羊瘙痒因子263K感染仓鼠终末期脑中胶质纤维酸性蛋白和神经元特异性烯醇化酶的表达和分布变化研究

为了探讨羊瘙痒因子263K感染仓鼠脑组织中星形胶质细胞和神经元的数量及功能改变,利用免疫印迹、免疫组化方法研究了胶质纤维酸性蛋白(glial fibrillary acidic protein,GFAP)和神经元特异性烯醇化酶(neuron-specific enolase,NSE)在受染仓鼠各脑区中表达变化的特点,同时比较其与神经病理学改变及PrPSc沉积的关系.结果表明,感染终末期仓鼠的脑组织中GFAP表达量明显增高,与正常对照相比,大脑皮质、脑干和小脑区域GFAP着色细胞数量分别增高3.69、2.41和1.56倍.感染仓鼠脑组织NSE表达量低于正常对照,小脑、海马CA1区和大脑皮质NSE着色细胞数量分别仅为正常对照相应区域的22.5%、54.2%和53.9%.这些变化与PrPSc在脑组织中的沉积程度和空泡样变性程度相吻合.结果提示,GFAP和NSE的检测可分别很好地反映星形胶质细胞和神经元的数量及功能状态,成为在朊病毒病发病过程中重要的病理变化指标.     

TnT-Hs和NSE在手足口病患儿中的表达水平及临床意义

目的：探讨TnT-Hs和NSE水平在手足口病患儿中的表达及临床意义。方法：选择我院2012年6月-2013年6月确诊为手足口病的住院患儿68例作为观察组,选择同期入院健康体检的68例正常儿童作为对照组,对比两组心肌钙蛋白T（TnT—Hs）与血清神经元特异性烯醇化酶（NSE）水平;并对观察组EV71阳性患儿与阴性患儿TnT-Hs与NSE水平进行比较。结果：①相比健康对照组,观察组TnT-Hs与NSE水平均较高,差异有统计学意义（P〈0．01）。②EV71阳性患儿46例,阴性患儿22例,阳性患儿相比阴性患儿TnT-Hs与NSE水平较高,差异均有统计学意义（P〈0．05）。结论：Tn—T-Hs和NSE水平可反映手足口病患儿病情进展变化,其可作为早期预测手足口病患儿心肌损害及脑损伤的依据及重症病例的预警指标。     

TnT-Hs和NSE在手足口病患儿中的表达水平及临床意义

目的:探讨TnT-Hs和NSE水平在手足口病患儿中的表达及临床意义。方法:选择我院2012年6月~2013年6月确诊为手足口病的住院患儿68例作为观察组,选择同期入院健康体检的68例正常儿童作为对照组,对比两组心肌钙蛋白T(TnT-Hs)与血清神经元特异性烯醇化酶(NSE)水平;并对观察组EV71阳性患儿与阴性患儿TnT-Hs与NSE水平进行比较。结果:1相比健康对照组,观察组TnT-Hs与NSE水平均较高,差异有统计学意义(P0.01)。2EV71阳性患儿46例,阴性患儿22例,阳性患儿相比阴性患儿TnT-Hs与NSE水平较高,差异均有统计学意义(P0.05)。结论:Tn-T-Hs和NSE水平可反映手足口病患儿病情进展变化,其可作为早期预测手足口病患儿心肌损害及脑损伤的依据及重症病例的预警指标。     

血清S100β蛋白和NSE水平与急性脑梗死患者预后关系的探讨

目的:探讨急性脑梗死(ACI)患者血清S100β蛋白及神经元特异性烯醇化酶(NSE)水平变化与预后的关系。方法:采用双抗体夹心ELISA法测对33例脑梗死患者及25例健康对照组的血清S100B蛋白水平进行测定;用电化学发光的方法对NSE含量的观察,并比较ACI患者在不同病情、不同梗死面积时的血清S100β蛋白和NSE含量变化,采用Pearson法对二者进行相关性分析。结果:脑梗死组患者血清S100β蛋和NSE水平均明显高于正常对照组(P<0.05)。并且随着神经功能损伤程度的增高和梗死面积的增加,血清S100β蛋白和NSE含量亦明显升;S100β蛋白水平和NSE水平呈正相关(P<0.01)。结论:急性脑梗死患者血清NSE和S-100B蛋白浓度均明显增高。血清S100β蛋白和NSE水平可作为疾病诊断、判断病情及评估预后的重要参数。尤其适用于无法进行影像学检查的急性脑梗死患者。     

