脊髓挫伤速度对颈脊髓原发性损伤影响的实验研究

目的　确定脊髓挫伤速度是脊髓损伤的因素,探讨不同速度的脊髓挫伤对大鼠颈脊髓原发性损伤的影响。  方法    20只成年雄性Sprague-Dawley大鼠随机分为快速组（500 mm/s,n=8）、慢速组（5 mm/s,n=8）和对照组（n=4）。用直径为4 mm的平头圆锥打击头在C5水平产生1.5 mm的挫伤位移。损伤后即行心脏固定,切取以挫伤部位为中心长约1.5 cm的脊髓组织。行连续矢状位冰冻切片。HE染色观察脊髓大体形态,计算出血量。β-APP免疫组化后观察轴索损伤程度。  结果　挫伤后观察到脊髓表面有一带状出血,且快速组出血带颜色更深。快速组挫伤位移为(1.50±0.05) mm,最大力为(5.3±1.2) N;慢速组挫伤位移为(1.51±0.04) mm,最大力为(2.8±0.6) N,两组间最大力的差异有显著性（P=0.001）。HE染色显示脊髓出血大部分都集中在灰质,白质相对较少。快速组脊髓总出血量、灰质出血量和白质出血量分别为0.94、0.71和0.23 mm3,慢速组分别为0.55、0.43和0.12 mm3,其中两组间总出血量和灰质出血量的差异有显著性（P＜0.05）。β-APP免疫组化观察到快速组轴索断裂比慢速组更为严重。  结论　脊髓挫伤速度是影响脊髓原发性损伤的因素,快速的脊髓挫伤导致的原发性脊髓损伤更为严重,导致更多的脊髓出血和轴索断裂。     

The relationship between exercise work intervals and duration of exercise on lower extremity training induced by electrical stimulation in humans with spinal cord injuries

A group of 90 male paraplegics were studied to determine the optimal training protocol for isokinetic exercise induced by functional electrical stimulation of the quadriceps muscles. The parameters that were varied were the number of training sessions a week, the length of the training sessions each day, and the work-rest intervals in each training session. Training for 3 days a week for 30 min a day with 6 s of exercise and 6 s of rest proved the optimal protocol. Training for 5 days or for 1 day a week was not as effective in training strength or endurance. A combination of 50% work and 50% rest produced a much greater gain in strength and endurance than work:rest ratios of 66%:33% or 25%:75%. When training was conducted for 5 min, 15 min or 30 min each day, the greatest increase was found when the muscles were exercised for 30 min each day. While more variables need to be examined, this study has provided some initial guidelines for isokinetic training of humans using electrical stimulation. Accepted: 9 April 2000     

Multivariate analysis of factors influencing physical work capacity in wheelchair-dependent paraplegics with spinal cord injury

The purpose of this study was to determine the main factors that influence physical work capacity (PWC) in wheelchair-dependent paraplegics with spinal cord injury (SCI) using multivariate analysis. Thirty-two male paraplegics with SCI (PSCI) performed a submaximal arm exercise test on an arm-cranking ergometer to determine their PWC (oxygen uptake: ml ·  kg⁻¹ · min⁻¹) at a heart rate of 150 beats · min⁻¹ (PWC150). Hayashi's Quantification first type was applied to analyze the effects on PWC150 of six factors: age, smoking, level of physical activity, occupation, level of SCI and period since SCI. This analysis revealed high partial correlation coefficients between PWC150 and the level of SCI (0.651) and physical activity level (0.583) compared to other factors. In addition, the multiple correlation coefficient for six factors in predicting PWC150 was 0.726. These results indicate that the level of SCI and physical activity are the most important factors in determining PWC in wheelchair-dependent male PSCI. Accepted: 28 June 1999     

Atorvastatin prevents early apoptosis after thoracic spinal cord contusion injury and promotes locomotion recovery

