狼疮性肾炎患者淋巴细胞亚群比率和免疫球蛋白水平的变化

目的 探讨狼疮性肾炎（ＬＮ）患者的淋巴细胞亚群和免疫球蛋白（Ｉｇ）的变化及其意义。方法采用淋巴细胞的膜抗原双标记染色法及ＥＬＩＳＡ，对６０例ＬＮ患者的细胞与体液免疫功能进行前瞻性研究。结果①与对照组相比较，活动期ＬＮ患者的ＣＤ３＋ＣＤ４＋细胞的比率（Ａ组：伴肾病综合征者）为（ｌ６．３ ±７．９）％，Ｂ组（不伴肾病综合征者）为（２０．８±１０．１）％］和ＣＤ１６＋＋ＣＤ５６＋细胞的比率［Ａ组为（８．６±５．７）％，Ｂ组为（１５．２±６．２）％明显减少；ＣＤ３+ ＣＤ8+”细胞的比率［Ａ组为（４８．３±１０．７）％，Ｂ组为（３５．９±９．８）％］明显增高；ＣＤ３+ ＣＤ４+ ／ＣＤ３+ ＣＤ８＋细胞的比值＜１（Ａ组为０．４３±０．２１，Ｂ组为０．８７±０．２５），且Ａ组与８组相比较差异明显（Ｐ＜０．０５）。②与活动期ＬＮ患者相比较，治疗后处于稳定期的 ＬＮ患者 ＣＤ３＋ＣＤ４＋细胞的比率卜组为（２８．８±８．ｌ）％，Ｂ组为（３２．８± ７．ｌ）％］和 ＣＤ１６＋＋ＣＤ５６＋细胞的比率［Ａ组为（１８．９ ± １２．５）％，Ｂ组为（２４．０±８． ９）％，以及 ＣＤ３＋ＣＤ４＋／ＣＤ３＋ＣＤ８＋细胞的比值（Ａ组为 ０．９７±２．３，Ｂ组     

兔脑缺血的视觉和听觉诱发电位的变化

阻断兔双侧椎动脉（ＢＶＡ）和左颈总动脉（ＬＣＣＡ）后，夹闭右颈总动脉（ＲＣＣＡ）３、５、７ｍｉｎ，松开ＲＣＣＡ再灌流，记录听觉脑干诱发电位（ＢＡＥＰｓ）、中潜伏期听觉诱发电位（ＭＡＥＰｓ）以及视觉诱发电位（ＶＥＰｓ）。发现不全阻断脑血流后２．５ｍｉｎ，ＭＡＥＰｓ Ｎ０消失；４．５ｍｉｎ，ＶＥＰｓ Ｎ１和Ｐ２消失，ＢＡＦＰ３ Ⅰ～Ⅴ波峰值潜伏期延长，而振幅无明显变化。完全阻断脑血流１．５ｍｉｎ，ＶＥ     

乳腺癌血管生成及组织蛋白酶D表达与转移的关系

目的：探讨乳腺癌组织微血管密度（ｍｉｃｒｏｖｅｓｅｌｄｅｎｓｉｔｙ，ＭＶＤ）及组织蛋白酶Ｄ（ｃａｔｈｅｐｓｉｎＤ，ＣＤ）表达与转移的关系。方法：应用免疫组织化学方法对乳腺癌组织的ＭＶＤ及ＣＤ进行定量和半定量研究。结果：乳腺癌组织ＭＶＤ及ＣＤ表达与淋巴结转移密切相关，腋下淋巴结转移组的ＭＶＤ（１３１．８±３９．８）明显高于腋下淋巴结阴性乳腺癌（ｎｏｄｅｎｅｇａｔｉｖｅｂｒｅａｓｔｃａｎｃｅｒ，ＮＮＢＣ）组的ＭＶＤ（７８．１±２７．１）（Ｐ＜０．００１）；腋下淋巴结转移组ＣＤ高表达者（３３／３６，９１．７％）明显多于ＮＮＢＣ组（１６／３６，４４．４％）（Ｐ＜０．０１）。乳腺癌组织ＭＶＤ与ＣＤ表达关系密切；远处转移及早期死亡者ＭＶＤ较高且ＣＤ表达极强。结论：乳腺癌组织ＭＶＤ的增加及ＣＤ高表达可能协同促进肿瘤转移。富于微血管及ＣＤ高表达的乳腺癌应作为远处转移及早期死亡的高危患者加以重视。     

