淋巴滞留性脑水肿大鼠认知功能改变与海马DND关系的研究

目的探讨淋巴滞留性脑水肿大鼠空间认知能力的改变及其与海马迟发性神经元死亡(DND)之间的关系。方法采用阻断脑淋巴引流的方法，建立淋巴滞留性脑水肿模型。术后第4—7d用Morris水迷宫及图像自动监视系统监测大鼠的行为，然后处死动物，光镜及电镜下观察海马神经元的病理变化。结果动物出现明显的行为改变，在：Morris水迷宫中搜索目标的反应时程和行程明显延长，搜索策略由随机式过渡到趋向式和直线式的进程明显滞后。海马CAl区正常神经元数量明显减少，且排列极不整齐，电镜下可见神经元皱缩，核固缩、深染，核染色质聚集等病理变化。结论淋巴滞留性脑水肿大鼠可出现明显的空间定向缺损和一定程度的记忆缺损，海马CAl区迟发性神经元死亡是其主要病理基础。     

淋巴滞留性脑水肿大鼠神经元

目的:探讨淋巴滞留性脑水肿发病过程中神经元的病理学改变。方法:采用结扎颈部浅、深淋巴管并摘除相应淋巴结的方法,复制Wistar大鼠的淋巴滞留性脑水肿模型,分别于术后不同时间取脑组织,进行光镜及电镜观察。结果:术后2d出现脑组织水肿,顶叶大脑皮质及海马CA1区可见到神经元的凋亡及坏死两种形态学改变,以术后5-7d最显著。结论:脑淋巴引流阻断可导致淋巴滞留性脑水肿,神经元的凋亡及坏死是其主要病理变化。     

淋巴滞留性脑水肿的动物模型

目的 建立一种简便易行、重复性好、符合人类发病条件的淋巴滞留性脑水肿模型。方法 采用阻断大鼠脑淋巴引流的方法,建立淋巴滞留性脑水肿的动物模型,观察其行为学变化,并从术后不同时间取脑标本,进行肉眼、普通光镜、透射及扫描电镜观察,证实脑水肿的存在。结果 所有动物均发生脑水肿,表现行为异常,脑膜脑脑组织肿胀、充血,小血管壁外膜及Virchow-Robin间隙增宽,内含大量水肿液,毛细血管基底膜肥厚,神经元固缩、轮廓不清晰或肿胀、坏死,胶质细胞增生、肿胀,硬脑膜表现凹凸不平、水肿明显。结论 阻断脑淋巴引流,可以制备淋巴滞留性脑水肿模型,其操作简便、成功率高、重复性好。     

大鼠淋巴滞留性脑水肿的病理学研究

目的：探讨淋巴滞留性脑水肿的发病过程及病理特点。方法：采用阻断大鼠脑淋巴引流的方法,建立淋巴滞留性脑水肿模型,观察其行为变化,并从术后不同时间取脑标本,进行肉眼观察、HE染色及TUNEL染色光镜观察、透射及扫描电镜观察。结果：自术后第2天动物出现明显行为改变;脑膜及脑组织肿胀、充血、小血管壁外膜及Virchow-Robin间隙增宽,内含大量水肿液,毛细血管基底膜肥厚,神经元固缩、凋亡及肿胀、坏死、胶质细胞增生,硬脑膜表面凹凸不平,水肿明显。上述变化以术后5天最显著。结论：脑淋巴引流阻断后,可以导致淋巴滞留性脑水肿,其发病机制与3种传统类型的脑水肿不同,属于另一独立类型的脑水肿。     

脑皮质微血管梗塞模型中的迟发性神经元死亡

目的 :探讨脑皮质微血管梗塞后迟发性神经元死亡的发生机制。方法 :应用光化学反应原理 ,静脉注射光敏染科孟加拉红 ,绿色激光透过颅骨对大鼠脑皮质感觉运动区作定向照射 ,形成脑皮质微血管梗塞模型 ,进行神经功能评分、TTC和HE染色光镜观察、透射电镜观察和原位末端标记。结果 :脑皮质微血管梗塞后 48h ,神经功能缺损发展至高峰 ,神经元和内皮细胞损伤最为严重 ,梗塞灶中心神经元以坏死为主 ,半暗带区凋亡细胞数目显著增加。结论 :光化学法诱导大鼠脑皮质微血管梗塞模型中皮质神经元迟发性死亡呈一定的时间和空间分布特征 ,缺血半暗带神经元凋亡与这种延迟损伤有关     