The systemic administration of atorvastatin has been shown to be neuroprotective after spinal cord injury (SCI), by decreasing the inflammatory response at the lesion site and by reducing neuronal and oligodendrocyte apoptosis. The latter effect spares white matter at the injury site and improves locomotion. The aim of this study was to confirm the neuroprotective efficacy of atorvastatin as well as its early action in limiting apoptosis with its administration post-SCI. Female Sprague-Dawley rats received an intra peritoneal injection of: (1) statin/saline (5 mg/kg) at 2 h after the contusion injury; (2) physiological saline at 2 h post-SCI; or (3) physiological saline without injury. Statin-treated rats showed significant (p < 0.05) improvement in locomotion at week 4 post-SCI compared to vehicle-treated animals. Explaining this outcome, caspase-3 activity decreased by 50% (p < 0.05), and the histological TUNEL method revealed a decrease of approximately 20% in apoptotic cells at the injury site (p < 0.01) at 4 h post-SCI in atorvastatin-treated rats in comparison to vehicle-treated controls. These data demonstrate that atorvastatin is effective after experimental spinal cord contusion injury in preventing early apoptosis at the injury site within 2 h post-administration.     

脊髓横断伤后Fos在脑内与内脏和心血管相关核团中的表达

目的为阐明急性脊髓损伤对内脏及心血管活动的影响机制提供形态学资料。方法脊髓T4节段横断术后3h,用免疫组织化学方法观察脑与脊髓内脏和心血管相关核团内Fos表达。结果T4水平损伤3h后,中央杏仁核、下丘脑室旁核、中缝背核、导水管周围灰质、臂旁核、蓝斑、孤束核、延髓腹外侧网状核与脊髓中间带外侧核等核团中Fos阳性神经元数目较假手术组显著增加(P<0.01)。结论急性脊髓损伤可引起中枢神经系统的内脏和心血管相关核团内神经元产生特异性反应,但反应的机制不同。     

白藜芦醇对大鼠脊髓损伤后氧化与抗氧化过程的影响

目的探讨白藜芦醇﹙RES﹚对脊髓损伤﹙SCI﹚后髓过氧化物酶﹙MPO﹚和超氧化物歧化酶﹙SOD﹚活性的影响。方法 2008年2月~2010年8月在武汉大学人民医院动物实验中心将96只SD健康成年雄性大鼠随机分成4组,根据Allen’s法制成中度脊髓损伤模型,术后立即管饲白藜芦醇100mg/kg或甲基强的松龙﹙MPSS﹚100mg/kg;通过比色法观察脊髓损伤8小时、1天、3天及7天后白藜芦醇组脊髓MPO及SOD活性的变化,并与MPSS﹙甲基强的松龙﹚组进行疗效对比。结果在脊髓损伤后8小时、1天、3天及7天白藜芦醇组MPO及SOD活性与损伤组差异均有统计学意义,显示白藜芦醇对脊髓损伤具有明显神经细胞保护作用,而且白藜芦醇组与MPSS组间损伤后1天差异具有统计学意义﹙<0.05﹚。结论白藜芦醇在脊髓损伤后能够有效抑制MPO活性的升高幅度,并提高SOD活性,对损伤后脊髓起保护作用。     

修复脊髓损伤的仿生多孔水凝胶的制备研究

目的水凝胶是含水量高和体表面积大的化学性惰性合成高分子,当植入到脊髓组织中,为细胞和轴突提供力学支持。本研究对修复脊髓损伤水凝胶制备、物理特性进行研究。方法本研究交联的水凝胶由2-甲基丙烯酸羟（HEMA）．2乙基三甲基氯化物（methacryloyloxy,MOETACL）共聚物合成。利用氯化钠（NaCl）微粒制备水凝胶的孔隙,用扫描电子显微镜观察其结构。结果计算水凝胶在单位体积上的孔隙数,孔的平均直径和平均体积。以HEMA．MOETACL为基础的水凝胶在其组成上具有显著特征。结论均质多孔的水凝胶,其在修复脊髓损伤的生物特性上具有显著特征。     

Initiating extension of the lower limbs in subjects with complete spinal cord injury by epidural lumbar cord stimulation

