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目的 探讨黏附分子CD44在实验性自身免疫性脑脊髓炎（EAE）发病中的作用。方法 将20只大鼠随机分为正常对照组及EAE组,EAE组采用粗制髓鞘碱性蛋白（MBP）抗原注入大鼠后足掌皮下（0.2 ml/100 g）制作EAE模型,观察大鼠的发病情况及病理表现;并采用免疫组织化学法检测两组大鼠脑组织CD44的含量。结果 正常对照组大鼠未发病,EAE组大鼠均有不同程度的发病。HE染色后,光镜下观察,正常对照组大鼠脑和脊髓无异常;EAE组大鼠可见脑及脊髓实质内小血管充血,小静脉周围有大量炎性细胞浸润,血管周围白质脱髓鞘改变。免疫组化显示,正常对照组大鼠脑和脊髓组织未发现CD44阳性细胞;EAE组大鼠中枢神经系统（CNS）白质及灰白质交界处可见大量CD44阳性细胞。结论 EAE模型中存在黏附分子CD44的高表达,其对EAE的发病可能起到促进作用。 相似文献
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目的探讨黏附分子CD44在实验性自身免疫性脑脊髓炎(EAE)发病中的作用。方法将20只大鼠随机分为正常对照组及EAE组,EAE组采用粗制髓鞘碱性蛋白(MBP)抗原注入大鼠后足掌皮下(0. 2 ml/100 g)制作EAE模型,观察大鼠的发病情况及病理表现;并采用免疫组织化学法检测两组大鼠脑组织CD44的含量。结果正常对照组大鼠未发病,EAE组大鼠均有不同程度的发病。HE染色后,光镜下观察,正常对照组大鼠脑和脊髓无异常; EAE组大鼠可见脑及脊髓实质内小血管充血,小静脉周围有大量炎性细胞浸润,血管周围白质脱髓鞘改变。免疫组化显示,正常对照组大鼠脑和脊髓组织未发现CD44阳性细胞; EAE组大鼠中枢神经系统(CNS)白质及灰白质交界处可见大量CD44阳性细胞。结论 EAE模型中存在黏附分子CD44的高表达,其对EAE的发病可能起到促进作用。 相似文献
3.
目的 探讨RRx-001对实验性自身免疫性神经炎（EAN）的保护作用及机制的影响。方法 采用人工合成P253～78肽段与完全弗氏佐剂混合免疫Lewis大鼠建立EAN模型，RRx-001腹腔注射给药。实验分为3组：对照组、模型组和实验组。通过检测大鼠体重和临床评分，评估病情进展。采用透射电镜观察坐骨神经脱髓鞘变化。检测血液异硫氰酸荧光素―右旋糖酐，评估肠道屏障通透性。检测肠道一氧化氮（NO）、谷胱甘肽（GSH）和超氧化物歧化酶（SOD），评估氧化应激水平。采用ELISA试剂盒检测白细胞介素（IL）-1β、IL-18和肿瘤坏死因子α（TNF-α）表达情况。采用流式细胞术分析CD3+ T细胞、CD3+CD4+ T细胞、CD3+CD8+ T细胞、CD4+CD44H+ T细胞、CD4+CD62L+ T细胞和CD11b+F4/80+巨噬细胞。结果 与模型组相比，RRx-001可以减少EAN大鼠体重丢失、降低临床评分（P<0.05）；缓解坐骨神经脱髓鞘；提高SOD活力，降低IL-1β和TNF-α表达水平，减轻肠道损伤而改善肠通透性（P<0.001）；降低CD4+ T/CD8+ T淋巴细胞和CD11b+F4/80+ 巨噬细胞比例，提升CD3+ T淋巴细胞的比例（P<0.05）。结论 RRx-001可以改善EAN大鼠临床症状，其机制可能与调节免疫细胞活化和抑制炎症因子释放有关，发挥对EAN大鼠的保护作用。国际神经病学神经外科学杂志, 2023, 50(6): 1-6] 相似文献
4.
