.
[45] Dambinova SA.Monitoring of brain spiking activity and autoantibodies to N-terminus domain of GIuRI suhunil of AMPA receptors i rl blood serunl of rats with cobalt-induced epilepsy[J].J Neurochen)。1998,7l:2088-2092.
[46] Momzov SG. Autoantibodies to brain tissue antigets in epilepsy palients[J].Zh ncuropatol Psikhiatr lm S S korsakova,l 996。96:7 l-76.
[47] Dehounlean P,Gerome P,Zammi|C,et al. Frequency of anticardiolipin,antinuclear and anti—beta2 GPI antibodies is not increased in unselected epileptic patients:a case—control study[J].Seizue.2004,13:205-207.
[1] Blondeau C, Gaillard S, Ternaux JP, et al. Expression and distribution of phocein and members of the striatin family in neurones of rat peripheral ganglia. Histochem Cell Biol[J]. 2003 Feb;119(2):131-8.
[2] Gaillard S, Bailly Y, Benoist M, et al. A mammalian homolog of yeast MOB1 is both a member and a putative substrate of striatin family-protein phosphatase 2A complexes. J Biol Chem[J]. 2001 Jun 29;276(26):24253-60.
[3] Lu Q, Pallas DC, Surks HK, et al. Striatin assembles a membrane signaling complex necessary for rapid, nongenomic activation of endothelial NO synthase by estrogen receptor alpha[J].Proc Natl Acad Sci U S A. 2004 Dec 7;101(49):17126-31.
[4] Gaillard S, Bartoli M, Castets F, et al. A mammalian homolog of yeast MOB1 is both a member and a putative substrate of striatin family-protein phosphatase 2A complexes.J Biol Chem[J]. 2001 Jun 29;276(26):24253-60.
[5] Chiueh CC, Andoh T, Lai AR, et al. Neuroprotective strategies in Parkinson's disease: protection against progressive nigral damage induced by free radicals.Neurotox Res[J]. 2000 May;2(2-3):293-310.
[6] Lu KT, Chiou RY, Chen LG, et al. Neuroprotective effects of resveratrol on cerebral ischemia-induced neuron loss mediated by free radical scavenging and cerebral blood flow elevation.J Agric Food Chem[J]. 2006 Apr 19;54(8):3126-31.
[7] Wainwright MS, Grundhoefer D, Sharma S, et al. A nitric oxide donor reduces brain injury and enhances recovery of cerebral blood flow after hypoxia-ischemia in the newborn rat[J].Neurosci Lett. 2007 Jan 11.
[8] Jung KH, Chu K, Ko SY, et al. Early intravenous infusion of sodium nitrite protects brain against in vivo ischemia-reperfusion injury[J].Stroke. 2006 Nov;37(11):2744-50.
[9] Mitchell GW, Williams GS, Bosch EP, et al. ClassⅡantigen expression in peripheral neuropathies[J]. J Neurol Sci, 1991;102:170.
[10] Yahyavi-Firouz-Abadi N, Tahsili-Fahadan P, Riazi K, et al. Involvement of nitric oxide pathway in the acute anticonvulsant effect of melatonin in mice[J].Epilepsy Res.
[11] Noh HS, Kim DW, Cho GJ, et al. Increased nitric oxide caused by the ketogenic diet reduces the onset time of kainic acid-induced seizures in ICR mice[J]. Brain Res. 2006 Feb 23;1075(1):193-200.
[12] Paul V, Ekambaram P, et al. Effects of sodium nitroprusside, a nitric oxide donor, on gamma-aminobutyric acid concentration in the brain and on picrotoxin-induced convulsions in combination with phenobarbitone in rats[J]. Pharmacol Biochem Behav. 2005 Mar;80(3):363-70.
[13] Royes LF, Fighera MR, Furian AF, et al. The role of nitric oxide on the convulsive behavior and oxidative stress induced by methylmalonate: An electroencephalographic and neurochemical study[J].Epilepsy Res. 2007 Mar;73(3):228-237.
[1] Cuellar R,Molinero M. The treatment of children with difficult to control epilepsy [J]. Rev Neurol. 2003 Aug 16-31;37(4):371-5.
[2] Mikati MA, Saab R, Fayad MN et al. Efficacy of intravenous immunoglobulin in Landau-Kleffner syndrome[J] .Pediatr Neurol. 2002 Apr;26(4):298-300.
[3]晏勇.癫痫的免疫学异常.见:吴逊,主编.癫痫和发作性疾病[M].北京:人民军医出版社,2001:46-50.
[4]金伯泉.神经、免疫及内分泌系统间的关系.见:金伯泉,主编.细胞和分子免疫学.北京:科学出版社,2001:11-21.
[5] Weigent DA, Blalock JE.Associations between the neuroendocrine and immune systems[J]. J Leukoc Biol. 1995 Aug;58(2):137-50. Review.
[6] Mitchell GW, Williams GS, Bosch EP, et al. ClassⅡantigen expression in peripheral neuropathies[J]. J Neurol Sci, 2001;102:170.
[7] Steinle A, Groh V, Spies T. Diversification, expression, andγδT cell recognition of evolutionarily distant members of the MIC family of major histocompatibility complex class I related molecules [ J ] . Proc Natl Acad Sci USA,1998, 95(9):12510 12515.
[8] Rlle A, Mousavi J, Eriksson M, et al. Effects of human cytomegalovirus infection on ligands for the activating NKG2D receptor of NK cells: up regulation of UL16 binding protein (ULBP)1 and ULBP2 is counteracted by the viral UL16 protein[J]. J Immunol,2003,171(2):902 908.
[9] Martín Pagola A, Ortiz L, Pérez de Nanclares G, et al. Analysis of the expression of MICA in small intestinal mucosa of patients with celiac disease[J]. J Clin Immunol,2003, 23(6):498 503.
[10] Cosman DJ, Mullberg CL, Sutherland W, et al. ULBPs, novel MHC class I-related molecules, bind to CMV glycoprotein UL16, and stimulate NK cytotoxicity through the NKG2D receptor[J]. Immunity. 2001;14:123.
[11] Bauer SV, Groh J, Steinle JH, et al. Activation of NK cells and T cells by NKG2D, a receptor for stress-inducible MICA[J]. Science 1999 ;285:727.
[12] Diefenbach AAM, Jamieson SD, Li N, et al. Ligands for the murine NKG2D receptor: expression by tumor cells and activation of NK cells and macrophages. Nat[J]. Immunol. 2000 ;1:119.