神经节苷脂联合咪达唑仑治疗重症颅脑损伤的临床疗效及对患者血清MMP-9、GFAP、MBP、NSE水平的影响

目的:探讨神经节苷脂联合咪达唑仑治疗重症颅脑损伤的临床疗效及对患者血清基质金属蛋白酶-9(MMP-9)、胶质纤维酸性蛋白(GFAP)、髓鞘碱性蛋白(MBP)、神经元特异性烯醇化酶(NSE)水平的影响。方法:选择2016年3月到2017年9月于我院进行治疗的85例重症颅脑损伤患者,将其按随机数表法分为观察组(n=45)和对照组(n=40),对照组使用神经节苷脂治疗,观察组采用神经节苷脂联合咪达唑仑治疗。比较两组治疗后疗效及血清GFAP、中枢神经特异蛋白(S100β)、NSE、MMP-9、MBP、C反应蛋白(CRP)、白细胞介素-6(IL-6)、肿瘤坏死因子α(TNF-α)水平、格拉斯哥昏迷评分(Glasgow Coma Scale,GCS)评分的变化及不良反应的发生情况。结果:治疗后,观察组临床疗效总有效率(93.33%)显著高于对照组(75.00%,P0.05);两组血清GFAP、S100β、NSE、MMP-9、MBP、CRP、IL-6及TNF-α水平均较治疗前明显下降,且观察组以上指标均显著低于对照组(P0.05);观察组GCS评分明显高于对照组(P0.05),且不良反应发生率明显低于对照组(6.67%vs. 30.00%,P0.05)。结论:神经节苷脂联合咪达唑仑治疗重症颅脑损伤患者的临床效果显著,明显优于单用神经节苷脂治疗,可能与其有效改善患者血清MMP-9、GFAP、MBP、NSE水平及抑制炎症因子的生成有关。     

血清S-100B蛋白和NSE含量变化评估脑损伤程度的意义

目的探讨颅脑损伤后血清S-100B蛋白、神经元特异性烯醇化酶(NSE)水平变化及其在损伤程度的临床意义。方法采用酶联免疫测定法检测90例颅脑损伤患者入院时及入院后6、12、24h和3、7天血清S-100B蛋白、NSE水平,并分析其与颅脑损伤严重程度的关系。同时选择30例健康体检者作为对照组进行比较分析。结果颅脑损伤后血清S-100B蛋白、NSE水平较对照组明显升高(P0.05或P0.01);重型组患者的血清S-100B蛋白和NSE水平明显高于轻、中型组患者(P0.05或P0.01);动态检测结果显示,血清S-100B蛋白在伤后12h达峰值(P0.05),NSE含量在伤后24h达峰值(P0.05),然后缓慢下降。GCS评分与S-100B、NSE浓度呈负相关(分别为r=-0.814,P0.01;r=-0.726,P0.05)。结论颅脑损伤后血清S-100B蛋白、NSE水平升高,其与脑损伤程度有较好的相关性,2种标记物水平对颅脑损伤程度有较高的评估价值。     

NSE 和NGF 在颅脑损伤后血清中含量变化及临床意义

创伤性颅脑损伤后外周血清中神经元特异性烯醇化酶(NSE)和神经生长因子(NGF)含量呈动态变化,在颅脑损伤(尤其是重型颅脑损伤)早期即可出现表达增加,其中NSE含量与颅脑损伤程度呈正相关,而NGF在颅脑损伤后的神经修复、再生和神经元保护等机制中起重要作用,其在血清中含量变化的临床意义明显不同。两者在血清中含量变化对于颅脑损伤后病情、治疗及预后评估有重要的作用,是颅脑损伤后评估病情、进行治疗的重要指标,因此监测血清中NSE及NGF的变化,可以为更准确判断病情、评估预后,并为临床治疗提供依据。本文就其在颅脑损伤患者血清中的含量变化及临床意义作以简要综述。     