We provide evidence that the human spinal cord is able to respond to external afferent input and to generate a sustained extension of the lower extremities when isolated from brain control. The present study demonstrates that sustained, nonpatterned electrical stimulation of the lumbosacral cord—applied at a frequency in the range of 5–15 Hz and a strength above the thresholds for twitches in the thigh and leg muscles—can initiate and retain lower-limb extension in paraplegic subjects with a long history of complete spinal cord injury. We hypothesize that the induced extension is due to tonic input applied by the epidural stimulation to primary sensory afferents. The induced volleys elicit muscle twitches (posterior root muscle-reflex responses) at short and constant latency times and coactivate the configuration of the lumbosacral interneuronal network, presumably via collaterals of the primary sensory neurons and their connectivity with this network. We speculate that the volleys induced externally to the lumbosacral network at a frequency of 5–15 Hz initiate and retain an extension pattern generator organization. Once established, this organization would recruit a larger population of motor units in the hip and ankle extensor muscles as compared to the flexors, resulting in an extension movement of the lower limbs. In the electromyograms of the lower-limb muscle groups, such activity is reflected as a characteristic spatiotemporal pattern of compound motor-unit potentials.Abbreviations C Cervical - CMUP Compound motor-unit potential - EMG Potential - CNS Central nervous system - EMG Electromyography, electromyographic - H Hamstring - L Lumbar - MLR Mesencephalic locomotor region - PARA Paraspinal muscles - Q Quadriceps - S Sacral - SCI Spinal cord injury, spinal cord-injured - SCS Spinal cord stimulation - T Thoracic - TA Tibialis anterior - TS Triceps surae     

Interleukin-17 deficiency improves locomotor recovery and tissue sparing after spinal cord contusion injury in mice

Following the initial impact, spinal cord injury (SCI) triggers a number of inflammatory responses which can exacerbate tissue damage in the cord and impair functional recovery. The involvement of several pro-inflammatory cytokines in the secondary degenerative mechanisms of SCI has been well established, although the role of interleukin-17 (IL-17) remains unclear. In the present study, we used IL-17 knockout (KO) and C57BL/6J wildtype (WT) mice to investigate the effects of IL-17 deficiency on locomotor recovery, lesion size, glial activation and inflammatory cell response following spinal cord contusion injury. Our results show that compared to WT mice, IL-17 KO mice had a significantly smaller lesion size, corresponding with significantly improved locomotor functional recovery following SCI. At 6 weeks after injury, recruitment of B cells, dendritic cells and neutrophils was significantly lower in IL-17 KO than WT mice, however there was no difference in the presence of activated microglia and reactive astrocytes, in the injured spinal cord. These findings suggest that IL-17 is a mediator of secondary degeneration, which contributes to neuroinflammation and hinders functional recovery, though its actions do not affect glial activation following SCI.     

Inhibitory effects on flexor reflexes in patients with a complete spinal cord lesion

Summary The inhibitory effects on flexors of electrical stimulation of a distal peripheral nerve were investigated in 7 paraplegic patients having a complete spinal cord section. The stimuli (3–50 mA) were applied to the sural nerve. Their effects were investigated on: 1) the ipsi- and contralateral H reflex of the Tibialis Anterior (TA); 2) the continuous EMG activity reflexly elicited in TA by a sustained pinch of the foot and 3) on the reflexes evoked in TA by contralateral sural nerve stimulation. Sural nerve stimulation induced two peaks of facilitation of the ipsilateral TA H reflex that could be replaced by inhibition as the stimulus intensity was increased. The comparison of the effect on H reflexes and the EMG activity suggests presynaptic inhibition of Ia fibres at time intervals longer than 300 ms. The stimulation could depress the sustained EMG reflex activity and induce a period of silence whose duration increased with the intensity of the stimulation. As shown in a previous study, a sural nerve stimulation induced a reflex in TA with a prolonged (more than 130 ms) latency. This late reflex could be selectively inhibited by a contralateral sural nerve stimulation, probably at an interneuronal level. These results confirm that the late reflex in TA is similar to the one observed after Flexor Reflex Afferent (FRA) stimulation in the acute spinal cat with DOPA. In addition, they show that at least some part of the half centre organization which has been described in the acute spinal cat with DOPA is also present in the human spinal cord chronically deprived of supraspinal control.     

Effects of motor imagery training after chronic,complete spinal cord injury

Abnormalities in brain motor system function are present following spinal cord injury (SCI) and could reduce effectiveness of restorative interventions. Motor imagery training, which can improve motor behavior and modulate brain function, might address this concern but has not been examined in subjects with SCI. Ten subjects with SCI and complete tetra-/paraplegia plus ten healthy controls underwent assessment before and after 7 days of motor imagery training to tongue and to foot. Motor imagery training significantly improved the behavioral outcome measure, speed of movement, in non-paralyzed muscles. Training was also associated with increased fMRI activation in left putamen, an area associated with motor learning, during attempted right foot movement in both groups, despite foot movements being present in controls and absent in subjects with SCI. This fMRI change was absent in a second healthy control group serially imaged without training. In subjects with SCI, training exaggerated, rather than normalized, baseline derangement of left globus pallidus activation. The current study found that motor imagery training improves motor performance and alters brain function in subjects with complete SCI despite lack of voluntary motor control and peripheral feedback. These effects of motor imagery training on brain function have not been previously described in a neurologically impaired population, and were similar to those found in healthy controls. Motor imagery might be of value as one component of a restorative intervention.     

