大鼠胎脑组织移植血管构筑形态研究

把 Wistar 胎鼠脑皮质组织移植到同种大鼠的脑缺损腔内.于移植后6月、16月分批活杀。采用 Niss 染色法、墨汁灌注法作光镜和电镜观察.部分作 ABS 灌注电子探针超微扫描观察.并与假手术组对照。结果:见脑移植组植入胎脑存活。移植物与受体脑之间有血循环重建。重建血管构筑特点为,从植入物周边向心性延伸分枝供血。为临床脑移植研究提供参考依据。     

大白鼠脑移植体血管重建的观察及其意义

本文观察了胎鼠脑组织移植大鼠眼前房及脑内后,移植体血循环的重建。移植后1、3、6个月进行切片染色,观察移植体的形态结构及血管构筑。结果表明,存活的脑移植体,重建血循环,但移植体的血管密度低于宿主相应的脑组织,微循环的形态不够完善,血循环不如宿主脑组织充分。个别脑移值体内未见血管长入,其神经细胞变性或消失。部分标本中可见慢性排异反应。结果提示,移植体血循环的建立是移植成功的关键。     

Collagen与胎脑神经细胞移植入脑缺血大鼠的形态学研究

目的：观察胶原蛋白（Collagen)与胎脑神经细胞（FBN）联合培养2天后，神经细胞与胶原蛋白的吸附情况；观察胶原蛋白与胎脑神经细胞（CFBN）移植入脑缺血大鼠后神经细胞的成活情况。方法：取孕14天的胎脑神经细胞，体外分离后与胶原蛋白进行联合培养；制备大脑中动脉闭塞（MCAO）模型。实验组在脑缺血2小时，再灌流48小时后植入CFBN，对照组同样条件未移植CFBN。实验组及对照组分别于2、6、10、30天后灌流取材，保证各时相点动物大于或等于3只。结果：CFBN植入2天后，机体发生轻微排斥反应，部分中性粒细胞和淋巴细胞浸润，6天后排斥反应消失。HE和尼氏染色可见实验组植入神经细胞生长良好。结论：CFBN在脑缺血大鼠中生长良好，CFBN可用作神经系统疾病的细胞移植治疗。     

胎脑移植治疗脑性瘫痪21例分析

本文报告采用胎脑移植治疗脑性瘫痪病人２１例。通过术后１～４年随访，其中疗效优４例，良８例，一般５例，无效４例。无并发症。并对移植作用的可能机制和手术要点进行讨论，主张复合移植。     

胎脑移植治疗脑性瘫痪21例分析

本文报告采用胎脑移植治疗脑性瘫痪病人２１例，通过术后１￣４年随访，其中疗效优４例，良８例，一般５例，无效４例，无并发症，并对移植作用的可能机制和手术要点进行讨论，主张复合移植。     

胎脑组织移植对额叶皮层损伤大鼠辨别学习、记忆之影响

本研究观察了胎脑组织移植对双侧额叶皮层损伤的大鼠学习、记忆功能的影响。学习、记忆再现测验在Y型迷宫中进行。结果表明,胎脑组织移植能促进双侧额叶皮层受损动物明—暗分辨学习及记忆再现功能的恢复,且移植时间长短与其功能恢复呈正相关。组织学检查表明,移植的胎脑组织不仅存活,且分化良好,移植3、6个月后,与宿主脑界面有部分融合,提示移植脑组织与宿主脑可能有纤维联系形成。     

胎脑组织移植若干因素研究

胎脑组织移植若干因素研究刘俊张可成以大鼠为研究对象进行同种及异种胎脑组织移植后在不同时间内检测了移植区局部Ｔ淋巴细胞浸润及ＭＨＣⅡ类抗原的表达情况，以此对脑组织移植后的免疫排斥反应状况进行了探讨。一、材料与方法受体动物用Ｗｉｓｔａｒ大鼠，雌雄不分，年...     