[13] Eisele G, Wischhusen J,Mittelbronn M, et al. TGF-beta and metalloproteinases differentially suppress NKG2D ligand surface expression on malignant glioma cells[J]. Brain. 2006 Sep;129(Pt 9):2416-25.
[14]金伯泉.神经和内分泌(或神经内分泌)系统对免疫系统的调控.见:金伯泉,主编.细胞和分子免疫学.北京:科学出版社,2001:11-21.
[15] HaskóG, Elenkov IJ, Vizi ES. Presynaptic receptors involved in the modulation of release of noradrenaline from the sympathetic nerve terminals of the rat thymus. Immunol Lett[J]. 1995 Jul-Aug;47(1-2):133-7.
[16] Espinosa E, Bermúdez-Rattoni F. Behavior-immunity relationship: the role of cytokines. Rev Invest Clin[J]. 2001 May-Jun;53(3):240-53.
[17] Di Comite G, Grazia Sabbadini M, Corti A, et al. Conversation galante: how the immune and the neuroendocrine systems talk to each other[J]. Autoimmun Rev. 2007 Nov;7(1):23-9.
[18] Schwartz M, Sela BA, Eshhar N. Antibodies to gangliosid and myelin autoantigens are produced in mice following sciatic nerve injury[J]. J Neurochem, 1982;38:1192.
[19] De Medinaceli L, Church AC, Yen-Nung Wang. Posttramatic autoimmune reaction in peripheral nerve: effect of single injury[J]. Exp Neurol, 1985;88:372.
[20] Ansselin AQ, Pollard JD. Immunopathological factors in peripheral nerve allograft rejection: quantification of lymphocyte invasion and major histocompatility complex expression[J]. J Neuro Sci, 1990;96:75.
[21]裴福兴,杨志明,黄富国,等.周围神经损伤后的免疫反应和神经再生.中华显微外科杂志,1995;18:146.
[22] Forsum U, Claesson K, Hjelm E, et al. ClassⅡtransplantation antigens:Distribution in tissue and involement disease [J].Scand J Immunol, 1985;21:389.
[23] de Graaf KL, Wallstr?m E, Muhallab S, et al. MHC and non-MHC gene regulation of disease susceptibility and disease course in experimental inflammatory peripheral neuropathy[J]. J Neuroimmunol. 2004 Oct;155(1-2):73-84.
[24] Scarpini E, Lisak RP, Benrttas S, et al. Quantitative assessment of classⅡMoleculars in normal and pathological nerves: immunohistochemical studies in vivo and in tissue cultures[J]. Brain, 2003;77:659.
[25] Lawrence JM, Keegan DJ, Muir EM,et al . Transplantation of Schwann cell line clones secreting GDNF or BDNF into the retinas of dystrophic Royal College of Surgeons rats[J]. Invest Ophthalmol Vis Sci. 2004 Jan;45(1):267-74.
[26] Mackinnon SE, Hudson AR. Clinical application of peripheral nerve t ransplantation[J]. Plast Reconstr Surg, 2004;90:695.
[27] Bain JR, Mackinnon SE, Hudson AR. The peripheral nerve allograft: An assessment of regeneration across nerve allograft in rats immunosuppressed with cyclosporin A[J]. Plast Reconstr Surg, 2005;82:1053.
[28] Buttemeyer R, Rao UN, Jones NF. Peripheral nerve allograft transplantation with FK506:functional,histological,and immunological results before and after discontinuation of immunosuppression[J]. Annals of Plastic Surgery, 1995;35(4):396.
[29] Nakao Y, Mackinnon SE, Mohanakumar T, et al. Monoclonal antibodies against ICAM-1 and LFA-1(CD11A) induce specific tolerance to peripheral nerve allograft in rats. Transplantation Proceedings, 1995;27(1):373. Jean-Michel Dubernard, Earl Owen, Guillaume Herzberg, et al. Human hand allograft:report on first 6 months[J]. The Lacent, 1999;353:1315.
[30] Tobin G, Breidenbach W, Barker J, et al. Clinical progress of the nation’s first hand transplant over the first year and a half[J]. Louisvil Medicine, 2000;48(2):57
[31]裴国献,顾立强,于立新.异体手移植二例前期报告.中华医学志,2000;80(6):1.
[32] Gold BG, Densmore V, Shou WN, et al. Immunophilin FK506-binding protein 52(not FK506-binding protein 12) mediates the neurotrophic action of FK505[J]. J of Pharmacology and Experimental Therapeutics, 1999;289:1202.
[33] Ishibashi T, Dakin KA, Stevens B. Astrocytes promote myelination in response to electrical impulses[J].Neuron. 2006 Mar 16;49(6):823-32.
[34] Olah M, Ping G, De Haas AH. Enhanced hippocampal neurogenesis in the absence of microglia T cell interaction and microglia activation in the murine running wheel model[J]. Glia. 2008 Dec 29.
[35] Kurkowska-Jastrzebska I, Joniec I, Zaremba M. Anti-myelin basic protein T cells protect hippocampal neurons against trimethyltin-induced damage[J].Neuroreport. 2007 Mar 26;18(5):425-9.
[36] Weller RO , Engelhardt B , Phillips MJ . Lymphocyte targeting of the central nervous system:a reviewof afferent and efferent CNS-immune pathways[J ] . Brain-pathol . 1996 ,6(3) :275～288
[37] Weller RO , Phillips MJ , Kida S , et al . Immunologic significance of lym2 phatic drainage of the brain[J ] . Bull Acad Natl Med. 1997 ,181(4) :661～671
[38] Harling-Berg C, Konpf PM, MerriamJ . Role of cervical lymph node in the systemic humoral immune response to human serum albumin microinfusedinto rat cerebrospinal fluid[J ] . J Neuroimmunol . 1998 ,25 :185～193
[39] Lake J , Weller RO , Phillips MJ ,et al . Lymphocyte targeting of the brain in adoptive transfer cryolesion-EAE[J ] . J pathol . 1999 ,187(2) :259～265
[40] Phillips MJ , Needham M, Weller RO. Role of cervical lymph nolds in autoimmune encephalomyelitis in lewis rat[J ] . J Pathol . 1997 ,182(4) :457～464
[41] De-Carvalho MC, Chimelli LM, Quirico-Santos T. Modulation of lewis rats with experimental autoimmune encephalomyelitis[J]. Braz J Med Biol Res.1999 ,32(5) : 583～592
[42] Tang FR, Chia SC, Zhang S. Glutamate receptor 1-immunopositive neurons in the gliotic CA1 area of the mouse hippocampus after pilocarpine-induced status epilepticus[J].Eur J Neurosci. 2005 May;21(9):2361-74.