目的 探讨白藜芦醇(RSV)对血管性痴呆(VD)大鼠认知功能的影响及其对沉默调节蛋白1(SIRT1)／叉头框转录因子O3a(FoxO3a)通路的影响。方法 清洁级健康雄性Sprague-Dawley大鼠40只随机分为4个组：假手术组、VD模型组、RSV低剂量(30 mg/kg)治疗组和RSV高剂量(60 mg/kg)治疗组,每组10只。采用双侧颈总动脉永久结扎术(BCCAO)制备VD大鼠模型,假手术组大鼠仅分离出双侧颈总动脉、套缝线,但不结扎。治疗组大鼠灌胃给予相应剂量RSV进行药物干预,假手术组和VD模型组给予等体积羧甲基纤维素钠溶液。采用Morris水迷宫检测各组大鼠的空间学习及记忆能力;HE染色观察各组大鼠海马CA1区神经元的病理改变及TUNEL染色观察各组大鼠海马CA1区神经元的凋亡情况;采用Western blotting方法检测各组大鼠海马组织中SIRT1、FoxO3a、B细胞淋巴瘤2(Bcl-2)、Bcl-2相关X蛋白(Bax)、微管相关蛋白1轻链3(LC3)、Beclin1蛋白的表达情况。结果 与假手术组大鼠相比,VD模型组大鼠逃避潜伏期延长(P<0.05);目标象限停留时间百分比降低(P<0.05);海马CA1区神经元病理性损害严重,凋亡神经元增多(P<0.05);SIRT1、FoxO3a、Bcl-2、Beclin1蛋白表达降低(P<0.05);Bax蛋白表达增加(P<0.05);Bcl-2/Bax、LC3Ⅱ/Ⅰ比值降低(P<0.05)。与VD模型组大鼠相比,RSV治疗组的逃避潜伏期缩短(P<0.05);目标象限停留时间的百分比有所升高(P<0.05);神经元病理性损害有所减轻,凋亡情况有所改善(P<0.05);SIRT1、FoxO3a、Bcl-2、Beclin1蛋白表达升高(P<0.05);Bax蛋白表达降低(P<0.05);Bcl-2/Bax、LC3Ⅱ/Ⅰ比值升高(P<0.05)。上述各项指标在RSV高、低剂量组间比较,差异无统计学意义(P>0.05)。结论 RSV能够改善VD大鼠的认知功能,减轻海马神经元凋亡,并激活自噬,发挥神经保护作用,其机制可能与激活SIRT1/FoxO3a通路有关。 相似文献
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目的 探讨褪黑素（melatonin,MT）在1-甲基-4-苯基-吡啶离子（1-methyl-4-phenylpyridinium ion,MPP+）诱导的帕金森病体外模型中的作用及分子机制。方法 将MN9D细胞分为对照组、MPP+组、MT组、治疗组。采用细胞计数试剂盒8检测MT和MPP+对细胞活力的影响;采用线粒体膜电位检测试剂盒（JC-1）评价线粒体功能;Hoechst/PI双染法检测细胞凋亡;通过免疫荧光蛋白质印迹法（Western blotting）检测凋亡相关蛋白［Cleaved-Caspase 3和细胞色素C（cytochrome C,CytC）］以及泛醌―细胞色素C还原酶核心蛋白1（ubiquinol-cytochrome C reductase core protein 1,UQCRC1）蛋白的表达;采用干扰RNA技术沉默MN9D细胞中UQCRC1的表达,然后采用Western blotting检测凋亡相关蛋白表达。结果 MT可以减轻MPP+诱导的细胞活力下降（P<0.05）;恢复MPP+造成的线粒体膜电位下降（P<0.05）;减少MPP+诱导的凋亡细胞数量（P<0.05）;抑制凋亡蛋白（CytC和Cleaved-Caspase3）的表达（P<0.05）;上调UQCRC1的表达（P<0.05）。沉默UQCRC1后,MT组和治疗组的UQCRC1表达均下降（P<0.05）;MT对MPP+诱导细胞凋亡的保护作用下降（P<0.05）;凋亡蛋白（CytC和Cleaved-Caspase3）的表达增加（P<0.05）。结论 MT对 MPP+诱导的多巴胺能神经元损伤具有保护作用,其机制可能是通过上调UQCRC1抑制神经元凋亡。 [国际神经病学神经外科学杂志, 2023, 50(3): 26-31] 相似文献
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目的 对CD58在胶质瘤中的表达及意义做初步研究。方法 从癌症基因组图谱（TCGA）数据库中获取胶质瘤相关样本的基因测序结果及临床信息,分析胶质母细胞瘤（GBM）组、低级别胶质瘤（LGG）组和非瘤脑组织（Non-tumor）组中CD58的表达差异及生存预后相关性,构建预后模型分析CD58表达与危险度评分关系及CD58高表达组和低表达组的总生存期差异,采用多变量Cox回归分析CD58表达对预后的影响;将40例临床样本分为三组：非瘤脑组织（Non-tumor）组,I、Ⅱ级胶质瘤为低级别胶质瘤（LGG）组,Ⅲ、Ⅳ级胶质瘤为高级别胶质瘤（HGG）组,运用免疫组织化学（免疫组化）检测三组中CD58的表达,并分析各组之间的表达差异。结果 表达差异分析显示,GBM组、LGG组和Non-tumor组的CD58表达依次降低（均P＜0.05）;危险度评分与CD58表达正相关,表达越高患者生存期越短（P＜0.05）;多变量Cox回归分析显示CD58表达水平是影响胶质瘤预后的因素,表达水平越高,死亡风险越大;免疫组化结果显示CD58阳性反应物位于细胞胞膜,HGG组阳性细胞数高于LGG组和Non-tumor组（均P＜0.05）,但三组的阳性例数无差别。结论 CD58在高级别胶质瘤中的表达高于低级别胶质瘤和非瘤脑组织,其表达差异与胶质瘤生存期相关,CD58高表达是胶质瘤预后的危险因素。CD58可以作为判定胶质瘤的恶性程度及预后的一项指标。