食欲素A促进短暂性全脑缺血大鼠的海马CA1区谷氨酸摄取并抑制迟发性神经元死亡

目的 探讨食欲素A(OX-A)对短暂性全脑缺血(tGCI)大鼠的海马CA1区胶质细胞谷氨酸转运体-1(GLT-1)的表达与功能以及迟发性神经元死亡(DND)的影响及机制.方法 将大鼠分为假手术(sham)组、模型(model)组、OX-A组和OX-A+LY294002组.用[3 H]-谷氨酸标记法检测海马CA1区GLT...     

硫酸镁和低分子肝素联合应用对海马迟发性神经元坏死的保护作用

目的 研究硫酸镁和低分子肝素在短暂局灶性脑缺血再灌注后海马迟发性神经元坏死中的保护作用。方法 新西兰大白兔夹闭单侧颈总动脉制成模型，缺血30min再灌注72h后通过HE染色进行组织观察，同时检测血清中IL-8的含量，探讨硫酸镁和低分子肝素对保护脑的作用机制。结果 硫酸镁联合低分子肝素治疗组迟发性神经元坏死程度显著低于盐水治疗组，低分子肝素能降低缺血再灌注后血清中的IL-8含量。结论 IL-8做为一种急性炎症的趋化因子，在脑缺血时升高，可作为脑缺血炎症期或再灌注损伤重要的观察指标之一。硫酸镁没有抗炎作用，单用硫酸镁或低分子肝素的治疗效果。没有联合应用的治疗效果显著。     

沙土鼠短暂性脑缺血后海马迟发性神经元死亡机理的研究

本实验通过结扎沙土鼠双侧颈总动脉20分钟后再灌流2天或7天造成海马迟发性神经元死亡(DND)模型,检测背侧海马Ca~(2 )及脂质过氧化物含量的变化,并用海马CA_1区神经元密度作为指标,观察尼莫地平及超氧化物歧化酶(SOD)对海马DND的影响。结果:再灌流2天后背侧海马组织Ca~(2 )及MDA含量增加;尼莫地平及SOD均可改善海马CA_1区DND,使海马CA_1区神经元密度增加。本实验提示:Ca~(2 )及氧自由基导致的脂质过氧化物在短暂性脑缺血后海马DND的发生中起重要作用,钙拮抗剂及自由基清除剂对海马DND有保护作用。     

对冲性额颞叶脑挫裂伤后迟发性脑水肿临床分析

对冲伤所致额颞部脑挫裂伤在临床上常见，治疗上并不困难。但我们发现部分此类患者在治疗1周左右出现病情加重，复查颅脑CT显示脑水肿加重，若不及时处理，预后极差。我们对山东省枣庄矿业集团滕南医院收治的22例患者的临床资料进行了回顾性分析，并对其发生原因和处理进行了探讨。     

迟发性运动障碍与DNA甲基化之间关系的研究进展

DNA甲基化是最常见的表观遗传学修饰之一,异常的甲基化影响基因的转录和表达。有研究表明DNA甲基化可能在精神疾病的发生机制中发挥着很大的作用。本文通过综述迟发性运动障碍的研究进展及DNA甲基化可能发挥的作用,为预测TD的发生发展及临床治疗和预防提供理论依据。     

短暂性前脑缺血再灌流后海马区cGMP反应细胞与DND的关系

目的3：观察短暂性前脑缺血再灌流后海区cGMP反应细胞与迟发性神经元坏死的分布,探讨两者间的关系。方法：钳夹沙土鼠的双侧颈总动脉制造脑缺血模型,应用放射免疫荧光法及尼氏染色分别观察前脑缺血再灌流1d,3d,7d后海马区cGMP的反应细胞分布及再灌流7d发性神经元坏死的分布,结果：脑缺血再灌流后cGMP阳性细胞主要分布在CA1始层,放射层及腔隙分子层,CA1区锥体细胞未见,cGMP阳性细胞,迟发性神经元坏死全部分布在CA1区锥体细胞。结论：cGMP阳性细胞可能比cGMP阴性细胞对缺血耐受。     