NSE和NGF在颅脑损伤后血清中含量变化及临床意义

创伤性颅脑损伤后外周血清中神经元特异性烯醇化酶（NSE）和神经生长因子（NGF）含量呈动态变化,在颅脑损伤（尤其是重型颅脑损伤）早期即可出现表达增加,其中NSE含量与颅脑损伤程度呈正相关,而NGF在颅脑损伤后的神经修复、再生和神经元保护等机制中起重要作用,其在血清中含量变化的临床意义明显不同。两者在血清中含量变化对于颅脑损伤后病情、治疗及预后评估有重要的作用,是颅脑损伤后评估病情、进行治疗的重要指标,因此监测血清中NSE及NGF的变化,可以为更准确判断病情、评估预后,并为临床治疗提供依据。本文就其在颅脑损伤患者血清中的含量变化及临床意义作以简要综述。     

脑血康胶囊联合巴曲酶对急性脑梗死患者血清 MBP、NSE水平的影响

摘要 目的：研究脑血康胶囊联合巴曲酶对急性脑梗死患者血清髓鞘碱性蛋白(myebin bosic protein,MBP)、神经元特异性烯醇化酶(neuron-specific enolase,NSE)水平的影响。方法：选择2018年3月～2019年3月我院收治的161例急性脑梗死患者,将其随机分为两组。对照组静脉滴注巴曲酶,首次给予10 BU,隔日给予5 BU,每两天给药1次;观察组在巴曲酶的基础上联合口服脑血康胶囊,每天3 次,每次3粒。观察和比较两组治疗总有效率、治疗前后血清MBP、NSE、全血黏度(whole blood viscosity,WBV)、红细胞压积(hematocrit,HCT)、血浆黏度(plasma viscosity,PV)和纤维蛋白原(fibrinogen,FIB)水平及NHISS和BI评分的变化。结果：治疗后,观察组的有效率为91.25 %,明显高于对照组(64.2%,P<0.05);两组血清MBP、NSE、WBV、HCT、PV和FIB水平均较治疗前明显降低(P<0.05),且观察组的以上指标明显低于对照组(P<0.05);两组的BI评分明显升高(P<0.05),NHISS评分明显降低(P<0.05),观察组BI评分明显高于对照组,而NHISS评分明显低于对照组(P<0.05)。结论：脑血康胶囊联合巴曲酶对急性脑梗死有显著的疗效,能明显降低患者血清MBP、NSE水平,促进神经功能的恢复。     

胎儿胰腺发育中CgA和NSE的表达及其意义

目的检测人胎儿胰腺中CgA和NSE的表达特征,初步探讨胎儿胰腺发育过程弥散神经内分泌系统的形成及其生物学作用.方法用免疫组织化学SP法,检测嗜铬素A(chromograin A,CgA)和神经元特异性烯醇化酶(neuron specific enolase,NSE)在不同胎龄胎儿胰腺组织中的表达.结果CgA在16-38周的胰腺中均有表达,随胎儿发育,CgA阳性细胞分布状态和反应程度均有差异变化;NSE在22-38周胎儿胰腺中表达,集中定位于胰腺的内分泌部细胞.结论CgA和NSE在人胎儿胰腺中的阳性表达,反映出弥散神经内分泌系统在胎儿胰腺中的形成过程;表明胎儿胰岛的形成及其DNES细胞的分泌,有调节胰腺外分泌部发育分化的作用,也提示胰岛DNES细胞通过调节血糖可能对胎儿个体发育具有重要影响.     