骶前区静脉丛的解剖学特点及临床意义

目的：研究骶前区静脉丛（Ｖｅｎｏｕｓ ｐｌｅｘｕｓ ｏｆ ｐｒｅｓａｃｒａｌ ｒｅｇｉｏｎ ，ＶＰＰＳＲ） 的解剖学特点，为骶前区静脉破裂大出血的防治提供解剖学基础。方法：在３４ 具成人尸体上，分虽观测ＶＰＰＳＲ 的组成、管壁、瓣膜、长度及直径。结果：ＶＰＰＳＲ 管壁薄、缺少静脉瓣，呈网状。ＶＰＰＳＲ Ｓ１～５ 横干的长度和直径（ Ｆ 检验） 均有显著差异，Ｐ＜ ０ ．０５ 。其长度平均（ 珋ｘ ±ｓ） ：Ｓ１ 为３ ．２ ±１ ．５ ｃｍ ，Ｓ２ 为４ ．４ ±１ ．０ ｃｍ ，Ｓ３ 为３ ．５ ±１ ．１ ｃｍ ，Ｓ４ 为２ ．３ ±０ ．９ ｃｍ ，Ｓ５ 为１ ．０ ±０ ．３ ｃｍ ；其直径平均（珋ｘ ±ｓ） ：Ｓ１ 为１ ．２ ±０ ．７ ｍ ｍ ，Ｓ２ 为２ ．５ ±１ ．５ ｍ ｍ ，Ｓ３ 为２ ．５ ±１ ．５ ｍ ｍ ，Ｓ４为１ ．７ ±１ ．５ ｍ ｍ ，Ｓ５ 为０ ．９ ±０ ．６ ｍ ｍ 。Ｓ４ 椎体前穿通支静脉口径２ ～４ ｍ ｍ 占８ ．８ ％ ，０ ．１ ～１ ．９ ｍ ｍ 占９１ ．２ ％ 。结论：ＶＰＰＳＲ 解剖变异多、血管壁薄、缺少静脉瓣是引起ＶＰＰＳＲ 损伤大出血甚至死亡的解剖学基础。     

脑干诱发电位V／I波幅比值和耳蜗电图对椎基底动脉供血不足的诊断价值

本文报告确诊为椎基底动脉供血不足者４２例（８４支耳），对其进行脑干诱发电位（ＡＢＲ）和耳蜗电图（ＥＣｏｃｈＧ）两项检测在本病时的应用价值研究。ＡＢＲ中Ⅰ—Ⅲ波ＩＰＬ延长（＞２．３０ｍｓ）占２０％．Ⅰ—Ⅴ波ＩＰＬ（＞４．５ｍｓ）占１２％，Ｉ／Ｖ比值）１．０占５８％。ＥＣｏｃｈＧ中ＡＰ（Ｎ１）下降占８４．５％，Ｎ２＞Ｎ１占２６％，ＳＰ／ＡＰ比值＞０．３７占２５％。认为利用单项ＡＢＲ或ＥＣｏｃｈＧ检测结果诊断椎基底动脉供血不足是不够全面的。     

MCP-1 mcAb和Losartan拮抗Ang Ⅱ介导的VSMCs的增殖与迁移效应的实验研究

目的探讨单核细胞趋化蛋白－１单克隆抗体（ＭＣＰ－１－ｍｅＡｂ）或Ｌｏｓａｒｔａｎ 拮抗血管紧张素Ⅱ（ＡｕｇⅡ）介导的血管平滑肌细胞（ＶＳＭＣｓ）增殖与迁移效应的可能性，为防治动脉硬化提供一定的理论依据。方法采用改良的Ｂｏｙｄｅｎ小室法检测 ＶＳＭＣｓ的迁移效应；以 ＭＴＴ法、~３Ｈ－ＴａＲ掺入法、~３Ｈ－脯氨酸标记法和ＶＳＭＣｓ计数评价ＶＳＭＣｓ的增殖效应。将培养ＶＳＭＣｓ分为 ５组； ２％胎牛血清（ ２％ＦＣＳ）组、 ＡｕｇⅡ组（其浓度为 １０－１０～１０－６ｍｏｌ／Ｌ）、Ｌｏｓａｒｔａｎ组（其浓度为 １０－７～１０－５ｍｏｌ／Ｌ）、ＭＣＰ－ｌｍｃＡｂ组（终浓度为 １０μｇ／ｍｌ）和阳性对照组（含５％的酵母多糖活化血清）。结果（１） ＡｕｇⅡ具有剂量依赖性的促进 ＶＳＭＣｓ的增殖与迁移效应；（２） ＭＣＰ－１ｍｃＡｂ或 Ｌｏｓａｒ－ｔａｎ能有效地拮抗ＡｕｇⅡ介导的ＶＳＭＣｓ增殖与迁移效应。结论 ＭＣＰ－１ｍｃＡｂ或Ｌｏｓａｒｔａｎ对动脉硬化性疾病可能具有较大的应用前景。     

