Lubeluzole对大鼠脑缺血再灌流时神经元的保护作用

目的 为了观察lubeluzole对大鼠脑缺血再灌流时神经元的保护作用。方法 本实验采用阻塞SD大鼠大脑中动脉2h，再灌流1、3、6、12、24、48h制成局灶性脑缺血动物模型，用免疫组化方法观察给药前后神经生长因子、脑源性神经营养因子在神经元的表达特点。结果 神经生长因子、脑源性神经营养因子在脑组织的分布相似。正常组和假手术组的皮质、丘脑等处的神经元为阴性；缺血模型组的缺血区皮质、丘脑的神经元为阴性或弱阳性，阳性神经元主要位于非大脑中动脉供血区和缺血周边区；治疗组缺血区的皮质、丘脑等处的神经元为弱阳性至中等阳性，缺血周边区为强阳性。结论 在缺血后6h内使用lubeluzole能降低神经元受损伤的程度，促进神经元的生长。     

c-fos和神经营养因子在大鼠脑缺血再灌流时的神经元表达特点

为了观察脑缺血再灌流时 c-fos和神经营养因子在神经元表达的时空特点 ,探讨其在缺血性神经元损伤中的作用 ,本研究用阻塞 SD大鼠大脑中动脉 2 h、再灌流 0 .5～ 48h制成局灶性脑缺血模型 ,用免疫组化方法观察了 c-fos和神经营养因子转化生长因子、神经生长因子和胶质源性神经营养因子在神经元的表达特点。结果表明 ,c-fos和转化生长因子分布相似 ,正常组无 c-fos和转化生长因子阳性神经元 ;缺血再灌流 0 .5～ 48h阳性的神经元主要位于非大脑中动脉供血区 ,缺血区皮质、纹状体和视前区神经元为阴性。而实验各组对照侧皮质神经元中等阳性。神经生长因子、胶质源性神经营养因子在缺血脑组织的分布相似。正常组、假性手术组 ,皮质、嗅结节、丘脑和下丘脑等区的神经元神经生长因子、胶质源性神经营养因子免疫反应为弱阳性乃至强阳性 ;再灌流 0 .5 h,缺血区皮质弱阳性 ,缺血周边区中等阳性 ;再灌流 3～ 48h,神经生长因子、胶质源性神经营养因子强阳性的神经元主要位于非大脑中动脉供血区和缺血周边区。此外 ,对照侧皮质大量的神经元呈强阳性。结论 ,上述资料提示即早基因 c-fos和神经营养因子具有促进神经元存活的作用     

大鼠脑缺血再灌流时即早基因c-fos在脑组织表达的免疫组织化学研究

为了研究 c-fos在大鼠缺血性脑损伤中的作用 ,本研究利用阻塞大鼠大脑中动脉 2 h后再灌流 0 .5～ 48h制成的局灶性脑缺血模型 ,用免疫组织化学技术观察了 c-fos的表达特点。结果证明 ,正常组、假性手术组 c-fos在神经元的表达呈阴性或弱阳性 ;再灌流 0 .5～ 48h组 ,胞核呈强阳性 ( +++)的神经元主要位于非大脑中动脉供血区 ,而缺血中心区的皮质、纹状体和视前区呈阴性 ( -)。缺血周边区 ,神经元胞核呈弱阳性 ( +)。正常组未发现 c-fos阳性的胶质细胞 ,假性手术组脑实质内胶质细胞团和侧脑室壁的胶质细胞 c-fos呈强阳性 ,再灌流 3h组脑室壁及深层的室管膜下区和皮质浅层、髓质等处胶质细胞为阳性 ,再灌流2 4～ 48h组缺血周边区和脑实质内的巨噬细胞、活化小胶质细胞呈强阳性 ;再灌流 48h组 ,白质如胼胝体内大量的反应性星形胶质细胞呈强阳性。本文结果提示 ,脑缺血时 c-fos对神经元具有神经保护作用 ,并且这种保护作用可能与小胶质细胞和星形胶质细胞的活化有关     

大鼠局灶性脑缺血MAP2表达及毛冬青黄酮的保护作用

目的：探讨大鼠局灶性脑缺血神经细胞MAP2表达，研究毛冬青黄酮对脑缺血的保护作用：方法：选用颈外动脉插入线栓法制备大鼠大脑中动脉梗塞模型，加只雄性Wistar大鼠，随机分成正常对照组、假手术组、盐水-缺血3h、6h、24h组，毛冬青黄酮-缺血3h、6h、24h组。本研究以MAP2染色为指标，评价大鼠局灶性脑缺血损伤情况以及毛冬青黄酮对大鼠局灶性脑缺血MAP2表达的影响。MAP2在大鼠神经元中表达丰富，对兴奋性氨基酸、生长因子等反应敏感，是细胞内信号传导的重要环节，参与经元的生长和损伤后修复过程。MAP2对缺血敏感，可显示缺血时神经元损伤情况。     