NDRG2与GFAP在不同脑区星形胶质细胞的表达与分布

目的:观察NDRG2(N-myc下游调节基因2)与GFAP(胶质纤维酸性蛋白)在不同脑区星形胶质细胞的表达与分布。方法:利用免疫荧光NDRG2与GFAP双标技术以及Western Blot技术观察皮层、海马及纹状体等不同脑区星形胶质细胞NDRG2和GFAP的表达与分布。结果:免疫荧光结果显示NDRG2阳性细胞广泛而均匀地分布于不同脑区,并与GFAP存在较好的共定位;NDRG2与GFAP标记的星形胶质细胞形态不尽相同。Western Blot结果显示NDRG2在皮层中表达比海马和纹状体多,而GFAP在海马中表达比皮层和纹状体多。结论:NDRG2广泛表达于不同脑区星形胶质细胞,并于GFAP存在较好的共定位。     

碘过量大鼠仔鼠垂体促甲状腺激素细胞的组织学研究

目的探讨不同剂量碘过量对大鼠20日龄仔鼠垂体促甲状腺激素细胞的形态学影响。方法将断乳1个月的Wistar大鼠,雌雄各半,随机分为4组：NI组、10HI组、50HI组、100HI组。饲养3个月的雌雄大鼠1：1合笼交配产生仔鼠,断乳后的仔鼠喂养同上述大鼠。测定20日龄仔鼠垂体TSH细胞的体密度和面数密度。结果100HI组仔鼠垂体TSH细胞的体密度高于NI组,10HI、50HI与NI组相比无差异,各碘过量组的面数密度与NI组相比也无差别。结论大剂量碘过量可造成大鼠仔鼠乖体TSH细胞分泌颗粒蓄积,细胞体积增大。     

Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice

Alexander disease is a fatal leukoencephalopathy caused by dominantly-acting coding mutations in GFAP. Previous work has also implicated elevations in absolute levels of GFAP as central to the pathogenesis of the disease. However, identification of the critical astrocyte functions that are compromised by mis-expression of GFAP has not yet been possible. To provide new tools for investigating the nature of astrocyte dysfunction in Alexander disease, we have established primary astrocyte cultures from two mouse models of Alexander disease, a transgenic that over-expresses wild type human GFAP, and a knock-in at the endogenous mouse locus that mimics a common Alexander disease mutation. We find that mutant GFAP, as well as excess wild type GFAP, promotes formation of cytoplasmic inclusions, disrupts the cytoskeleton, decreases cell proliferation, increases cell death, reduces proteasomal function, and compromises astrocyte resistance to stress.     

碘缺乏或碘过量对小鼠子二代生长发育的影响

目的探讨碘缺乏和碘过量所致的甲状腺功能低下对小鼠子二代生长发育的影响。方法将断乳1个月Baldb／c小鼠,随机分为5组（LI,NI,5HI,10HI,50H1）。给以不同浓度碘水喂养3个月后,连续传二代。观察碘缺乏和碘过量对子二代小鼠生长发育的影响。结果20日龄时,各组子二代鼠与NI组相比,LI组与50HI组的T4明显降低;LI组的体重明显降低,50HI组体重、身长、尾长、胸腺、脾均明显降低,脑相对重量增加。40日龄时,各组子二代鼠与NI组相比,LI组T4明显降低;碘缺乏组的体重、身长、胸腺、脾、肾上腺的重量均明显降低,脑相对重量明显增加;50HI组体重、身长、尾长明显降低。结论碘缺乏,高剂量碘过量均可引起甲状腺功能低下,使子二代鼠的生长发育延迟。碘缺乏对生长发育的影响比碘过量更为明显。但小鼠对碘过量有较强的耐受性,当碘摄入量为正常的50倍时,才会影响下一代的生长发育。     

Reciprocal pathway between medullary visceral zone and hypothalamic supraoptic nucleus or paraventricular nucleus involved in hyperosmotic regulation