Increase in bFGF-responsive neural progenitor population following contusion injury of the adult rodent spinal cord

The number of neural progenitor cells, especially nestin+ cells or BrdU-uptake cells is sparse in the normal adult rodent spinal cord. However, in the present study, we show that after spinal cord injury (SCI), many ordinarily quiescent cells were activated to become nestin+ and undergo mitosis (BrdU+) in the ependymal layer as well as in the parenchyma of the spinal cord. Nestin+ cells and BrdU+ cells were in most cases immunohistochemically GFAP+, some of which displayed radial glial cell morphology and partly participated in the border formation of the lesion. The culturing of injured rat spinal cord tissues generated more neurospheres earlier than did the culturing of intact tissues, and these neurosphere cells were multipotent and bFGF-responsive. Immunohistochemical analysis showed that there existed many bFGF+ cells after SCI, the number of which were almost 15 times greater than that in an intact spinal cord. Increased bFGF production after SCI might activate quiescent progenitor cells, and thus initiate their cell proliferation. Finally, SCI to the nestin-promoter green fluorescent protein (GFP) transgenic mice showed broad proliferation of progenitor cells that were induced in the injured spinal cord. The culturing of injured spinal cord tissues from these transgenic mice provides direct evidence that neurospheres can be generated by SCI-activated nestin+ cells. Thus, the activation of bFGF-responsive progenitor cells and the concomitant increase in the population of bFGF+ cells following SCI might be beneficial for spinal cord repair if these progenitor cells are properly manipulated.     

Gene expression alterations of neurotrophins, their receptors and prohormone convertases in a rat model of spinal cord contusion

We have used a semi-quantitative RT-PCR approach to investigate the alterations in the expression of the main regulators of neuronal survival and death, neurotrophins (NTs), NT receptors, and prohormone convertases (PC), in a rat model of spinal cord contusion. Our results revealed that the expression of the members of NT family (Nerve-Growth Factor (NGF), Brain-Derived Neurotrophic Factor (BDNF), and Neurotrophin-3 (NT-3)) is significantly declined in the injured spinal cord, as early as 6h after the induction of the contusion. The expression was recovered afterward to that of the control levels. Furthermore, the expression of all NTs high-affinity Trk receptors decreased severely after the contusion. While the expression of TrkA and TrkC were completely shut down after 6 and 12h after injury respectively, the expression of TrkB receptor declined at 12h after injury and remained at this low level thereafter. In contrast to the pattern of Trk receptor expression, p75NTR receptor showed a significant upregulation after contusion. The expression of PC members functioning in the constitutive secretory pathway, i.e. furin, PACE4 and PC7, increased after damage, while the expression of PC members acting in regulated secretory pathway, PC1 and PC2, reduced after spinal cord injury. All together, the down-regulation of NTs, their designated Trk receptors and PC1/PC2 enzymes along with an upregulation of p75NTR promote neuronal death after injury. Our results suggest that either overexpression of NTs, Trk receptors and PC1/PC2 or interfering with the expression of p75NTR in host and/or grafted cells before transplantation could increase the success of the transplantation.     

脊髓缺血再灌注损伤对大鼠水通道蛋白4表达的影响

目的:在整体水平研究脊髓缺血再灌注损伤对大鼠水通道蛋白4表达水平的影响.方法:SD大鼠72只随机分为空白组、假手术组和SCⅡ组,每组24只.建立大鼠脊髓缺血再灌注损伤模型,并于1、3、5、7天四个时间点分别处死6只.BBB评分评价神经功能,Western blot和免疫荧光方法检测AQP4的表达情况.结果:空白对照组和假手术组在不同时间点的BBB评分均为21分,SCⅡ组的BBB评分在1天时最低,随时间推移逐渐增加,3天明显优于1天(P＜0.05),5天明显优于3天(P＜0.05),5天明显优于7天(P＜0.05).Western blot在34 kD及43 kD分子量处可见特异性条带,SCⅡ组早期AQP4的表达水平显著下降,即在1、3、5、7天四个时间点AQP4的表达显著低于空白对照组和假手术组,但呈逐渐增加趋势;在7天仍显著低于正常空白组和假手术组(P＜0.05).免疫荧光检测AQP4的表达变化趋势与Western blot的检测结果相似.结论:SCⅡ存在AQP4低表达,这可能是造成SCⅡ神经功能障碍的重要原因.     