[43] Takahashi Y, Mori H, Mishina M, Watanabe M.Autoantibodies andcell-mediated autoimmunity to NMDA-type GluRepsilon2 in patients with Rasmussen's encephalitis and chronic progressive epilepsia partialis continua[J]. Epilepsia. 2005;46 Suppl 5:152-8.
[44] Xu X, Sun R, Jin R. The effect of the ketogenic diet on hippocampal GluR5 and Glu(6 mRNA expression and Q/R site editing in the kainate-induced epilepsy model[J].Epilepsy Behav. 2008 Oct;13(3):445-8.
[45]姚君茹,潘j强,吕束清,等.癫痫夫鼠海马结构谷氨酸和nNOS神经元的动态变化.解剖学杂志,2004,27:505 506.
[46] Takahashi Y, Mori H, Mishina M. Autoantibodies to NMDA receptor in patients with chronic forms of epilepsia partialis continua.Neurology[J]. 2003 Oct 14;61(7):891-6.
[47] Dambinova SA.The presence of autoantibodies to N-terminus domain of G1uRI subunit of AMPA receptor in the blood serum of palienls with epiepsy[J].J Neurol Sci,1997,152:93-96.
[48] Dambinova SA.Monitoring of brain spiking activity and autoantibodies to N-terminus domain of GIuRI suhunil of AMPA receptors i rl blood serunlof rats with cobalt-induced epilepsy[J].J Neurochen。1998,7l:2088-2092
[49] Pehola J . Autoantibodies to glutamic acid decarboxylase in patients with therapy-resistant epilepsy[J].Neurology.2000,55:46-50.
[50] McKnight K, Jiang Y, Hart Y. Serum antibodies in epilepsy and seizure-associated disorders.Neurology[J]. 2005 Dec 13;65(11):1730-6.
[51] Proia RL. Gangliosides help stabilize the brain[J].Nat Genet. 2004 Nov;36(11):1147-8.
[52] Yamamoto HA, Mohanan PV. Ganglioside GT1B and melatonin inhibit brain mitochondrial DNA damage and seizures induced by kainic acid in mice.Brain Res[J]. 2003 Feb 21;964(1):100-6.
[53] Momzov SG. Autoantibodies to brain tissue antigets in epilepsy palients[J].Zh ncuropatol Psikhiatr lm S S korsakova,l 996。96:7 l-76.
[54] Dehounlean P,Gerome P,Zammi|C,et al. Frequency of anticardiolipin,antinuclear and anti—beta2 GPI antibodies is not increased in unselected epileptic patients:a case—control study[J].Seizue.2004,13:205-207.
[55] McKnight K, Jiang Y, Hart Y. Serum antibodies in epilepsy and seizure-associated disorders[J]. Neurology. 2005 Dec 13;65(11):1730-6.
[56] Mokran V , Simko M , Nyulassy S. Seizures and immune disorders J . B ratisl Lek L isty ,1997 ,98 (4) :229.
[57] Chapman J ,Cohen2Armon M , Shoenfeld Y ,et al. Antipholipid antibodies permeabilize depolarize brain synaptoneurosomes [J] .L upus ,1999 ,8 (2) :127.
[58]曾常茜.消炎痛对癫痫保护作用的免疫学研究J .中国神经免疫学和神经病学杂志,2002 ,9 (3) :135.
[59]刘保群.免疫调节剂辅助治疗癫痫J .中国神经免疫学和神经病学杂志,2002 ,9 (3) :141.
[60] Bien CG, Granata T, Antozzi C. Pathogenesis, diagnosis and treatment of Rasmussen encephalitis: a European consensus statement[J]. Brain. 2005 Mar;128(Pt 3):454-71.
[61] Dalakas MC. The role of IVIg in the treatment of patients with stiff person syndrome and other neurological diseases associated with anti-GAD antibodies[J]. J Neurol. 2005 May;252 Suppl 1:I19-25.
[62] Zou LP, Zhang WH, Wang HM. Maternal IgG suppresses NMDA-induced spasms in infant rats and inhibits NMDA-mediated neurotoxicity in hippocampal neurons[J]. J Neuroimmunol. 2006 Dec;181(1-2):106-11.
[63] Kanwar JR. Anti-inflammatory immunotherapy for multiplesclerosis/experimental autoimmune encephalomyelitis (EAE) disease[J]. Curr Med Chem. 2005;12(25):2947-62.
[64] Lorigados Pl ,Morales CL,Parch FN,et a1.Immunological disorders in epileptic patients are associated to the epileptogenic focus localization[J].Rev Neurol,2004,39:101一104.
[65] Hosokawa M,Klegcrls A,Maguire J,et al,Expression of complement tnessenger RNAs and proleins by human oligodendroglial cells[J].Gila.2003,42:417-423.
[66] Levite M.Autoimmune in Epilepsy Nat[J].Immunol,2002,3:500-505.
[1] F L M Ricciardolo. Multiple roles of nitric oxide in the airways [J].Thorax, 2003 Feb, 58:75.
[2] Panaro MA, Brandonisio O, Acquafredda A, et al. Evidences for iNOS Expression and Nitric Oxide Production in the Human Macrophages[J].Curr Drug Targets Immune Endocr Metabol Disord. 2003 Sep,3(3):20.
[3] Beckman JS ,Koppenol WH. Nitric oxide, superoxide, and peroxynitrit: the good, the bad, and ugly [J].Am J Physiol, 1996 Nov;27(5 Pt ):C424.
[4] Crowell JA, Steele VE, Sigman CC, et al. Is Inducible Nitric Oxide Synthase a Target for Chemoprevention? [J].Mol Cancer Ther, 2003 Aug;2(8):85.
[5] Murashima YL, Yoshii M, Suzuki J. Role of nitric oxide in the epileptogenesis of EL mice[J]. Epilepsia. 2000;41 Suppl 6:S195-9.
[6] Chiueh CC, Andoh T, Lai AR, et al. Neuroprotective strategies in Parkinson's disease: protection against progressive nigral damage induced by free radicals[J].Neurotox Res. 2000 May;2(2-3):293-310.
[7] Lu KT, Chiou RY, Chen LG, et al. Neuroprotective effects of resveratrol on cerebral ischemia-induced neuron loss mediated by free radical scavenging and cerebral blood flow elevation.J Agric Food Chem[J]. 2006 Apr 19;54(8):3126-31.
[8] Wainwright MS, Grundhoefer D, Sharma S, et al. A nitric oxide donor reduces brain injury and enhances recovery of cerebral blood flow after hypoxia-ischemia in the newborn rat.Neurosci Lett[J]. 2007 Jan 11.