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目的 探讨重复经颅磁刺激（repetitive transcranial magnetic stimulation,rTMS）通过调控DJ-1的表达,使小鼠缺血性脑损伤后的神经功能缺损得到恢复的机制。方法 选取8~12周健康雄性C57BL/6J小鼠30只,随机分为3组：假手术组（Sham组）、缺血再灌注组（MCAO组）和治疗组（rTMS组）,每组10只。MCAO组使用线栓法制备大脑中动脉闭塞（middle cerebral artery occlusion,MCAO）小鼠模型,Sham组小鼠处理同MCAO组但不插入线栓。Sham组和rTMS组给予rTMS治疗,MCAO组不予治疗。造模后1 h拔出线栓进行再灌注,再灌注24 h后开始给予 rTMS 治疗,频率为1 Hz,每次持续25 s,每日5 次,连续治疗7 d。在治疗前后对各组小鼠进行神经功能缺损评分;使用TTC染色确定各组小鼠脑组织梗死灶面积;并采用免疫组化技术检测梗死灶周围区域神经元中DJ-1表达变化;使用免疫印迹技术检测DJ-1的蛋白水平表达变化。结果 与Sham组（0.50±0.53）比较,MCAO组（2.80±0.63）和rTMS组（2.10±0.32）的神经功能缺损评分显著增高（P<0.05）;与MCAO组比较,rTMS组的神经功能缺损评分显著降低（P<0.05）。与MCAO组比较,rTMS组的梗死灶面积明显减小,DJ-1表达显著提高（P<0.01）。结论 rTMS可有效促进缺血性脑损伤的小鼠神经功能恢复,并显著减少梗死灶面积,可能分子机制是通过上调神经DJ-1蛋白表达干预损伤预后。国际神经病学神经外科学杂志, XXXX, XX(XX): 1-5] 相似文献
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目的 探索丙氨酰―谷氨酰胺配合高压氧治疗对中青年缺血性脑卒中患者恢复期外周血T淋巴亚群及微小RNA-124(miR-124)、miR-181c的影响。方法 选取2017年7月至2021年7月该院128例中青年缺血性脑卒中恢复期患者作为研究对象，依据随机数字表法分为4组：阴性对照组、对照A组、对照B组、观察组，每组32例。阴性对照组予以脑卒中恢复期常规治疗；在此基础上，对照A组予以丙氨酰―谷氨酰胺治疗；对照B组予以高压氧治疗；观察组予以丙氨酰―谷氨酰胺配合高压氧治疗，均连续治疗4周。比较4组治疗前、治疗2周后、4周后神经功能［美国国立卫生研究院卒中量表(NIHSS)评分］、日常生活能力［Barthel指数(BI)］、肢体运动功能［Fugl-Meyer 运动功能评分量表(FMA)评分］、炎症因子［肿瘤坏死因子-α(TNF-α)、单核细胞趋化蛋白-1(MCP-1)、白细胞介素12(IL-12)］、外周血T淋巴亚群（CD4+、CD8+、CD4+/CD8+）、脑血流动力学［颈动脉最小血流速度(Vmin)、最小血流量(Qmin)］、miR-124、miR-181c表达。结果 观察组治疗2周后、4周后NIHSS评分低于对照A组、对照B组和阴性对照组(P<0.05)；BI指数高于对照A组、对照B组和阴性对照组(P<0.05)；上、下肢肢体运动功能评分高于对照A组、对照B组和阴性对照组(P<0.05)。观察组治疗2周后、4周后血清TNF-α、MCP-1、IL-12水平低于对照A组、对照B组和阴性对照组(P<0.05)；CD4+、CD4+/CD8+水平高于对照A组、对照B组和阴性对照组；CD8+低于对照A组、对照B组和阴性对照组(P<0.05)。治疗2周后、4周后对照A组CD4+、CD4+/CD8+高于对照B组和阴性对照组(P<0.05)；CD8+低于对照B组和阴性对照组(P<0.05)。 观察组治疗2周后、4周后Vmin、Qmin高于对照A组、对照B组和阴性对照组(P<0.05)，且对照B组Vmin、Qmin高于对照A组和阴性对照组(P<0.05)。观察组治疗2周后、4周后miR-124、miR-181c表达低于对照A组、对照B组和阴性对照组(P<0.05)。结论 丙氨酰―谷氨酰胺配合高压氧治疗能进一步改善恢复期中青年缺血性脑卒中患者细胞免疫功能，下调miR-124、miR-181c表达水平，改善患者神经功能及日常生活能力。 相似文献
9.