T细胞性淋巴瘤组织CD56的检测及其与EB病毒的关系

目的探讨Ｔ细胞性淋巴瘤（ＴＣＬ）中ＣＤ５６的表达情况及ＣＤ５６阳性表达同爱波斯坦－巴尔病毒（ＥｐｓｔｅｉｎＢａｒＶｉｒｕｓ,ＥＢＶ）感染的关系。方法对４６例ＴＣＬ进行ＣＤ５６的免疫组织化学ＬＳＡＢ法检测及ＥＢＥＲｓ的原位杂交检测。结果（１）４６例ＴＣＬ中８例ＣＤ５６阳性（１７．４％）,其中鼻腔、咽部和口腔阳性率最高（５／１７例,２９．４％）。弥漫性大细胞型淋巴瘤ＣＤ５６阳性率最高（６／１６例,３７．５％）。（２）４６例ＴＣＬ中２４例ＥＢＥＲｓ阳性（５２．２％）。（３）８例ＣＤ５６阳性病例中,４例ＥＢＥＲｓ阳性。结论ＣＤ５６的表达同ＴＣＬ发生部位和类型有一定关系。ＣＤ５６阳性表达与ＥＢ病毒感染未发现相关性     

HBV感染与IgA肾病肾小管间质病变的关系

目的探讨ＩｇＡ肾病ＨＢＶ感染与肾小管间质病变的关系。方法利用原位分子杂交（ＨＢＶＤＮＡ）、免疫组化（ＨＢＡｇ、ＣＤ３、ＣＤ８）以及ＨＢＶＤＮＡＨＢＡｇ和ＨＢＡｇＣＤ４３双标记技术，对９１例ＩｇＡ肾病肾穿刺标本进行研究。结果肾组织内ＨＢＡｇ阳性率为６９．２％。ＨＢＶＤＮＡ原位杂交阳性率为４２９％。ＨＢＶＤＮＡ阳性的病例，双重标记染色发现ＨＢＶＤＮＡ阳性的肾小管上皮细胞可表达ＨＢｃＡｇ或／和ＨＢｓＡｇ。ＨＢＶ感染标记（ＨＢＶＤＮＡ、ＨＢｃＡｇ、ＨＢｓＡｇ）阳性组ＣＤ３阳性细胞和ＣＤ８阳性细胞数明显高于阴性组（Ｐ＜００１），并可见数量不等的Ｔ淋巴细胞入侵ＨＢｃＡｇ及ＨＢｓＡｇ阳性肾小管管壁或围绕其周围。结论感染ＨＢＶ的肾组织细胞能够表达ＨＢＡｇ，并诱导ＣＤ３阳性细胞和ＣＤ８阳性细胞浸润，从而加重肾小管、间质损害。ＨＢＶ感染对ＩｇＡ肾病的发生发展可能起着重要作用     

病毒性心肌炎、扩张型心肌病患者T细胞及其亚群和免疫球蛋白的改变

本研究用ＣＤ系统ＭＣＡＢ间接免疫荧光法对柯萨奇Ｂ病毒中和抗体阳性的病毒性心肌炎（Ｂ型），扩张型心肌病（Ｃ组）患者检测其周围Ｔ淋巴细胞及其亚群并与正常人（Ａ组）相对照，结果不论是Ｂ组或Ｃ组其ＣＤ３、ＣＤ４、ＣＤ３均较Ａ组为低，Ｐ值均＜０．０１，Ｃ组比Ｂ组更低，两者相比亦有统计学意义，Ｐ值分别为＜０．０５，＜０．００１。至于ＣＤ４／ＣＤ８，Ｃ组＞Ｂ组＞Ａ组，Ｐ值为＜０．０５，＜０．０１。在急性恢复期者与正常人相近，分别为１．７８±０．０５、１．７３±０．０８，而慢性反复发作期者与扩张型心肌病者相近，分别为２．２２±０．３及２．２９±０．２６。免疫球蛋白测定在扩张型心肌病中较在病毒性心肌炎息者明显增高，并有统计学意义     