白细胞介素-10通过乙二醛酶1影响脊髓钝挫伤大鼠运动功能的恢复

目的　用慢病毒介导的方法抑制白细胞介素-10（IL-10）的RNA,观察IL-10通过乙二醛酶1（GLO1）影响大鼠脊髓损伤后运动功能恢复。 方法　SD大鼠66只,采用Allen’s法制备脊髓钝挫伤（spinal cord contusion,SCC）模型,随机分为Sham组（n=9）、SCC组（n=27）、Vector组（n=15）和IL-10 SH组（n=15）,分别注射空质粒和包装IL-10 siRNA的质粒;每组再分为3 d、7 d和28 d 亚组。采用BBB（Basso,Beattie,Bresnahan）评分评估大鼠后肢运动功能;免疫组织化学和qRT-PCR技术定位和定量测定IL-10和GLO1的表达变化;用慢病毒包装的RNA构建IL-10的RNA干扰模型（IL-10-SH-LV）评估IL-10和GLO1在脊髓损伤后的功能,GeneMANIA生物信息学预测IL-10和GLO1的关系。 结果　SCC后大鼠双后肢截瘫,后肢运动功能消失,BBB评分在损伤后1 d,3 d,7 d,14 d逐渐恢复,但低于对照组。qRT-PCR结果显示IL-10在脊髓损伤后表达显著降低;SCC后,免疫组织化学结果显示IL-10主要在脊髓前角的神经元和神经胶质细胞中表达。慢病毒干扰IL-10的表达后,随着时间推移,GLO1表达增加,大鼠运动功能BBB评分也逐渐恢复。GeneMANIA结果显示GLO1和IL-10通过共表达的Hpd和Klk1c2、Kcns1、Proc相互作用。 结论　IL-10通过上调抗氧化应激因子GLO1的表达促进脊髓损伤大鼠运动功能恢复。     

原位胶原凝胶对大鼠脊髓损伤后功能恢复的影响

目的研究脊髓损伤后原位形成胶原凝胶对神经功能恢复的影响。方法15只健康雌性SD大鼠随机分为胶原组、对照组和假手术组．Allen撞击法制作脊髓损伤模型。用微量注射器将胶原溶液注入损伤部位,在体温作用下让其原位形成凝胶,对照组注入PBS溶液,每周进行运动评分,6周后取脊髓组织进行免疫荧光染色,观察损伤部位的胶质瘢痕和轴突生长情况。结果胶原组大鼠第5周起BBB评分显著高于对照组,免疫荧光显示损伤部位胶质瘢痕少于对照组,且长入损伤部位的轴突也多于对照组。结论原位形成的胶原凝胶能抑制损伤部位胶质瘢痕的形成,并能促进轴突再生长入损伤部位。证明胶原是一种较好的能用于修复脊髓损伤的可注射材料。     

Metallothionein-II improves motor function recovery and increases spared tissue after spinal cord injury in rats

After spinal cord injury (SCI), a complex cascade of pathophysiological processes rapidly damages the nervous tissue. The initial damage spreads to the surrounding tissue by different mechanisms, including oxidative stress. We have recently reported that the induction of metallothionein (MT) protein is an endogenous rapid-response mechanism after SCI. Since the participation of MT in neuroprotective processes after SCI is still unknown, the aim of the present study was to evaluate the possible neuroprotective effect of exogenously administered MT-II during the acute phase after SCI in rats. Female Wistar rats weighing 200-250g were submitted to spinal cord contusion by means of a computer-controlled device (NYU impactor). Rats received several doses of MT-II (3.2, 10 and 100μg) at 2 and 8h after SCI. Results of the BBB scale were statistically analysed using an ANOVA of repeated-measures, followed by Tukey's test. Among the three doses tested, only 10 and 100μg were able to significantly increase (p<0.05) BBB scale scores eight weeks after SCI from a mean of 7.88 in the control group, to means of 12.63 and 10.88 for the 10 and 100μg doses of MT-II, respectively. The amount of spared tissue was also higher in the groups treated with 10 and 100μg, as compared to the control group values. Results from the present study demonstrate a significant neuroprotective effect of exogenously administered MT-II. Further studies are needed in order to characterize the mechanisms involved in this neuroprotective action.     