目的 探讨初发脑梗死患者与复发脑梗死患者在氯吡格雷治疗后,血小板膜糖蛋白CD62p、CD63及血栓弹力图指标变化特点及其临床意义。方法 纳入2019年7月至2021年1月在该院住院的急性缺血性脑卒中患者103例,分为复发脑梗死组（43例）和初发脑梗死组（60例）。入院后服用氯吡格雷(75 mg/d),服药后第8天采用流式细胞术测定患者血浆中血小板膜糖蛋白CD62p和CD63表达率,并行血栓弹力图(TEG)检测,包括血小板ADP抑制率(%)、血细胞凝集块形成时间(K)、凝血反应时间(R)、血细胞凝集块形成速率(α角)和血凝块最大硬度或强度(MA)等指标,分析TEG各参数与CD62P、CD63表达率特点及其相关性。结果 初发组和复发组治疗后血小板糖蛋白CD62p、CD63表达阳性率较治疗前均下降,差异具有统计学意义(P<0.05)。与初发组相比,复发组治疗后CD62p、CD63的表达阳性率下降幅度更小,差异具有统计学意义(P<0.05)。与初发组相比,复发组治疗后第8天检测血小板ADP抑制率更低、K值更短、MA更高,差异具有统计学意义(P<0.05)。初发组与复发组治疗第8天TEG检测中凝血反应时间R与CD63表达阳性率均呈负相关;CD62p表达阳性率与ADP抑制率均呈负相关。复发组ADP抑制率与CD63表达阳性率呈负相关。结论 复发性脑梗死患者在氯吡格雷治疗后具有更高的血小板反应性、血小板活性和血凝状态,CD62p、CD63联合血栓弹力图指标检测有一定的临床意义。引用格式:471-475.] 相似文献
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目的 探讨虚拟现实（VR）技术结合肢体协调辅助装置训练对缺血性脑卒中患者脑灰质含量、运动功能、认知功能和日常生活能力的影响。方法 选取2022年2月至2023年1月合肥市第二人民医院收治的122例缺血性脑卒中患者作为研究对象，按照随机数字表法分为对照组（61例）和观察组（61例），其中对照组患者采取肢体协调辅助装置训练，观察组采取VR结合肢体协调辅助装置训练，治疗周期为2个月。对比治疗前后2组患者睁眼1 min轨迹面积、睁眼1 min摆动长度、上下肢运动功能、神经功能、认知功能和日常生活能力。结果 治疗后2组的睁眼1 min轨迹面积、睁眼1 min摆动长度均较治疗前显著减少（P<0.05），且观察组的轨迹面积和摆动长度均小于对照组（P<0.05）。治疗后2组的上下肢运动评分、脑灰质含量、蒙特利尔认知评估量表（MoCA）评分和日常生活能力均较治疗前显著提高（P<0.05），且观察组的这些指标水平均高于对照组（P<0.05）。治疗后神经功能评分均较治疗前显著降低（P<0.05），且观察组的该评分低于对照组（P<0.05）。结论 VR结合肢体协调辅助装置训练可有效促进缺血性脑卒中患者平衡功能的恢复，提高患者肢体运动功能，改善患者神经功能、认知功能和日常生活能力。 [国际神经病学神经外科学杂志, 2023, 50(6): 19-23] 相似文献
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Claude Steriade Jeffrey Britton Russell C. Dale Avi Gadoth Sarosh R. Irani Jenny Linnoila Andrew McKeon Xiao-Qiu Shao Viviana Venegas Christian G. Bien 《Epilepsia》2020,61(7):1341-1351
Seizures are a well-recognized and often prominent manifestation of autoimmune encephalitic syndromes. Progress in detection of pathogenic neural autoantibodies has led to increased awareness of autoimmune causes of seizures. Clinical studies of patients with these autoantibodies have improved our understanding of the seizure characteristics, treatments, and seizure prognosis in these disorders. The International League Against Epilepsy (ILAE) Autoimmunity and Inflammation Taskforce proposes conceptual definitions for two main diagnostic entities: (a) acute symptomatic seizures secondary to autoimmune encephalitis, and (b) autoimmune-associated epilepsy, the latter of which suggests an enduring predisposition to seizures. Such a distinction is relevant when discussing the pathophysiology, treatment, prognosis, and social consequences of these disorders. We discuss the role of biomarkers in the application of these conceptual definitions and illustrate their use in patients cared for by members of the task force. 相似文献
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Seizures resulting from cerebral autoimmunity are either acutely symptomatic in the context of autoimmune encephalitis (AIE) with neural surface antibodies, or they are indicative of an enduring predisposition to seizures, that is, epilepsy. Here, we propose a practical definition for autoimmune encephalitis-associated epilepsy (AEAE): Seizures associated with antibodies against glutamic acid decarboxylase, paraneoplastic syndromes, or Rasmussen encephalitis are classified as AEAE. AEAE secondary to AIE with antibodies against the N-methyl-D-aspartate receptor, leucine-rich glioma inactivated protein 1, contactin-associated protein-2, or γ-aminobutyric acid-B receptor can be diagnosed if the following criteria are met: seizures persist for at least 2 years after immunotherapy initiation; no signs of encephalitis on magnetic resonance imaging and no fluorodeoxyglucose positron emission tomography hypermetabolism; normal cerebrospinal fluid cell count; and a substantial decrease in antibody titers. This classification corresponds