针刺对局灶性脑缺血模型大鼠神经元的保护作用

目的：研究探讨针刺对局灶性脑缺血模型大鼠神经元的保护作用。方法：应用栓线法栓塞大鼠大脑中动脉（MCAO）造成局灶性脑缺血模型，分为三组：假手术对照组、模型组、电针组。观察电针对局灶性脑缺血大鼠神经体征的促恢复作用，电针对局灶性脑缺血大鼠海马CAI段神经元的影响，采用免疫组织化学法检测局灶性脑缺血大鼠神经元凋亡相关基因bcl-2、bax蛋白的表达。     

线栓法制备SD大鼠局灶性脑缺血再灌注损伤模型

背景：线栓法制备大鼠局灶性脑缺血再灌注损伤模型的方法尚无统一标准,寻找一种操作简单,稳定性好,成功率高的局灶性脑缺血再灌注模型方法在缺血性脑病研究中有重要意义。 目的：采用线栓法制备SD大鼠局灶性脑缺血再灌注损伤模型,分析模型制作的成功率和稳定性。 方法：对传统Zea Longa模型制作方法进行改进,选用鱼线作为栓线,结扎颈外动脉及颈总动脉近心端,不剪断颈外动脉,不结扎翼腭动脉,栓线通过颈总动脉进入大脑中动脉造成缺血,拔出线栓形成再灌注。 结果与结论：建模型时间均在20 min内完成,建模后大鼠神经功能缺损明显,红四氮唑染色示脑梗死区苍白,病理学检查有典型的病理表现,模型成功率为75%,在制作过程中易出现蛛网膜下腔出血、脑缺血不完全等问题。结果表明,线栓法制备SD大鼠局灶性脑缺血再灌注损伤模型的方法成功率高,缺血效果明确,时间短,是一种简单方便的制作局灶性脑缺血再灌注损伤模型的方法。     

对微球囊栓塞大脑中动脉制作猕猴局灶性脑缺血再灌注模型的评价

目的 建立一种理想的猕猴局灶性脑缺血再灌注模型. 方法 成年健康猕猴12只(雌雄各半).经颈总动脉或股动脉介入手术,将标准微球囊导管插入大脑中动脉(MCA)的起始部,然后充盈微球囊阻断MCA血流,退出微球囊后实现MCA血流再灌注,建立大脑中动脉闭塞再灌注(MCAO/R)模型.通过脑血管造影、磁共振血管成像(MRA)、磁共振扫描成像(MRI)、氯化三苯基四氮唑(TIC)染色和神经行为功能评分对动物模型进行评价.结果 经颈总动脉或股动脉介入手术,可以在荧光屏直视下准确地将微球囊导管插入大MCA阻断其血流,MCA在MRA上不显像.MCA供血区磁共振T1、T2、DWI出现高信号区,TFC染色显示脑梗夕匕病灶,动物出现相应的神经功能障碍.该方法 成功率高、重复性好、操作简单. 结论 经股动脉微球囊导管介入手术建立猕猴MCAO/R模型是一种较为理想的方法 .     

大鼠脑缺血再灌流时神经元损伤与星形胶质细胞的反应

为探讨星形胶质细胞在缺血性神经元损伤中的作用及其与神经元损伤的关系 ,本实验阻塞大鼠大脑中动脉 2 h,再灌流0 .5～ 48h建立短暂局灶性脑缺血模型 ,进行 H-E染色 ;通过胶质原纤维酸性蛋白和细胞核增殖抗原免疫组化单重或双重反应 ,TU NEL和胶质原纤维酸性蛋白免疫组化双重反应观察了神经元和星形胶质细胞的反应。结果表明 :再灌流 2 4h缺血区面积最大 ,再灌流 6h开始出现神经元不可逆变性 ,2 4h梗塞成熟 ;星形胶质细胞表现为反应性、营养不良性和退形变三种不同的形态特点。再灌流 48h时星形胶质细胞数量开始增多。 48h之内星形胶质细胞无增生 ,且有少量星形胶质细胞凋亡。这些结果提示脑缺血时星形胶质细胞反应与神经元损伤密切相关 ,反应性星形胶质细胞是其积极应答神经元损伤的结果 ,在维持神经元存活中起作用。     