胎脑皮质移植物神经元发育的组织学观察

本实验用E_(15)胎脑皮质作供体植入到中年Wistar大鼠大脑皮质3、1、2区内,移植后7天的移植物中成熟的神经元数量少,未成熟神经元占大多数,15天的移植物成熟神经元占多数,未成熟神经元数量少.30天神经元发育成熟.神经元发育过程比原位大脑皮质神经元至少推迟8天.移植后30天内神经元发育过程占主导地位.     

神经节苷脂GM1对新生大鼠缺氧缺血性脑病的作用研究

目的 探讨单唾液酸四己糖神经节苷脂（GM1）对新生大鼠缺氧缺血性脑病（HIE）及其后的癫痫发作是否具有保护和预防作用以及可能作用机理，为临床应用GM1治疗HIE提供理论依据。方法 建立新生大鼠HIE模型。用组织化学方法和免疫组织化学方法观察缺氧缺血后脑损害的形态学改变，兴奋性氨基酸Glu阳性（Glu-IR)神经元和抑制性氨基酸GABA阳性（GABA-IR）神经元表达和GM1对上述变化的影响。结果 盐水处理组与GM1治疗组相比病变较重，Glu-IR神经元和GABA-IR神经元数目减少与GMI治疗组差异有显著性意义。结论 GM1能够在一定程度上减轻新生大鼠缺氧拭岂血后病损灶，保护Glu-IR神经元和GABA-IR神经元，尤其是对GABA-IR神经元的保护作用，提示GM1对新生大鼠缺氧缺血后的癫痫发作具有一定的预防作用。但尚需进一步探讨研究。     

Areas of Cartilaginous and Osseous Metaplasia After Experimental Myocardial Infarction in Rats

The presence of hyaline cartilage has been previously documented in heart tissue of different vertebrates, ranging from birds to superior mammals. However, there is scarce published data regarding the appearance of focal deposits of hyaline-like cartilage within the hearts of laboratory rats. Few mechanisms that could trigger the appearance of this type of cartilage in heart were hypothesized (e.g., mechanical stress, ageing). Using different microscopy techniques this report confirms the presence of hyaline cartilage and bone in Wistar rats, which underwent left anterior coronary artery ligation for experimental myocardial infarction. The presented (ultra)structural evidence of focal chondroid metaplasia in the papillary muscles and close to the insertion point in the ventricular mass of the infarcted heart suggests a structural adaptation of cardiac myocardium to the newly acquired kinetics of left ventricular wall, after experimental myocardial infarction. Specific cartilaginous matrix proteins are known to mediate cardiac extracellular matrix remodeling, and this study provides evidence of a complete transition to a cartilaginous pattern in postinfarcted heart, which may nonetheless constitute a supplemental risk factor of a further heart failure condition. Moreover, for heart focal chondrogenesis, we also presume the involvement of the cellular and molecular inflammatory milieu that dominates the first 24 hr border zone landscape of the experimental myocardial infarction lesion. Anat Rec, 302:947–953, 2019. © 2018 Wiley Periodicals, Inc.     