to different disease mechanisms. While AIE results from the pathogenic effects of neural antibodies, AEAE is probably the consequence of encephalitis-related tissue damage and thereby mainly structurally mediated. The distinction between AIE and AEAE also has practical consequences: In AIE, immunotherapy is usually highly beneficial, whereas anti-seizure medication has little effect. In AEAE, immunotherapy is less promising and the usual anti-seizure interventions are preferable. In addition, the diagnosis of AEAE has social consequences in terms of driving and professional limitations. 相似文献
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Experimental autoimmune encephalomyelitis (EAE) is an inflammatory disease of the central nervous system (CNS) that is mediated by T helper 1 (Th1) CD4+ T cells. Lewis rats can be protected from actively induced EAE by coimmunization with the encephalitogenic myelin basic protein (MBP) epitope 73–84 and its single alanine-substituted analog 1028. Although analog 1028 cannot induce either active or passive EAE, it does elicit a Th1-like response that is cross-reactive with MBP73–84. Analog 1028 can effectively inhibit clinical EAE in a dose-dependent manner when rats are coimmunized with the encephalitogenic peptide MBP73–84 and 1028 in complete Freund adjuvant (CFA). Stimulation of cells from MBP73–84:1028—coimmunized protected rats proliferate and secrete interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) in vitro in response to MBP73–84. Furthermore, coimmunized protected rats harbor a population of MBP73–84—reactive potentially encephalitogenic T cells, because splenocytes from these rats can be stimulated to transfer passive EAE to naive recipients. Thus, the protection of coimmunized rats by analog 1028 is not due to the inhibition of priming of MBP73–84—reactive T cells or alteration of the cytokine secretion profile of the MBP73–84—reactive cell population. Rather, MBP73–84—reactive potentially encephalitogenic T cells are primed in these protected animals. © 1996 Wiley-Liss, Inc. 相似文献
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A case of post‐leptospirosis autoimmune epilepsy presenting with sleep‐related hypermotor seizures 
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下载免费PDF全文 Prashant Makhija Siby Gopinath Sudheeran Kannoth Kurupath Radhakrishnan 《Epileptic Disord》2017,19(4):456-460
This video‐illustrated case report concerns a 49‐year‐old woman who presented with sleep‐related hypermotor seizures. The antecedent history of leptospirosis, high frequency of new‐onset seizures, presence of an unclassified anti‐neuronal antibody, and dramatic response to steroids strongly supported post‐infectious immune‐mediated pathogenesis in our patient. To the best of our knowledge, post‐leptospirosis autoimmune epilepsy presenting as sleep‐related hypermotor seizures has not hitherto been reported. [Published with video sequence on www.epilepticdisorders.com ]. 相似文献
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C. Ioppoli G. Meucci S. Mariotti E. Martino A. Lippi L. Gironelli A. Pinchera A. Muratorio 《The Italian Journal of Neurological Sciences》1990,11(1):31-36
Multiple sclerosis (MS) is associated with complex abnormalities of immunore-gulation and a role of autoimmunity in its pathogenesis
has been accepted. MS is reportedly associated with several autoimmune diseases, but few studies are available on the prevalence
of organ-specific autoantibodies in this condition. The aim of this study was to assess the frequency of anti-thyroglobulin
(TgAb), anti-thyroid microsomal (MAb) and gastric parietal cell (PCA) antibodies in 113 patients (63 females, 50 males, age