9例脑组织移植患者临床免疫学初步观察

本文观察了9例胎脑移植患者移植后的一般临床表现(首例移植迄今已有3年零9个月)。测定移植前与移植后外周血中的淋巴细胞计数(Lym)、淋巴细胞转化率(LTT)、血清免疫球蛋白IgG、IgA、IgM,补体C_3、C_4,抗核杭体(AnAb)等常规免疫指标。采用荧光抗体技术检测抗脑抗体。结果:在本组病人中未发现有临床免疫排斥反应(HVGR)和移植物抗宿主反应(GVHR)的临床表现。患者移植前、后的常规免疫指标测定值与正常人对照,无显著性差异(P>0.05)。仅有1例移植前、后抗核抗体均出现阳性反应,但滴度不变,都是1:20。患者移植前、后的荧光抗脑抗体检测也呈阴性结果。因此,初步认为,本组病例的移植免疫效应与“大脑为免疫特免器官”的论点相一致的。     

双侧肾上腺切除大鼠脑缺血后血脑屏障破坏的研究

目的观察脑缺血时体内自身的糖皮质激素变化对血脑屏障（ＢＢＢ）的影响。方法采用线栓法造成脑缺血模型，用辣根过氧化物酶组织化学染色的方法，观察双侧肾上腺切除大鼠局灶脑缺血后血脑屏障的改变。结果双侧肾上腺切除后脑缺血组（Ａ组）大鼠ＢＢＢ破坏的范围为１０．１０１±１．４１１ｍｍ２；单纯脑缺血组（Ｂ组）大鼠ＢＢＢ破坏范围为６．１９１±１．０４５ｍｍ２，Ａ组大鼠ＢＢＢ破坏的范围大于Ｂ组大鼠ＢＢＢ破坏的范围（Ｐ＜０．０１）。结论脑缺血时体内自身的糖皮质激素升高对ＢＢＢ具有保护作用。     

脑内移植治疗顽固性癫痫的临床研究

目的：寻找提高治疗癫痫的疗效方法。方法：本组采用癫痫灶切除和脑移植结合，治疗此类病人６２例。结果：显示总有效率达９５％，而常规治疗组为９２％，与常规治疗组比有显著差异（Ｐ＜００１）。结论：癫痫灶切除术加脑移植治疗顽固性癫痫是一种有效的治疗方法     

Cadmium induced endothelial cell alterations in the fetal brain from prenatal exposure

Summary Pregnant rats received a single administration of 0.5, 1.0, or 2.0 mg/kg of cadmium on day 18 or 20 or gestation Maternal animals were killed on day 21 and samples of the caudate nucleus from fetal brains were examined using the transmission electron microscope. A 2.0 mg/kg dose of cadmium administered to maternal rats on day 20 of gestation caused the formation of vacuoles in the endothelial cells of capilaries in the fetal brain. Significant endothelial cell vacuolization was not observed in the brain of fetuses from other treatment groups. The vacuoles occurred singly, were spherical in shape, were located adjacent to the intercellular junctions and caused focal distortion of the endothelial cell. Vacuoles were the only ultrastructural alteration observed in the caudate nucleus of fetal brains.     

神经生长因子在胎脑组织保存和移植中的应用

大鼠胚胎脑组织放入神经生长因子（ＮＧＦ）溶液或ＤＭＥＭ培养液中保存１～６天，观察不同时间细胞存活率，ＮＧＦ组均高于ＤＭＥＭ组。将这两种液体中保存５天的组织分别植入两组成年大鼠脑内，６～８周后组织学观察发现，ＮＧＦ组移植成活４／１０，对照组移植物成活３／９．尽管两组移植物成活率比较差别不显著（Ｐ＞０．０５），但是移植物生存质量ＮＧＦ组明显优于对照组。     

大鼠颅脑创伤后脑红蛋白表达变化的实验研究

目的研究弥漫性颅脑创伤后大鼠脑组织中脑红蛋白的核酸与蛋白表达变化情况，初探脑红蛋白与颅脑创伤的关系。方法选择Marmarou’s自由落体打击装置复制弥漫性颅脑创伤模型，采用实时定量PCR及Westernblotting分别检测伤后不同时间（30min、1h、2h、6h、12h、24h、48h、72h、5d）脑组织中脑红蛋白核酸及蛋白水平的表达情况，并对所得数据进行统计学分析。结果在伤后30min，脑组织中脑红蛋白的核酸表达m现首个高峰，相应地其蛋白表达于伤后1h增高，于伤后2h达峰值；伤后12h，脑红蛋白的核酸表达再次升高，于伤后48h达高峰，其蛋白表达亦于伤后24h增高，至72h达峰值。结论颅脑创伤后脑组织中脑红蛋白呈“双峰”样表达。提示脑红蛋白可拮抗对神经元的创伤应激及伤后继发缺血、缺氧性损害，对创伤后脑组织具有一定的保护作用。     