新生大鼠海马神经干细胞的分离培养及分化研究

研究新生大鼠海马区脑组织中神经干细胞体外培养方法,为治疗神经系统疾病寻找合适的细胞来源。取新生SD大鼠的海马区脑组织,采用accutase结合机械分离法获取神经干细胞,在含有B－27、碱性成纤维生长因子和表皮生长因子的DMEM／F12无血清培养液中培养;Accutase酶消化后传代培养,取第3代细胞行抗巢蛋白免疫荧光染色鉴定并以含10％胎牛血清培养液诱导分化,神经元特异烯醇化酶和胶质纤维酸性蛋白免疫荧光染色检测NSCs向神经元及胶质细胞分化的能力。分离的新生大鼠海马区脑组织中细胞,在无血清培养液中形成大量的神经球,部分神经球出现融合及贴壁分化现象,细胞呈典型NSCs 形态。经巢蛋白染色鉴定,大部分为阳性细胞。神经细胞球经含有胎牛血清培养液培养后,可分化为神经元特异烯醇化酶和胶质纤维酸性蛋白表达阳性的细胞。从新生大鼠海马组织分离培养的NSCs具有自我更新和增殖能力,在含胎牛血清培养液中具有向神经元和神经胶质细胞分化的潜能。     

糖尿病大鼠海马超微结构观察及胰岛素治疗作用

目的 观察实验性糖尿病大鼠海马超微结构改变。方法 将成年ＳＤ大鼠随机分为正常对照组（５只）、糖尿病组（１２只,经腹腔注射链脉佐菌素制备实验性糖尿病大鼠模型）、糖尿病治疗组门 只,给子部分成模大凤长效胰岛素２－３Ｕ／日治疗,使空腹血糖低于 １０ｍｍｏｌ／Ｌ）,于成模第３月末及第６月末灌注固定取脑,透射电镜下观察梅马起微结构。结果 电镜下可见糖尿病大鼠海马发生锥体细胞退变。６月组病变较三月组更显著,相应治疗组改变较轻傲。结论 糖尿病可导致大鼠海马锥体细胞退变,早期应用胰岛素治疗可延缓其发生。     

Specific Suppression of Humoral and Delayed Hypersensitivity Responses by Cyclophosphamide in an Experimental Model of Autoimmunity

ABSTRACT: The aim of this report is to investigate the effect of cyclophosphamide (CY) in an experimental model of autoimmunity to rat male accessory glands. The results indicated that 100 mg/kg of this drug suppressed humoral immune response that persisted for at least 45 days when administered 3 days after the first immunization of rats with modified rat male accessory glands (MRAG) in complete Freund's adjuvant (CFA). Administration of the drug 3 days before ID injection of antigen caused a shorter suppression of antibody formation. Delayed type hypersensitivity (DTH) studied 13 days after the first immunization was suppressed only in the animals that were administered CY after the antigen. The specificity of the immunosuppression was studied in rats treated with CY after the first immunization with MRAG using aggregated human γ-globulin (AHGG) as an unrelated antigen. The studies demonstrated significant suppression of DTH (p < 0.005) and humoral immunity only against MRAG. On the contrary, the response to AHGG was not significantly modified.     

Delayed peripheral administration of the N-terminal tripeptide of IGF-1 (GPE) reduces brain damage following microsphere induced embolic damage in young adult and aged rats

We have previously reported that peripheral administration of GPE prevents neuronal injury after ischemic reperfusion injury in young adult rats. This study examined the ameliorating effects of GPE-treatment after embolic injury induced by microsphere injection in young adult and aged male rats. Unilateral injury was induced by injecting microspheres into the right internal carotid artery in both young adult (3–4 months) and aged (16–17 months) male rats. Either GPE (12 mg/kg) or the vehicle was infused intravenously over 1 h starting 3 h after embolic injury and the degree of brain injury, astrocytosis and vascular remodeling were examined using histological and immunohistochemical analysis 8 days later. Changes in core temperature, blood glucose concentration, oxygen saturation and heart rate were monitored. Microsphere injection induced multiple sites of focal damage in the ipsilateral subcortical regions. Massive numbers of microglia accumulated within the core of the tissue damage whereas astrocytes were located in the penumbra. There was no difference in the degree of brain injury between the young and aged control rats. However the aged rats showed less injury-induced astrocytosis and greater vascular remodeling. Intravenous infusion of GPE 3 h after the injury reduced overall damage scores in both young (p < 0.01) and aged rats (p < 0.05). GPE-treatment reduced astrocytosis in young, but not aged animals and did not significantly alter the vascular remodeling in either age group. The data suggested that the neuroprotection of the tripeptide is independent of cerebral reperfusion and is not age selective.