ranging 15–62 years) with MS and in 51 neurological controls. The diagnosis of MS was made according to McDonald and Halliday
criteria. TgAb and/or MAb were detected by passive hemagglutination in 19 (16.8%) patients with MS and in 3 (5.9%) of the
controls. All positive TgAb and/or MAb were observed in MS females (19/63=30.1%), with significantly higher frequency than
in female controls (X2=5.15, p<0.025). The presence of circulating thyroid antibodies was higher in patients with clinically definite or progressive
probable MS and in those with long standing disease. In contrast with thyroid antibodies, no difference in the frequency of
PCA, as assessed by radioimmunoassay, was observed between MS and controls. These data support a specific association between
thyroid autoimmunity and MS. The appearance of thyroid autoimmune phenomena seems to be related to the reliability of the
diagnosis of MS and the duration of the disease.
Sommario La Sclerosi Multipla (MS) è associata a complesse alterazioni della immunoregolazione e nella sua patogenesi è stato accettato l'intervento di meccanismi autoimmunitari. Sono state anche riportate associazioni tra MS e numerose malattie autoimmuni, ma pochi sono i dati relativi alla presenza di autoanticorpi organospecifici nella MS. Con questo studio è stata verificata l'incidenza di anticorpi anti-Tireoglobulina (TgAb), anti-microsomi di tiroide (MAb) e anti-cellule parietali gastriche (PCA) in 113 casi con MS (63 femmine e 50 maschi, di età compresa fra 15 e 62 anni) e in 51 controlli neurologici. I criteri per la diagnosi di MS erano quelli di McDonald e Halliday. Con la metodica dell'emoagglutinazione passiva sono stati rilevati TgAb e/o MAb in 19 (16.8%) pazienti con MS e in 3 (5.9%) controlli. Tutte le positività anticorpali sono state osservate nei soggetti con MS di sesso femminile (19/63=30.1%), con un'incidenza significativamente maggiore rispetto ai soggetti di controllo di sesso femminile (X2=5.15; p<0.025). Gli anticorpi antitiroide circolanti sono stati rilevati con maggior frequenza nei pazienti con MS clinicamente definita o progressiva probabile, e in quelli con maggiore durata di malattia. Nessuna differenza tra i casi di MS e i controlli è stata osservata per l'incidenza di PCA, dosati con metodica RIA. Questi dati confermano una specifica associazione tra autoimmunità tiroidea e MS. La comparsa di fenomeni autoimmuni tiroidei sembra in relazione con il grado di certezza diagnostica della MS e con la durata di malattia.相似文献
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Variation in experimental autoimmune encephalomyelitis scores in a mouse model of multiple sclerosis
Multiple sclerosis (MS) is a common demyelinating central nervous system disease associated with progressive physical impairment. To study the mechanism underlying disease pathogenesis and develop potential treatments, experimental autoimmune encephalomyelitis (EAE) is often used as an animal model. EAE can be induced in various species by introducing specific antigens, which ultimately result in motor dysfunction. Although the severity of the paralysis is indicated using the EAE score, there is no standard scoring system for EAE signs, and there is variability between research groups with regard to the exact EAE scoring system utilized. Here, we describe the criteria used for EAE scoring systems in various laboratories and suggest combining EAE score with another quantitative index to evaluate paralysis, such as the traveled distance, with the goal of facilitating the study of the mechanisms and treatment of MS. 相似文献