[9] Jung KH, Chu K, Ko SY, et al. Early intravenous infusion of sodium nitrite protects brain against in vivo ischemia-reperfusion injury[J].Stroke. 2006 Nov;37(11):2744-50. Epub 2006 Sep 28.
[10] ereira de Vasconcelos A, Riban V, Wasterlain C, et al. Role of endothelial nitric oxide synthase in cerebral blood flow changes during kainate seizures: a genetic approach using knockout mice[J]. Neurobiol Dis. 2006 Jul;23(1):219-27.
[11] Hosseinzadeh H, Karimi GR, Rakhshanizadeh M, et al. Anticonvulsant effect of Hypericum perforatum: role of nitric oxide[J].J Ethnopharmacol. 2005 Apr 8;98(1-2):207-8.
[12] Yahyavi-Firouz-Abadi N, Tahsili-Fahadan P, Riazi K, et al. Involvement of nitric oxide pathway in the acute anticonvulsant effect of melatonin in mice[J].EpilepsyRes. 2006 Feb;68(2):103-13.
[13] Noh HS, Kim DW, Cho GJ, et al. Increased nitric oxide caused by the ketogenic diet reduces the onset time of kainic acid-induced seizures in ICR mice[J]. Brain Res. 2006 Feb 23;1075(1):193-200.
[14] Paul V, Ekambaram P, et al. Effects of sodium nitroprusside, a nitric oxide donor, on gamma-aminobutyric acid concentration in the brain and on picrotoxin-induced convulsions in combination with phenobarbitone in rats[J]. Pharmacol Biochem Behav. 2005 Mar;80(3):363-70.
[15] Royes LF, Fighera MR, Furian AF, et al. The role of nitric oxide on the convulsive behavior and oxidative stress induced by methylmalonate: An electroencephalographic and neurochemical study[J].Epilepsy Res. 2007 Mar;73(3):228-237.
[2] Rolle A, Mousavi-Jazi M, Eriksson M et al. Effects of human cytomegalovirus infection on ligands for the activating NKG2D receptor of NK cells: up-regulation of UL16-binding protein (ULBP)1 and ULBP2 is counteracted by the viral UL16 protein[J]. J Immunol. 2003 Jul 15;171(2):902-8.
[3] Borchers MT,Harris NL,Wesselkamper SC et al. The NKG2D-activating receptor mediates pulmonary clearance of Pseudomonas aeruginosa[J]. Infect Immun. 2006 May;74(5):2578-86.
[4] Von Strandmann EP, Hansen HP, Reiners KS et al. A novel bispecific protein (ULBP2-BB4) targeting the NKG2D receptor on natural killer (NK) cells and CD138 activates NK cells and has potent antitumor activity against human multiple myeloma in vitro and in vivo[J]. Blood. 2006 Mar 1;107(5):1955-62.
[5] Vankayalapati R, Garg A, Porgador A et al. Role of NK cell-activating receptors and their ligands in the lysis of mononuclear phagocytes infected with an intracellular bacterium [J]. J Immunol. 2005 Oct 1;175(7):4611-7.
[6] Sutherland CL, Rabinovich B, Chalupny NJ et al. ULBPs, human ligands of the NKG2D receptor, stimulate tumor immunity with enhancement by IL-15 [J]. Blood. 2006 Aug 15;108(4):1313-9.
[7] Eisele G, Wischhusen J, Mittelbronn M et al.TGF-beta and metalloproteinases differentially suppress NKG2D ligand surface expression on malignant glioma cells[J]. Brain.2006 Sep;129(Pt 9):2416-25.
[8] Maasho K, Opoku-Anane J, Marusina AI et al. NKG2D is a costimulatory receptor for human naive CD8+ T cells[J]. Immunol. 2005 Apr 15;174(8):4480-4.
[9] Mitchell GW, Williams GS, Bosch EP, et al. ClassⅡantigen expression in peripheral neuropathies[J]. J Neurol Sci, 1991;102:170.
[10] Levite M,Mishina M,Watanabe M,et al.Autoimmune in Epilepsy Nat Immunol[J]. J Neurol Sci,2002,3:500-505.
[11] Mokran V , Simko M , Nyulassy S. Seizures and immune disordersJ[J] . B ratisl Lek L isty ,1997 ,98 (4) :229.
[12]晏勇.癫痫的免疫学异常.见:吴逊,主编.癫痫和发作性疾病.北京:人民军医出版社,2001.
[13] Mokran V , Simko M , Nyulassy S. Seizures and immune disorders [J]. B ratisl Lek L isty ,1997 ,98 (4) :229.
[14] Chapman J ,Cohen2Armon M , Shoenfeld Y ,et al. Antipholipid antibodies permeabilize depolarize brain synaptoneurosomes [J] .L upus ,1999 ,8 (2) :127
[15] Tang FR, Chia SC, Zhang S. Glutamate receptor 1-immunopositive neurons in the gliotic CA1 area of the mouse hippocampus after pilocarpine-induced status epilepticus[J].Eur J Neurosci. 2005 May;21(9):2361-74.
[16] Takahashi Y, Mori H, Mishina M, et al.Autoantibodies andcell-mediated autoimmunity to NMDA-type GluRepsilon2 in patients with Rasmussen's encephalitis and chronic progressive epilepsia partialis continua[J]. Epilepsia.2005;46 Suppl 5:152-8.
[17] Xu X, Sun R, Jin R,et al. The effect of the ketogenic diet on hippocampal GluR5 and Glu6 mRNA expression and Q/R site editing in the kainate-induced epilepsy model.Epilepsy Behav[J]. 2008 Oct;13(3):445-8.
[18] Krestel HE, Shimshek DR, Jensen V,et al A genetic switch for epilepsy in adult mice[J].J Neurosci. 2004 Nov 17;24(46):10568-78.
[19]姚君茹,潘强,吕束清,等.癫痫夫鼠海马结构谷氨酸和nNOS神经元的动态变化.解剖学杂志,2004,27:505 506.
[20] Takahashi Y, Mori H, Mishina M,et al. Autoantibodies to NMDA receptor in patients with chronic forms of epilepsia partialis continua.Neurology[J]. 2003 Oct 14;61(7):891-6.
[21] Pehola J.Autoantibodies to glutamic acid decarboxylase in patients with therapy-resistant epilepsy[J].Neurology.2000,55:46-50,
[22] McKnight K, Jiang Y, Hart Y. Serum antibodies in epilepsy and seizure-associated disorders[J].Neurology. 2005 Dec 13;65(11):1730-6.
[23] Proia RL. Gangliosides help stabilize the brain[J].Nat Genet. 2004 Nov;36(11):1147-8.