阈值强度刺激BAEP检测在梅尼埃病的应用

目的：探讨阈值强度刺激在梅尼埃病（ＭＤ）ＢＡＥＰ检测中的应用价值。方法：对３６例ＭＤ患者４６只耳同时进行阈上强度刺激ＢＡＥＰ检测和阈值强度刺激检测,并和２５例正常人５０只耳检测结果进行比较。结果：ＭＤ组４６只耳阈上强度刺激ＢＡＥＰ检测２只耳Ⅰ波潜伏期延长,１３只耳Ⅰ波缺失,异常率３３％。而阈值强度刺激时ＢＡＥＰ反应阈增高者３６只耳,异常率７２％,两者差异显著（Ｐ＜００１）。与正常对照组Ｖｔ波潜伏期（均值７９５ｍｓ）比较,ＭＤ组Ｖｔ波潜伏期（均值６６５ｍｓ）缩短,有显著差异Ｐ＜００１）。结论：阈值强度刺激可显著提高ＭＤＢＡＥＰ检测阳性率,Ｖｔ波潜伏期＜７０ｍｓ可作为判断蜗性损害的一项客观指标     

电针促进坐骨神经中不同纤维成分再生—电生理和形态学研究

本实验运用屈肌反射-HRP逆行追踪结合实验,对电针促进大鼠坐骨神经干中躯体运动及感觉纤维成分的再生进行了观察。结果显示:电针组足底施予45±5V屈肌反射阈刺激,可引起短潜伏期的A类及长潜伏期的C类纤维传入反应;对照组足底经65±5V屈肌反射阈刺激后,仅见C类纤维传入所引起的屈肌反射。电针组右侧脊神经节内主要为大、小两种圆形细胞被标记,而对照组右侧脊神经节内标记细胞却均为淡染的小圆形细胞。电针组脊髓前角内浓染的标记细胞呈大多角状。电针组脊神经节及脊髓前角内标记细胞百分率及神经再生率明显高于对照组。上述结果表明,电针组坐骨神经干中感觉纤维及躯体运动纤维终末向各自支配区的再生速度明显快于对照组。本文结果提示:电针促进坐骨神经中不同纤维成分的再生可能具有定向诱导轴突支芽、加快神经细胞蛋白质合成及转运等双重功能。     

纯化蝎毒素Ⅳ对神经损伤康复的促进作用

实验用大鼠２０只，结扎坐骨神经以造成神经慢性机械压迫－痛觉过敏动物模型。实验组从手术后第２天开始经腹腔注射纯化蝎毒素Ⅳ，每日注射６００ｍｇ／ｋｇ，持续用药，选用辐射热测痛．本实验用电生理学方法结合ＨＲＰ逆行追踪技术进行研究。结果显示，纯化蝎毒素Ⅳ对神经损伤后形态和功能的恢复以及对神经损伤性痛觉过敏的解除都具有促进作用．     

糖尿病性NA-AION的图形视觉诱发电位的研究

目的 研究糖尿病非动脉炎性前段缺血性视神经病变(NA-AION)的图形视觉诱发电位(P-VEP)P100波潜伏期和振幅的变化。方法 将有糖尿病且无糖尿病性视网膜病变的NA-AION患者17例纳入A组,将非增生期糖尿病视网膜病变的NA-AION患者21例纳入B组,将增生期糖尿病视网膜病变的NA-AION患者20例纳入C组,将无糖尿病的NA-AION患者25例纳入D组,行PVEP检查。结果 A、B、C、D组P100波0.25度方格平均潜伏期分别为127.27 ms、132.37 ms、139.58 ms、125.46 ms,振幅分别为119.13 μv、124.61μv、135.62 μv、116.08 μv,A、B、C组与D组P100波潜伏期、振幅分别比较,差异有统计学意义（P＜0.05）,1度方格结果同0.25度方格。结论 糖尿病性NA-AION患者视神经功能较非糖尿病性NA-AION患者下降更为明显,控制糖尿病可能会有效的减少NA-AION的发生。     

Localization of dopamine D1A and D1B receptor mRNAs in the forebrain and midbrain of the domestic chick