巴曲酶对脑缺血再灌注大鼠海马CA1区的影响

目的 通过观察大鼠局灶性脑缺血再灌注不同时段，巴曲酶对海马CAl神经元及星形胶质细胞数目、形态等方面的影响，从而探讨巴曲酶对局灶性脑缺血再灌注损伤的保护作用。方法 采用改良的线栓法制备大脑中动脉阻塞(MACO)2h、不同再灌注时间段(3h、6h、12h、24h、48h、72h、7d)的大鼠短暂局灶性脑缺血(transient focal cerebral isehemia)模型，随机设立巴曲酶组(Bat)、生理盐水对照组(N．S)、假手术组(sham-operated)，通过HE染色及胶质原纤维酸性蛋白(GFAP)和神经元特异核抗原(NeuN)的免疫组化染色，观测CAl区神经元和星形胶质细胞的形态、数目的动态变化。结果巴曲酶能显提高再灌注早期(6～24h)CAl区GFAP阳性细胞的数目，再灌注7d组存活锥体细胞的数量较盐水对照组有明显提高，提示局灶性脑缺血后早期反应性星形胶质细胞的增多对维持神经元的存活有积极意义，巴曲酶对短暂局灶性脑缺血再灌注引起的海马CAl区延迟性神经元坏死(DND)有一定的抑制作用。     

线栓法制作大鼠局灶性脑缺血再灌注模型的改进与探讨

目的提供一种比较简易的大鼠局灶性脑缺血／再灌注模型制备方法。方法应用SD雄性大鼠，线栓法制作局灶性脑缺血再灌注模型，选择在颈总动脉（CCA）分叉处切口，使线栓从CCA顺行进入颈内动脉（ICA）。造模后直接将栓线缝合在皮内，再灌注时拔出一定长度拴线，使栓线回至CCA即可。通过神经功能检测，红四氮唑（TTC）染色和病理学检查等方法评价该模型的可靠性。结果大鼠手术后神经功能缺损明显，TTC染色清楚显示了梗死病灶，病理学检查显示典型病理改变。结论该改良方法术式简便，缺血效果可靠，可以用于脑缺血再灌注的研究。     

Cerebral ganglioglioma

Summary The morphological characteristics of neurons revealed by Golgi's method are reported in a case of cerebral ganglioglioma.Spindle-shaped (leptodendritic) neurons and radiated type I neurons form the bulk of this tumour. According to Ramon-Moliner (1968) isodendritic neurons (both leptodendritic and radiate type I) are philogenetically primitive cells and differ greatly from those observed in most of the deep cerebral nuclei of the mammalian's brain.     

小儿颅脑疾病与头颅计算机断层成像术

目的 探讨头颅ＣＴ检查在小儿颅脑疾病诊断中的重要意义。方法 以３７０例头颅ＣＴ异常的非外伤性病变的患儿为研究对象,按疾病增将其归类、比较、分析,从中揭示其关系。结果 各类癫痫的主要ＣＴ改变是脑萎缩,脑软化次之;小儿颅脑肿瘤以幕下、中线部位多见,颅高压征出现象,定位体征少见,易于误诊;新生儿颅脑损伤发病率高,头颅ＣＴ检查得于新生儿缺氧缺血性脑病和新生儿颅内出血的诊断。结论 头颅ＣＴ是小儿颅脑疾病的首选检查方法,安的应用使颅脑疾病的诊断水平明显提高。     

Cerebral neuroblastoma

Summary A cerebral neuroblastoma removed surgically from a female child is presented. Electron microscopy showed numerous neuronal processes with growth cones which are a feature of the developing neurone. In addition there were some rosettes with distinct lumina. The luminal surfaces were covered with a smooth plasma membrane lacking any surface differentiation and the lateral surface of these cells had many cell junctions (terminal bars), reminiscent of a primitive neural tube. These features in a nerve cell tumor help to substantiate it as a neuroblastoma arising from immature rather than differentiated cells.The nature of this rare tumor is discussed.     