[24] Yamamoto HA, Mohanan PV. Ganglioside GT1B and melatonin inhibit brain mitochondrial DNA damage and seizures induced by kainic acid in mice[J].Brain Res. 2003 Feb 21;964(1):100-6.
[25] Okada K, Yamashita U, Tsuji S, et al, et al. Ameliorative effect of pioglitazone on seizure responses in genetically epilepsy-susceptible EL mice[J]. Brain Res. 2006 Aug 2;1102(1):175-8.
[26]曾常茜.消炎痛对癫痫保护作用的免疫学研究J .中国神经免疫学和神经病学杂志,2002 ,9 (3) :135.
[27]刘保群.免疫调节剂辅助治疗癫痫J .中国神经免疫学和神经病学杂志,2002 ,9 (3) :141.
[28] Bien CG, Granata T, Antozzi C. Pathogenesis, diagnosis and treatment of Rasmussen encephalitis: a European consensus statement[J]. Brain. 2005 Mar;128(Pt 3):454-71.
[29] Dalakas MC. The role of IVIg in the treatment of patients with stiff person syndrome and other neurological diseases associated with anti-GAD antibodies[J]. J Neurol. 2005 May;252 Suppl 1:I19-25.
[30] Zou LP, Zhang WH, Wang HM, et al. Maternal IgG suppresses NMDA-induced spasms in infant rats and inhibits NMDA-mediated neurotoxicity in hippocampal neurons[J]. J Neuroimmunol. 2006 Dec;181(1-2):106-11.
[31] KanwarJR.Anti-inflammatory immunotherapy for multiplesclerosis/experimental autoimmune encephalomyelitis (EAE) disease[J]. Curr Med Chem. 2005;12(25):2947-62.
[32] Cosman DJ, Mullberg CL, Sutherland W, et al. ULBPs, novel MHC class I-related molecules, bind to CMV glycoprotein UL16, and stimulate NK cytotoxicity through the NKG2D receptor. Immunity[J]. 2001;14:123.
[33] Bauer SV, Groh J, Steinle JH, et al. Activation of NK cells and T cells by NKG2D, a receptor for stress-inducible MICA[J]. Science 1999 ;285:727.
[34] Diefenbach AAM, Jamieson SD, Li N, et al. Ligands for the murine NKG2D receptor: expression by tumor cells and activation of NK cells and macrophages. Nat. Immunol. 2000 ;1:119.
[35] Romphruk AV, Romphruk A, Choonhakarn C, et al. Major histocompatibility complex class I chain-related gene A in Thai psoriasis patients: MICA association as a part of human leukocyte antigen-B-Cw haplotypes. Tissue Antigens, 2004, 63(6):547-554.
[36] Okada K, Yamashita U, Tsuji S et al. Ameliorative effect of pioglitazone on seizure responses in genetically epilepsy-susceptible EL mice[J].Brain Res. 2006 Aug 2;1102(1):175-8.
[37] Jamali S, Bartolomei F, Robaglia-Schlupp A et al. Large-scale expression study of human mesial temporal lobe epilepsy: evidence for dysregulation of the neurotransmission and complement systems in the entorhinal cortex[J]. Brain. 2006 Mar;129(Pt 3):625-41.
[38] Di Loreto S, Balestrino M, Pellegrini P. Blockade of N-methyl-D-aspartate receptor prevents hypoxic neuronal death and cytokine releas [J]. Neuroimmunomodulation. 1997 Jul-Aug;4(4):195-9.
[39] Lipton SA. HIV-related neuronal injury. Potential therapeutic intervention with calcium channel antagonists and NMDA antagonists[J]. Mol Neurobiol. 1994 Apr-Jun;8(2-3):181-96.
[40] Hermsen CC, Mommers E, van de Wiel T et al. Convulsions due to increased permeability of the blood-brain barrier in experimental cerebral malaria can be prevented by splenectomy or anti-T cell treatment[J]. J Infect Dis. 1998 Oct;178(4):1225-7.
[41] Ishibashi T, Dakin KA, Stevens B. Astrocytes promote myelination in response to electrical impulses[J].Neuron. 2006 Mar 16;49(6):823-32.
[42] Olah M, Ping G, De Haas AH. Enhanced hippocampal neurogenesis in the absence of microglia T cell interaction and microglia activation in the murine running wheel model[J]. Glia. 2008 Dec 29.
[43] Kurkowska-Jastrzebska I, Joniec I, Zaremba M. Anti-myelin basic protein T cells protect hippocampal neurons against trimethyltin-induced damage[J].Neuroreport. 2007 Mar 26;18(5):425-9.
[44] Dambinova SA.The presence of autoantibodies to N-terminus domain of G1uRI subunit of AMPA receptor in the blood serum of palienls with epiepsy[J].J Neurol Sci,1997,152:93-96.
[45] Dambinova SA.Monitoring of brain spiking activity and autoantibodies to N-terminus domain of GIuRI suhunil of AMPA receptors i rl blood serunl of rats with cobalt-induced epilepsy[J].J Neurochen)。1998,7l:2088-2092.
[46] Momzov SG. Autoantibodies to brain tissue antigets in epilepsy palients[J].Zh ncuropatol Psikhiatr lm S S korsakova,l 996。96:7 l-76.
[47] Dehounlean P,Gerome P,Zammi|C,et al. Frequency of anticardiolipin,antinuclear and anti—beta2 GPI antibodies is not increased in unselected epileptic patients:a case—control study[J].Seizue.2004,13:205-207.
[1] Blondeau C, Gaillard S, Ternaux JP, et al. Expression and distribution of phocein and members of the striatin family in neurones of rat peripheral ganglia. Histochem Cell Biol[J]. 2003 Feb;119(2):131-8.
[2] Gaillard S, Bailly Y, Benoist M, et al. A mammalian homolog of yeast MOB1 is both a member and a putative substrate of striatin family-protein phosphatase 2A complexes. J Biol Chem[J]. 2001 Jun 29;276(26):24253-60.
[3] Lu Q, Pallas DC, Surks HK, et al. Striatin assembles a membrane signaling complex necessary for rapid, nongenomic activation of endothelial NO synthase by estrogen receptor alpha[J].Proc Natl Acad Sci U S A. 2004 Dec 7;101(49):17126-31.
[4] Gaillard S, Bartoli M, Castets F, et al. A mammalian homolog of yeast MOB1 is both a member and a putative substrate of striatin family-protein phosphatase 2A complexes.J Biol Chem[J]. 2001 Jun 29;276(26):24253-60.