缺血预处理快速效应对兔急性缺血脊髓的保护作用

目的:探讨缺血预处理快速相对兔腹主动脉短暂阻断致缺血脊髓的保护作用。方法:36只雄性新西兰兔随机分成3组(n=12):即缺血再灌注损伤组(IR组)、缺血预处理组(IPC+IR组)及假手术组(Sham组)。IR组阻闭兔腹主动脉肾下段20min,复制兔脊髓缺血损伤模型;IPC+IR组预先阻闭腹主动脉肾下段6min,再灌注30min后再次阻闭腹主动脉肾下段20min;Sham组除不夹闭腹主动脉外,其余处理同IR组。再灌注后8h、12h、24h和48h分别对动物神经功能评分,然后,处死动物取脊髓(L_5-7),分别行组织病理学观察及测定脊髓组织中Na⁺,K⁺-ATP酶的活性。结果:Sham组及IPC+IR组神经功能评分各时点均明显高于IR组(P＜0.01);Sham组及IPC+IR组脊髓前角正常神经细胞数明显多于IR组(P＜0.01);Sham组及IPC+IR组脊髓组织中Na⁺,K⁺-ATP酶的活性明显高于IR组(P＜0.01)。结论:缺血预处理快速相对兔急性缺血脊髓有显著的保护作用,这种保护作用可能与稳定Na⁺,K⁺-ATP酶的活性有关。     

A new model of severe neurogenic pulmonary edema in spinal cord injured rat

We describe a new model of neurogenic pulmonary edema in spinal cord injured Wistar male rats. The pulmonary edema was elicited by an epidural thoracic balloon compression spinal cord lesion, performed under a low concentration of isoflurane (1.5 or 2%) in air. Anesthesia with 1.5% isoflurane promoted very severe interstitial and intraalveolar neurogenic pulmonary edema with a significantly increased thickness of the alveolar walls and massive pulmonary hemorrhage. In this group, 33% of animals died. Anesthesia with 2% isoflurane promoted severe interstitial and intraalveolar neurogenic pulmonary edema with less thickening of the alveolar walls and pulmonary hemorrhage. For evoking severe neurogenic pulmonary edema in spinal cord injured rats, 2% isoflurane anesthesia would be more suitable. However, if very severe neurogenic pulmonary edema needs to be evoked, spinal cord injury under 1.5% isoflurane anesthesia could be used, but one-third of the animals will be lost.     

Implications of immunotherapy with high-dose glatiramer acetate in acute phase of spinal cord injury in rats

Objective: Recently, many researches with different viewpoints have focused on application of immunotherapy agents in treatment of spinal cord injury (SCI) according to neuroprotective results in some neurodegenerative disease. Glatiramer acetate (GA) is the most commonly used drug for Multiple sclerosis (MS) patients that exerts an immunomodulatory effect against Myelin basic protein (MBP) antigen.

Materials and methods: High-dose (2mg/kg) treatment of GA for 28 consecutive days after SCI was compared with its low-dose (0.5?mg/kg) treatment, SCI control and Sham control rat groups.

Results: High-dose GA group had significantly worsened outcome in standard functional recovery evaluation test (BBB) 12 weeks after SCI compared to SCI control and low-dose GA groups, which was confirmed by augmented spinal cavity volume and reduced ventral horn motor neurons in high-dose GA group; however, there was no significant difference between low-dose GA and control SCI group. In addition, proliferation test performed on lymphocytes from spleen and lymph nodes one week after SCI showed that high-dose GA injection has more significant effect on Division Index (DI) in response to MBP stimulation compared to low-dose GA and control SCI groups, which was associated with significant increase in IFN-γ, IL-4, and IL-17A secretion.

Conclusion: Along with confirmation of deleterious aspects of autoimmunity resulting from autoreactive lymphocytes against myelin antigens in SCI, this study has shown that high-dose immunotherapy using GA, especially in acute phase after SCI, overwhelms any neuroprotective effect of adoptive immune system.