小儿颅脑疾病与头颅计算机断层成像术

目的探讨头颅CT检查在小儿颅脑疾病诊断中的重要意义.[ BF] 方法以370例头颅CT异常的非外伤性病变的患儿为研究对象,按疾病增将其归类、比较、分析,从中揭示其关系.结果各类癫痫的主要CT改变是脑萎缩,脑软化次之;小儿颅脑肿瘤以幕下、中线部位多见,颅高压征出现晚,定位体征少见,易于误诊;新生儿颅脑损伤发病率高,头颅CT检查利于新生儿缺氧缺血性脑病和新生儿颅内出血的诊断.结论头颅CT是小儿颅脑疾病的首选检查方法,它的应用使颅脑疾病的诊断水平明显提高.     

Cerebral vasospasm

Cerebral vasospasm (specifically, intracranial arterial spasm) is variously defined as: (1) an arteriographically evident narrowing of the lumen of one or more of the major intracranial arteries at the base of the brain due to contraction of the smooth muscle within the arterial wall, or due to the morphological changes in the arterial wall and along its endothelial surface that occur in response to vessel injury; (2) the delayed onset of a neurological deficit following subarachnoid hemorrhage, thought to be due to ischemia or infarction of a portion of the brain; or (3) the combination of these two features (symptomatic vasospasm). The arterial contraction of intracranial arterial spasm typically develops a few days after the rupture of an intracranial aneurysm and lasts 2 to 3 weeks. Such arterial spasm can also occur in other conditions such as head trauma. If it is severe enough it can lead to cerebral infarction. The pathogenesis of this condition is still unclear. Many ingenious attempts have been made to prevent or treat cerebral vasospasm, but most have failed. The best current approach is to ensure adequate blood volume, and to elevate the patient's blood pressure (especially if the aneurysm has been secured by an early operation). The continuing investigation of drugs such as calcium channel blocking agents to improve the cerebral circulation has begun to provide additional help.     

Cerebral malaria

Cerebral malaria is a rapidly progressive potentially fatal complication of Plasmodium falciparum infection. It is characterized by unarousable and persistent coma along with symmetrical motor signs. Children, pregnant women and non-immune adults are more susceptible to have cerebral malaria. Several clinical, histopathological and laboratory studies have suggested that cytoadherence of parasitized erythrocytes (mechanical hypothesis), and neuronal injury by malarial toxin and excessive cytokine (e.g. tissue necrosis factor-alpha) production (cytotoxic hypothesis) are possible pathogenic mechanisms. Several associated systemic complications like hypoglycemia, hypovolemia, hyperpyrexia, renal failure, bleeding disorders, anemia, lactic acidosis and pulmonary oedema may contribute in the pathogenesis of coma, and are responsible for high mortality. The meticulous supportive care along with intravenous administration of antimalarial drugs are corner-stone of the treatment. Quinine is currently, drug of choice. Artimisinin derivatives are equally effective and can be used by intramuscular route. In severe cases exchange blood transfusion may be an effective alternative. Corticosteroids has no place in the management of cerebral malaria. The occurrence of convulsions are common in children, these can be prevented with the use of single intramuscular administration of phenobarbitone. Despite advances in the management mortality and morbidity have not changed much. A large number of surviving patients are left with permanent neurological sequelae. There is a need to search for effective malaria prevention and interventional strategies to avert high mortality and morbidity associated with cerebral malaria.     

Cerebral Malaria

Malaria infection of the Central Nervous System (CNS) can cause a severe neurological syndrome termed Cerebral Malaria (CM). The central neuropathological feature of CM is the preferential sequestration of parasitised red blood cells (PRBC) in the cerebral microvasculature. The level of sequestration is related to the incidence of cerebral symptoms in severe malaria. Other neuropathological features of CM include petechial hemorrhages in the brain parenchyma, ring hemorrhages and Diirck's granuloma's. Immunohisto-chemical and electron microscopy studies have shown widespread cerebral endothelial cell activation and morphological changes occur in CM, as well as focal endothelial cell damage and necrosis. The immune cell response to intravascular sequestration appears to be limited, although activation of pigment-phagocytosing monocytes is a late feature. The mechanisms by which PRBC cause coma in malaria remain unclear. In vitro parasitised erythrocytes bind to endothelial cells by specific, receptor mediated interactions with host adhesion molecules such as ICAM-1, whose expression on cerebral endothelial cells is increased during CM as part of a systemic endothelial activation. Induction of local neuro-active mediators such as nitric oxide and systemic cytokines like TNFα may be responsible for the rapidly reversible symptoms of the coma of CM. The recent cloning of the parasite ligand PfEMP-1, thought to mediate binding to host sequestration receptors, promises further insight into the relationship between patterns of sequestration and the incidence and pathogenesis of coma in cerebral malaria.