[5] Chiueh CC, Andoh T, Lai AR, et al. Neuroprotective strategies in Parkinson's disease: protection against progressive nigral damage induced by free radicals.Neurotox Res[J]. 2000 May;2(2-3):293-310.
[6] Lu KT, Chiou RY, Chen LG, et al. Neuroprotective effects of resveratrol on cerebral ischemia-induced neuron loss mediated by free radical scavenging and cerebral blood flow elevation.J Agric Food Chem[J]. 2006 Apr 19;54(8):3126-31.
[7] Wainwright MS, Grundhoefer D, Sharma S, et al. A nitric oxide donor reduces brain injury and enhances recovery of cerebral blood flow after hypoxia-ischemia in the newborn rat[J].Neurosci Lett. 2007 Jan 11.
[8] Jung KH, Chu K, Ko SY, et al. Early intravenous infusion of sodium nitrite protects brain against in vivo ischemia-reperfusion injury[J].Stroke. 2006 Nov;37(11):2744-50.
[9] Mitchell GW, Williams GS, Bosch EP, et al. ClassⅡantigen expression in peripheral neuropathies[J]. J Neurol Sci, 1991;102:170.
[10] Yahyavi-Firouz-Abadi N, Tahsili-Fahadan P, Riazi K, et al. Involvement of nitric oxide pathway in the acute anticonvulsant effect of melatonin in mice[J].Epilepsy Res.
[11] Noh HS, Kim DW, Cho GJ, et al. Increased nitric oxide caused by the ketogenic diet reduces the onset time of kainic acid-induced seizures in ICR mice[J]. Brain Res. 2006 Feb 23;1075(1):193-200.
[12] Paul V, Ekambaram P, et al. Effects of sodium nitroprusside, a nitric oxide donor, on gamma-aminobutyric acid concentration in the brain and on picrotoxin-induced convulsions in combination with phenobarbitone in rats[J]. Pharmacol Biochem Behav. 2005 Mar;80(3):363-70.
[13] Royes LF, Fighera MR, Furian AF, et al. The role of nitric oxide on the convulsive behavior and oxidative stress induced by methylmalonate: An electroencephalographic and neurochemical study[J].Epilepsy Res. 2007 Mar;73(3):228-237.
[1] Cuellar R,Molinero M. The treatment of children with difficult to control epilepsy [J]. Rev Neurol. 2003 Aug 16-31;37(4):371-5.
[2] Mikati MA, Saab R, Fayad MN et al. Efficacy of intravenous immunoglobulin in Landau-Kleffner syndrome[J] .Pediatr Neurol. 2002 Apr;26(4):298-300.
[3]晏勇.癫痫的免疫学异常.见:吴逊,主编.癫痫和发作性疾病[M].北京:人民军医出版社,2001:46-50.
[4]金伯泉.神经、免疫及内分泌系统间的关系.见:金伯泉,主编.细胞和分子免疫学.北京:科学出版社,2001:11-21.
[5] Weigent DA, Blalock JE.Associations between the neuroendocrine and immune systems[J]. J Leukoc Biol. 1995 Aug;58(2):137-50. Review.
[6] Mitchell GW, Williams GS, Bosch EP, et al. ClassⅡantigen expression in peripheral neuropathies[J]. J Neurol Sci, 2001;102:170.
[7] Steinle A, Groh V, Spies T. Diversification, expression, andγδT cell recognition of evolutionarily distant members of the MIC family of major histocompatibility complex class I related molecules [ J ] . Proc Natl Acad Sci USA,1998, 95(9):12510 12515.
[8] Rlle A, Mousavi J, Eriksson M, et al. Effects of human cytomegalovirus infection on ligands for the activating NKG2D receptor of NK cells: up regulation of UL16 binding protein (ULBP)1 and ULBP2 is counteracted by the viral UL16 protein[J]. J Immunol,2003,171(2):902 908.
[9] Martín Pagola A, Ortiz L, Pérez de Nanclares G, et al. Analysis of the expression of MICA in small intestinal mucosa of patients with celiac disease[J]. J Clin Immunol,2003, 23(6):498 503.
[10] Cosman DJ, Mullberg CL, Sutherland W, et al. ULBPs, novel MHC class I-related molecules, bind to CMV glycoprotein UL16, and stimulate NK cytotoxicity through the NKG2D receptor[J]. Immunity. 2001;14:123.
[11] Bauer SV, Groh J, Steinle JH, et al. Activation of NK cells and T cells by NKG2D, a receptor for stress-inducible MICA[J]. Science 1999 ;285:727.
[12] Diefenbach AAM, Jamieson SD, Li N, et al. Ligands for the murine NKG2D receptor: expression by tumor cells and activation of NK cells and macrophages. Nat[J]. Immunol. 2000 ;1:119.
[13] Eisele G, Wischhusen J,Mittelbronn M, et al. TGF-beta and metalloproteinases differentially suppress NKG2D ligand surface expression on malignant glioma cells[J]. Brain. 2006 Sep;129(Pt 9):2416-25.
[14]金伯泉.神经和内分泌(或神经内分泌)系统对免疫系统的调控.见:金伯泉,主编.细胞和分子免疫学.北京:科学出版社,2001:11-21.
[15] HaskóG, Elenkov IJ, Vizi ES. Presynaptic receptors involved in the modulation of release of noradrenaline from the sympathetic nerve terminals of the rat thymus. Immunol Lett[J]. 1995 Jul-Aug;47(1-2):133-7.
[16] Espinosa E, Bermúdez-Rattoni F. Behavior-immunity relationship: the role of cytokines. Rev Invest Clin[J]. 2001 May-Jun;53(3):240-53.
[17] Di Comite G, Grazia Sabbadini M, Corti A, et al. Conversation galante: how the immune and the neuroendocrine systems talk to each other[J]. Autoimmun Rev. 2007 Nov;7(1):23-9.
[18] Schwartz M, Sela BA, Eshhar N. Antibodies to gangliosid and myelin autoantigens are produced in mice following sciatic nerve injury[J]. J Neurochem, 1982;38:1192.
[19] De Medinaceli L, Church AC, Yen-Nung Wang. Posttramatic autoimmune reaction in peripheral nerve: effect of single injury[J]. Exp Neurol, 1985;88:372.
[20] Ansselin AQ, Pollard JD. Immunopathological factors in peripheral nerve allograft rejection: quantification of lymphocyte invasion and major histocompatility complex expression[J]. J Neuro Sci, 1990;96:75.
[21]裴福兴,杨志明,黄富国,等.周围神经损伤后的免疫反应和神经再生.中华显微外科杂志,1995;18:146.