The distribution and cellular localization of dopamine D1A and D1B receptor mRNAs in the forebrain and midbrain of the domestic chick were examined using in situ hybridization histochemistry with ³⁵[S]-dATP labeled oligonucleotide probes, visualized with film and emulsion autoradiography. Labeling for D1A receptor mRNA was intense in the medial and lateral striatum, and moderately abundant in the pallial regions termed the archistriatum and the neostriatum, in the hypothalamic paraventricular nucleus region, and in the superficial gray layer of optic tectum of the midbrain. D1B receptor mRNA was abundant in the medial and lateral striatum, and in the pallial region termed the hyperstriatum ventrale, and moderately abundant in the intralaminar dorsal and posterior thalamus and in the superficial gray of the optic tectum. At the cellular level, about 75% of neurons in the medial striatum and 59% of neurons in the lateral striatum were labeled for D1A receptor mRNA, whereas about 39% of the neurons in the medial striatum and 21% in the lateral striatum were labeled for D1B receptor mRNA. Large striatal neurons were not labeled for D1A or D1B receptor mRNA. The data suggest that while both D1A and D1B receptors mediate dopaminergic responses in many neurons of the avian striatum, primarily D1A receptors mediate dopaminergic responses in the archistriatum and the neostriatum, while primarily D1B receptors mediate dopaminergic responses in the hyperstriatum ventrale and the thalamus.     

嗅鞘细胞移植对大鼠脊髓半横断损伤后轴突再生及后肢功能恢复的作用

为了对嗅鞘细胞移植治疗大鼠脊髓损伤(spinal cord injury, SCI)后轴突再生及后肢功能恢复进行综合性的评价,本实验采用22只雌性成年SD大鼠,并随机分成A、B、C、D 4组。其中A、B、D组行左侧T11 ～T12节段脊髓半横断手术,然后A组移植嗅鞘细胞(olfactory ensheathing cells,OECs)悬液;B组移植DMEM/F12培养液;D组移植核荧光试剂(Hoechst33342)标记的嗅鞘细胞,用于鉴定嗅鞘细胞在体内的存活情况;C组作为正常对照组。术后6周内,对大鼠进行BBB评分、IP斜板试验并观察皮质体感诱发电位(cortical somatosensory evoked potential, CSEP)、运动诱发电位(motor evoked potential, MEP)的潜伏期。将辣根过氧化物酶(HRP)注射到横断面尾段脊髓,逆行追踪观察横断面头段脊髓及对侧中脑红核内HRP逆标细胞数,并观察左侧后肢小腿三头肌肌细胞横截面积及直径的变化。结果显示:(1)移植后的OECs数量未见明显减少,细胞核形态较好,细胞未向头、尾侧迁移;(2)移植3周后BBB评分及IP斜板,试验A、B组较C组明显低(P<0.05),但A组明显高于B组(P<0.05);(3)A、B组的CSEP及MEP潜伏期较C组明显延长(P<0.05),但A组要比B组明显缩短(P<0.05);(4)HRP逆行追踪观察到对侧中脑红核大细胞区及脊髓T9 ～T11节段逆标细胞的数量,A组明显多于B组,但A、B组均少于C组;(5)左侧后肢小腿三头肌肌细胞的横截面积及直径,A、B组均较C组减少,但A组减小的幅度明显小于B组。以上结果表明OECs移植能促进半横断脊髓轴突的再生及后肢功能的恢复。     

健康青年人四肢远端神经F波特征

目的:观察健康青年志愿者的正中、尺、腓、胫神经F波最短潜伏期以及出现率与年龄、性别的关系.方法:选择延边大学医学院健康志愿者996名为研究对象,采用美国NICOLET公司出产的Portabook肌电图诱发电位仪,检测正中神经、尺神经、腓神经和胫神经F波,比较分析男18～21岁组、女18～21岁组与男22～25岁组、女2...     

超声辐照微泡对肝细胞生长因子转染大鼠损伤面神经的促进作用

目的 观察超声微泡介导肝细胞生长因子(HGF)基因促进大鼠受损面神经修复的可行性及有效性.方法 将40只SD大鼠随机分成4组,A组:单纯手术组(PBS);B组:HGF+微泡组;C组:HGF+超声组;D组:HGF+超声+微泡组,每组10只.建立大鼠面神经损伤模型,以HGF作为治疗基因.基因转染后28 d,观察各组大鼠的一般情况,检测面神经传导速度、潜伏期及神经电位波幅的变化.处死各组大鼠,采用Westem blot和RT-PCR检测损伤面神经HGF蛋白和mRNA的表达.结果 经行为学检测,D组大鼠在触须摆动及鼻尖位置均明显优于其余3组.D组面神经传导速度、神经电位波幅明显高于其余3组,潜伏期明显低于其余3组(p＜0.05).D组中HGF蛋白和mRNA的表达量明显高于其他3组(P＜0.05).结论 微泡在一定频率和强度的超声作用下能够安全、有效的将目的基因转染进入损伤后的面神经,有利于受损面神经的修复.     