急性创伤性脑损伤大鼠血脑屏障通透性变化与Claudin-5的相关性研究

目的 研究大鼠急性创伤性颅脑损伤(TBI)后血脑屏障(BBB)通透性的变化和机制.方法 雄性Wistar大鼠96只按随机数字表法分为假手术组和TBI组,TBI模型参照Feeney自由落体致伤法制作,假手术组仅行开颅术不行打击致伤.每组按伤后处死时间的不同分为3h、6h、12h 、24 h、48 h、72h6个亚组,每亚组4只.采用干湿重比法测定脑组织含水量,Western blotting检测脑皮质紧密连接蛋白Claudin-5的表达,伊文思蓝(EB)法检测脑组织BBB通透性变化. 结果 与假手术组比较,TBI组大鼠创伤后不同时间点脑组织含水量、EB含量均增多.组内比较显示二者创伤后3h开始增多,24 h达高峰,随后下降,差异有统计学意义(P＜0 05);与假手术组比较,TBI组大鼠创伤后6h、12h、24 h、48 h、72 h紧密连接蛋白Claudin-5表达降低.组内比较显示其创伤后6h表达降低,24 h达最低值,随后回升,差异有统计学意义(P＜0.05);大鼠脑Claudin-5蛋白的相对表达水平和脑组织水含量、脑组织EB含量呈负相关关系(r=-0.994,P=0.000;r=-0.846,P=0.036).脑组织含水量和EB含量呈正相关关系(=0.863,P=0.027). 结论 TBI后大鼠BBB通透性变化和脑损伤程度具时间依赖性,紧密连接蛋白Claudin-5与BBB变化具有一定程度的相关性.     

Prenatal sodium arsenite affects early development of serotonergic neurons in the fetal rat brain

Prenatal arsenite exposure has been associated with developmental disorders in children, including reduced IQ and language abnormalities. Animal experiments have also shown that exposure to arsenite during development induced developmental neurotoxicity after birth. However, the evidence is not enough, and the mechanism is poorly understood, especially on the exposure during early brain development. This study assessed effects of sodium (meta) arsenite shortly after exposure on early developing fetal rat brains.Pregnant rats were administered 50 mg/L arsenite in their drinking water or 20 mg/kg arsenite orally using a gastric tube, on gestational days (GD) 9–15. Fetal brains were examined on GD16.Pregnant rats administered 20 mg/kg arsenite showed reductions in maternal body weight gain and food consumption during treatment, but not with 50 mg/L arsenite. Arsenite did not affect fetal development, as determined by body weight, mortality and brain size. Arsenite also did not induce excessive cell death or affect neural cell division in any region of the fetal neuroepithelium. Thyrosine hydroxylase immunohistochemistry revealed no difference in the distribution of catecholaminergic neurons between fetuses of arsenite treated and control rats. However, reductions in the number of serotonin positive cells in the fetal median and dorsal raphe nuclei were observed following maternal treatment with 20 mg/kg arsenite. Image analysis showed that the serotonin positive areas decreased in all fetal mid- and hind-brain areas without altering distribution patterns. Maternal stress induced by arsenite toxicity did not alter fetal development. These results suggest that arsenite-induced neurodevelopmental toxicity involves defects in the early development of the serotonin nervous system.     

Rat brain slicer. A simple device for rapidly obtaining serial slabs of fresh brain

A simple, two-part device is described which has been used to provide rapid serial sectioning of fresh rat brain in experiments in which identifiable brain regions were microdissected for biochemical analysis. This device is easily constructed at low cost, and offers several advantages over other devices and techniques.     

Persistence of phencyclidine in fetal brain

Phencyclidine residues were found in the brains of rat pups of mothers dosed with this drug during pregnancy. These levels were significant at times after dosing when maternal levels of phencyclidine in serum or brain were low or undetectable. The persistence of this compound in fetal serum was also not prolonged. Maternal ingestion of PCP for a relatively brief time may result in an extended exposure of the developing nervous system.