[22] Forsum U, Claesson K, Hjelm E, et al. ClassⅡtransplantation antigens:Distribution in tissue and involement disease [J].Scand J Immunol, 1985;21:389.
[23] de Graaf KL, Wallstr?m E, Muhallab S, et al. MHC and non-MHC gene regulation of disease susceptibility and disease course in experimental inflammatory peripheral neuropathy[J]. J Neuroimmunol. 2004 Oct;155(1-2):73-84.
[24] Scarpini E, Lisak RP, Benrttas S, et al. Quantitative assessment of classⅡMoleculars in normal and pathological nerves: immunohistochemical studies in vivo and in tissue cultures[J]. Brain, 2003;77:659.
[25] Lawrence JM, Keegan DJ, Muir EM,et al . Transplantation of Schwann cell line clones secreting GDNF or BDNF into the retinas of dystrophic Royal College of Surgeons rats[J]. Invest Ophthalmol Vis Sci. 2004 Jan;45(1):267-74.
[26] Mackinnon SE, Hudson AR. Clinical application of peripheral nerve t ransplantation[J]. Plast Reconstr Surg, 2004;90:695.
[27] Bain JR, Mackinnon SE, Hudson AR. The peripheral nerve allograft: An assessment of regeneration across nerve allograft in rats immunosuppressed with cyclosporin A[J]. Plast Reconstr Surg, 2005;82:1053.
[28] Buttemeyer R, Rao UN, Jones NF. Peripheral nerve allograft transplantation with FK506:functional,histological,and immunological results before and after discontinuation of immunosuppression[J]. Annals of Plastic Surgery, 1995;35(4):396.
[29] Nakao Y, Mackinnon SE, Mohanakumar T, et al. Monoclonal antibodies against ICAM-1 and LFA-1(CD11A) induce specific tolerance to peripheral nerve allograft in rats. Transplantation Proceedings, 1995;27(1):373. Jean-Michel Dubernard, Earl Owen, Guillaume Herzberg, et al. Human hand allograft:report on first 6 months[J]. The Lacent, 1999;353:1315.
[30] Tobin G, Breidenbach W, Barker J, et al. Clinical progress of the nation’s first hand transplant over the first year and a half[J]. Louisvil Medicine, 2000;48(2):57
[31]裴国献,顾立强,于立新.异体手移植二例前期报告.中华医学志,2000;80(6):1.
[32] Gold BG, Densmore V, Shou WN, et al. Immunophilin FK506-binding protein 52(not FK506-binding protein 12) mediates the neurotrophic action of FK505[J]. J of Pharmacology and Experimental Therapeutics, 1999;289:1202.
[33] Ishibashi T, Dakin KA, Stevens B. Astrocytes promote myelination in response to electrical impulses[J].Neuron. 2006 Mar 16;49(6):823-32.
[34] Olah M, Ping G, De Haas AH. Enhanced hippocampal neurogenesis in the absence of microglia T cell interaction and microglia activation in the murine running wheel model[J]. Glia. 2008 Dec 29.
[35] Kurkowska-Jastrzebska I, Joniec I, Zaremba M. Anti-myelin basic protein T cells protect hippocampal neurons against trimethyltin-induced damage[J].Neuroreport. 2007 Mar 26;18(5):425-9.
[36] Weller RO , Engelhardt B , Phillips MJ . Lymphocyte targeting of the central nervous system:a reviewof afferent and efferent CNS-immune pathways[J ] . Brain-pathol . 1996 ,6(3) :275～288
[37] Weller RO , Phillips MJ , Kida S , et al . Immunologic significance of lym2 phatic drainage of the brain[J ] . Bull Acad Natl Med. 1997 ,181(4) :661～671
[38] Harling-Berg C, Konpf PM, MerriamJ . Role of cervical lymph node in the systemic humoral immune response to human serum albumin microinfusedinto rat cerebrospinal fluid[J ] . J Neuroimmunol . 1998 ,25 :185～193
[39] Lake J , Weller RO , Phillips MJ ,et al . Lymphocyte targeting of the brain in adoptive transfer cryolesion-EAE[J ] . J pathol . 1999 ,187(2) :259～265
[40] Phillips MJ , Needham M, Weller RO. Role of cervical lymph nolds in autoimmune encephalomyelitis in lewis rat[J ] . J Pathol . 1997 ,182(4) :457～464
[41] De-Carvalho MC, Chimelli LM, Quirico-Santos T. Modulation of lewis rats with experimental autoimmune encephalomyelitis[J]. Braz J Med Biol Res.1999 ,32(5) : 583～592
[42] Tang FR, Chia SC, Zhang S. Glutamate receptor 1-immunopositive neurons in the gliotic CA1 area of the mouse hippocampus after pilocarpine-induced status epilepticus[J].Eur J Neurosci. 2005 May;21(9):2361-74.
[43] Takahashi Y, Mori H, Mishina M, Watanabe M.Autoantibodies andcell-mediated autoimmunity to NMDA-type GluRepsilon2 in patients with Rasmussen's encephalitis and chronic progressive epilepsia partialis continua[J]. Epilepsia. 2005;46 Suppl 5:152-8.
[44] Xu X, Sun R, Jin R. The effect of the ketogenic diet on hippocampal GluR5 and Glu(6 mRNA expression and Q/R site editing in the kainate-induced epilepsy model[J].Epilepsy Behav. 2008 Oct;13(3):445-8.
[45]姚君茹,潘j强,吕束清,等.癫痫夫鼠海马结构谷氨酸和nNOS神经元的动态变化.解剖学杂志,2004,27:505 506.
[46] Takahashi Y, Mori H, Mishina M. Autoantibodies to NMDA receptor in patients with chronic forms of epilepsia partialis continua.Neurology[J]. 2003 Oct 14;61(7):891-6.
[47] Dambinova SA.The presence of autoantibodies to N-terminus domain of G1uRI subunit of AMPA receptor in the blood serum of palienls with epiepsy[J].J Neurol Sci,1997,152:93-96.
[48] Dambinova SA.Monitoring of brain spiking activity and autoantibodies to N-terminus domain of GIuRI suhunil of AMPA receptors i rl blood serunlof rats with cobalt-induced epilepsy[J].J Neurochen。1998,7l:2088-2092
[49] Pehola J . Autoantibodies to glutamic acid decarboxylase in patients with therapy-resistant epilepsy[J].Neurology.2000,55:46-50.
[50] McKnight K, Jiang Y, Hart Y. Serum antibodies in epilepsy and seizure-associated disorders.Neurology[J]. 2005 Dec 13;65(11):1730-6.
[51] Proia RL. Gangliosides help stabilize the brain[J].Nat Genet. 2004 Nov;36(11):1147-8.