In this study we try to simultaneously investigate the response of neurons and astrocytes of rats following hyperosmotic stimulation and test the possibility that the reciprocal pathways between medullary visceral zone (MVZ) and hypothalamic paraventricular nucleus (PVN) or supraoptic nucleus (SON). Hyperosmotic pressure animal model was established by administering 3% sodium chloride as drinking water to rats. The distribution and expression of the HRP retrogradely labeled neurons, Fos, tyrosine hydroxylase (TH) or vasopressin (VP) positive neuron and glial fibrillary acidic protein (GFAP) positive astrocytes in the MVZ, SON and PVN were observed by quadruplicate-labeling methods of WGA-HRP retrograde tracing combined with anti-Fos, TH (or VP) and GFAP immunohistochemical technique. Fos positive neurons within the MVZ, PVN and SON increased markedly. There were also a large number of GFAP positive structures in the brain and their distribution pattern was fundamentally similar or analogous to Fos positive neurons in the above-mentioned areas. The augmented GFAP reactivities took on hypertrophic cell bodies, thicker and longer processes. Quadruplicate immunohistochemical staining showed that a neuron could be closely surrounded by many astrocytes and they formed neuron-astrocytic complex (N-ASC). Fos+/TH+/HRP+/GFAP+ and Fos+/VP+/HRP+/GFAP+ quadruplicate labeled N-ASC could be found in the MVZ, PVN and SON, respectively. The present results indicated that the neurons and astrocytes might be very active following hyperosmotic pressure and N-ASC as a functional unit might serve to modulate osmotic pressure. There were reciprocal osmoregulation pathways between the MVZ and SON or PVN in the brain.     

S100和GFAP在猫上丘表浅层表达差异的免疫组织化学观察

目的比较青、老年猫上丘表浅层（superricial Superior Colliculus,sSC）星形胶质细胞中S100蛋白与胶质原纤维酸性蛋白（glial fibrillary acidic protein,GFAP）表达的老年性变化,并探讨其在动物视觉功能衰退中的意义。方法采用免疫组织化学方法（SABC法）示青、老年猫上丘表浅层S100免疫阳性反应（S100-immunoreactive,S100-IR）细胞及胶质纤维酸性蛋白免疫反应阳性（GFAP-immunoreactive,GFAP-IR）细胞。光镜下观察、拍照,并利用Image-ProExpress图像分析软件对上丘表浅层各层S100和GFAP免疫反应阳性细胞密度及其灰度值进行测量。结果与青年猫相比,老年猫上丘表浅层中S100蛋白与GFAP表达均有不同程度的显著增强（P〈0.01）。结论衰老进程中,上丘表浅层出现S100、GFAP表达增强,星形胶质细胞存在明显的反应性活化与增生,这对维持上丘表浅层神经元的活性和神经元之间的通讯联系,从而延缓老年性视觉功能衰退具有重要意义。     

Ganglioside Modulation of Cyclic AMP-Dependent Protein Kinase and Cyclic Nucleotide Phosphodiesterase In Vitro

The expression of glial fibrillary acidic protein (GFAP)-mRNA during mouse brain development and in astroglial primary cultures has been investigated by using two approaches: Northern-blot evaluation using a specific cDNA probe, and cell-free translation associated with immunoprecipitation. During brain maturation (4-56 days postnatal), the GFAP-mRNA underwent a biphasic evolution. An increase was observed between birth and day 15 (i.e., during the period of astroglial proliferation), which was followed by a decrease until day 56 (i.e., during astroglial cell differentiation). At older stages (300 days), an increase was observed, which might reflect gliosis. During astroglial in vitro development (7-32 days in culture), the GFAP-mRNA showed similar variations. An increase, observed during the period of astroglial proliferation (7-18 days), was followed by a decrease which occurred in parallel to marked changes in cell shape, cell process outgrowth, and the organization and accumulation of gliofilaments. During the same culture period (7-32 days), alpha-tubulin mRNA, which was used as an internal standard, did not vary significantly. These results show that the increase of the GFAP protein and of gliofilaments observed both in vivo and in vitro during astroglial differentiation cannot be ascribed to an accumulation of the GFAP-mRNA. It might be that more than one mechanism regulates the levels of free and polymerized GFAP and of its encoding mRNA.