Influence of auditory precuing on automatic postural responses

An experiment was conducted to determine the influence of auditory precuing on posture control. Specifically, the influence of a warning signal on the onset latencies of the gastrocnemius (G) and tibialis anterior (TA) muscles was determined. An audible 50-ms tone was presented to subjects standing on a moveable platform and preceded a perturbation to standing balance by 500 ms. The perturbations were produced by an anterior or posterior translation (3 cm at 30 cm/s) of the support surface. Unilateral electromyographic activity was recorded from G and TA muscles. In the first series of trials (series A), the muscle onset latencies following perturbations with a nondirectionally specific precue, an invalid precue, and no precue were compared. In the second series of trials (series B), muscle onset latencies following perturbations with a directionally specific precue, invalid precue, and no precue perturbations were compared. In series A, mean muscle onset latencies decreased following nondirectionally specific precues during forward and backward platform perturbations; respectively, TA 6% (91±9 ms to 86±9 ms) and G 7% (93±6 ms to 87±5 ms). During series B, the TA and G muscle onset latencies decreased following directionally specific precues by 10.4% (92±12 ms to 82±6ms) and 9.8% (92±9ms to 83±6ms), respectively. There were no significant differences between the types of precues. Thus, prior knowledge of a forthcoming balance perturbation reduces postural muscle onset latency times. In addition, specific prior knowledge reduces muscle onset latency time in the same manner as does nonspecific prior knowledge.     

Spinal and supraspinal reflex pathways of cardio-cardiac sympathetic reflexes

In anaesthetized cats recordings were made of reflex responses recorded in the inferior cardiac nerves of one side while stimulating the inferior cardiac nerves of the opposite side. Three reflex potentials were observed: an early (about 25 ms) reflex and a later (about 60 ms) reflex due to A afferent fibre excitation and a reflex with a much longer latency (about 180 ms) due to C afferent fibre excitation. Following spinal transection at C2 only the early A reflex remained and this was augmented.     

Motor cortex excitability following repetitive electrical stimulation of the common peroneal nerve depends on the voluntary drive

Previously, long-term changes in the motor cortex have been reported after repetitive electrical nerve stimulation (rES) as well as after motor exercise. The purpose of this study was to investigate whether the effects of voluntary motor cortical drive and of rES on the motor cortical output in healthy subjects interact with each other. A 30-min exercise session was performed during the following conditions: rES of the right common peroneal nerve (CPN) during rES at rest (A); voluntary exercise of the right ankle dorsiflexors alone (B); rES combined with voluntary dorsiflexion exercise (C); voluntary exercise of ankle plantar flexors alone (D); and plantar flexion exercise combined with rES (E). Motor evoked potentials (MEPs) were obtained before and after the exercise with a stimulation intensity of 125% of the threshold of the relaxed right tibialis anterior (TA). rES was ON for 1 s and OFF for 2 s in a cycle, and consisted of trains of five pulses, duration 1 ms and frequency 30 Hz, as applied in functional electrical stimulation (FES). MEPs of the TA muscle elicited after the training were increased in A by 38%, in B by 35%, and in C by 66%. In D and E, the MEPs of TA were decreased by 29% and 35%, respectively. The effect was maintained for at least 30 min after the nerve stimulation was completed. Consistent with previous studies (Khaslavskaia et al. (2002) Exp Brain Res 145:309–315), MEPs after the CPN rES are shown to be partly due to increased TA cortical excitability. These results suggest that the effect of FES on motor cortical excitability depends on the concurrent motor cortical drive present at the time of FES, and the combination of these factors modulates neural excitability and probably reorganization. The decrease in motor cortical excitability after plantar flexor exercise probably means that voluntary effort antagonistic to the electrical exercise is stronger and cancels out the effects of rES. Improving FES effects through an agonist voluntary drive implies an enhancement of sensorimotor reorganization through the addition of a voluntary component to a trained movement. Possible mechanisms and implications of these results on the rehabilitation of patients with paralysis and spasticity are discussed.