[52] Yamamoto HA, Mohanan PV. Ganglioside GT1B and melatonin inhibit brain mitochondrial DNA damage and seizures induced by kainic acid in mice.Brain Res[J]. 2003 Feb 21;964(1):100-6.
[53] Momzov SG. Autoantibodies to brain tissue antigets in epilepsy palients[J].Zh ncuropatol Psikhiatr lm S S korsakova,l 996。96:7 l-76.
[54] Dehounlean P,Gerome P,Zammi|C,et al. Frequency of anticardiolipin,antinuclear and anti—beta2 GPI antibodies is not increased in unselected epileptic patients:a case—control study[J].Seizue.2004,13:205-207.
[55] McKnight K, Jiang Y, Hart Y. Serum antibodies in epilepsy and seizure-associated disorders[J]. Neurology. 2005 Dec 13;65(11):1730-6.
[56] Mokran V , Simko M , Nyulassy S. Seizures and immune disorders J . B ratisl Lek L isty ,1997 ,98 (4) :229.
[57] Chapman J ,Cohen2Armon M , Shoenfeld Y ,et al. Antipholipid antibodies permeabilize depolarize brain synaptoneurosomes [J] .L upus ,1999 ,8 (2) :127.
[58]曾常茜.消炎痛对癫痫保护作用的免疫学研究J .中国神经免疫学和神经病学杂志,2002 ,9 (3) :135.
[59]刘保群.免疫调节剂辅助治疗癫痫J .中国神经免疫学和神经病学杂志,2002 ,9 (3) :141.
[60] Bien CG, Granata T, Antozzi C. Pathogenesis, diagnosis and treatment of Rasmussen encephalitis: a European consensus statement[J]. Brain. 2005 Mar;128(Pt 3):454-71.
[61] Dalakas MC. The role of IVIg in the treatment of patients with stiff person syndrome and other neurological diseases associated with anti-GAD antibodies[J]. J Neurol. 2005 May;252 Suppl 1:I19-25.
[62] Zou LP, Zhang WH, Wang HM. Maternal IgG suppresses NMDA-induced spasms in infant rats and inhibits NMDA-mediated neurotoxicity in hippocampal neurons[J]. J Neuroimmunol. 2006 Dec;181(1-2):106-11.
[63] Kanwar JR. Anti-inflammatory immunotherapy for multiplesclerosis/experimental autoimmune encephalomyelitis (EAE) disease[J]. Curr Med Chem. 2005;12(25):2947-62.
[64] Lorigados Pl ,Morales CL,Parch FN,et a1.Immunological disorders in epileptic patients are associated to the epileptogenic focus localization[J].Rev Neurol,2004,39:101一104.
[65] Hosokawa M,Klegcrls A,Maguire J,et al,Expression of complement tnessenger RNAs and proleins by human oligodendroglial cells[J].Gila.2003,42:417-423.
[66] Levite M.Autoimmune in Epilepsy Nat[J].Immunol,2002,3:500-505.
[1] F L M Ricciardolo. Multiple roles of nitric oxide in the airways [J].Thorax, 2003 Feb, 58:75.
[2] Panaro MA, Brandonisio O, Acquafredda A, et al. Evidences for iNOS Expression and Nitric Oxide Production in the Human Macrophages[J].Curr Drug Targets Immune Endocr Metabol Disord. 2003 Sep,3(3):20.
[3] Beckman JS ,Koppenol WH. Nitric oxide, superoxide, and peroxynitrit: the good, the bad, and ugly [J].Am J Physiol, 1996 Nov;27(5 Pt ):C424.
[4] Crowell JA, Steele VE, Sigman CC, et al. Is Inducible Nitric Oxide Synthase a Target for Chemoprevention? [J].Mol Cancer Ther, 2003 Aug;2(8):85.
[5] Murashima YL, Yoshii M, Suzuki J. Role of nitric oxide in the epileptogenesis of EL mice[J]. Epilepsia. 2000;41 Suppl 6:S195-9.
[6] Chiueh CC, Andoh T, Lai AR, et al. Neuroprotective strategies in Parkinson's disease: protection against progressive nigral damage induced by free radicals[J].Neurotox Res. 2000 May;2(2-3):293-310.
[7] Lu KT, Chiou RY, Chen LG, et al. Neuroprotective effects of resveratrol on cerebral ischemia-induced neuron loss mediated by free radical scavenging and cerebral blood flow elevation.J Agric Food Chem[J]. 2006 Apr 19;54(8):3126-31.
[8] Wainwright MS, Grundhoefer D, Sharma S, et al. A nitric oxide donor reduces brain injury and enhances recovery of cerebral blood flow after hypoxia-ischemia in the newborn rat.Neurosci Lett[J]. 2007 Jan 11.
[9] Jung KH, Chu K, Ko SY, et al. Early intravenous infusion of sodium nitrite protects brain against in vivo ischemia-reperfusion injury[J].Stroke. 2006 Nov;37(11):2744-50. Epub 2006 Sep 28.
[10] ereira de Vasconcelos A, Riban V, Wasterlain C, et al. Role of endothelial nitric oxide synthase in cerebral blood flow changes during kainate seizures: a genetic approach using knockout mice[J]. Neurobiol Dis. 2006 Jul;23(1):219-27.
[11] Hosseinzadeh H, Karimi GR, Rakhshanizadeh M, et al. Anticonvulsant effect of Hypericum perforatum: role of nitric oxide[J].J Ethnopharmacol. 2005 Apr 8;98(1-2):207-8.
[12] Yahyavi-Firouz-Abadi N, Tahsili-Fahadan P, Riazi K, et al. Involvement of nitric oxide pathway in the acute anticonvulsant effect of melatonin in mice[J].EpilepsyRes. 2006 Feb;68(2):103-13.
[13] Noh HS, Kim DW, Cho GJ, et al. Increased nitric oxide caused by the ketogenic diet reduces the onset time of kainic acid-induced seizures in ICR mice[J]. Brain Res. 2006 Feb 23;1075(1):193-200.
[14] Paul V, Ekambaram P, et al. Effects of sodium nitroprusside, a nitric oxide donor, on gamma-aminobutyric acid concentration in the brain and on picrotoxin-induced convulsions in combination with phenobarbitone in rats[J]. Pharmacol Biochem Behav. 2005 Mar;80(3):363-70.
[15] Royes LF, Fighera MR, Furian AF, et al. The role of nitric oxide on the convulsive behavior and oxidative stress induced by methylmalonate: An electroencephalographic and neurochemical study[J].Epilepsy Res. 2007 Mar;73(3):228-237.
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