小神经胶质

Between P14 and P21,CIAPIN1 immunoreaction in the brain,heart and liverbecame much lower. However,between P21 and P28,CIAPIN1 immunoreactionin the heart,brain,liver and skeletal muscle became much lower,while with thekidney development,CIAPIN1 immunoreaction in the kidney became higher. Invarious tissues from adult mouse,CIAPIN1 immunoreaction could be seen incardiac muscle cell,brain,hepatocyte,epithelium of renal tubule,skeletal muscle,lung tissue,gastric mucosa and gland,acinus lienalis.2. Distribution of CIAPIN1 in normal fetal and adult human tissuesTo reveal the possible physiological role of CIAPIN1,we examined theexpression and distribution of CIAPIN1 in fetal and adult human tissues usingimmunohistochemistry. We found that CIAPIN1 was ubiquitously distributed infetal and adult tissues,and was localized in both the cytoplasm and the nucleus.

然而，在3个月大的成年鼠中，CIAPIN1阳性反应物在心、脑、肝和肾小管中的表达强度要低于P28小鼠；但CIAPIN1阳性反应物在成年鼠骨骼肌中较P28小鼠高。2、CIAPIN1蛋白在人5个月胚胎及成人多器官组织内的表达在人5月胚胎多器官组织中，CIAPIN1阳性反应物见于心脏、胆囊单层柱状上皮和粘膜、结肠粘膜、小肠粘膜和绒毛、肝脏、直肠腺体、胃粘膜、肾上腺束状带、甲状腺滤泡、脾索、胸腺小叶间隔、皮肤真皮层和汗腺、睾丸白膜和间质、脑组织内神经元和神经胶质、肺小支气管和肺泡、骨骼肌、肾脏皮髓质和肾小管、子宫内膜、胰腺腺泡和胰岛、卵巢、输卵管粘膜等绝大多数组织细胞。

Microglial activation may play a role in the pathogenesis of Huntington's disease.

小神经胶质细胞的活化可能在亨廷顿舞蹈病的病理发生中起一定作用。

Iron in the form of ferritin is highly toxic and may cause neural death and reactive gliosis. Astrocytes and microglia are responsible for uptake of excessive CSF iron in superficial siderosis.

星形胶质细胞和小胶质细胞可摄取脑脊液中过多的铁，而铁蛋白中铁的毒性又可导致神经元坏死和反应性神经胶质增生。

In addition, the inventive compounds can reduce the inflammatory component of diseases that affect the nervous system, for example, by reducing activation of the microglia and/or astrocytes and/or by reducing reactive gliosis.

另外，根据本发明的化合物特别通过减少小胶质细胞和/或星形细胞的活化和/或通过减少反应性的神经胶质增生而能够减少影响神经系统的疾病的炎性物质。

RESULTS The degenerative changes of nerve ending in Meissner's corpuscles were observed after 1 month of denervation, and the basic structure of the corpuscles had no obvious changes. After 3 months, the axons of corpuscles were disappeared, and the volume of corpuscles was shrunk. The basic structure of nerves was disappeared, and the lemmocyte and neurolemma plate were changed after 5 months.

结果 失神经1个月时触觉小体内的神经末梢已有溃变，触觉小体的基本结构无明显改变；3个月时轴突消失，触觉小体的体积开始萎缩；5个月时神经结构消失，膜细胞及其膜板亦开始改变；8个月时触觉小体内胶原纤维含量逐渐增多；12个月时触觉小体内膜结构与膜间基质完全消失，被胶原纤维代替。

After the cell growth curves was recorded, RPE cells of the 3-5th passages were utilized. 2、Three different siRNA (siRNAl,siRNA2,siRNA3) targeting against human cx43 gene and one negative control siRNA were designed and transfected into cultured human RPE cells via liposome reagent. The most effective siRNA can be determined by semi-quantitative reverse transcription PCRRT-PCR. 3、To the most effective siRNA, after transfected into human RPEs with different concentration, the cellular proliferate activities were messured by MTT colorimetry ; the percentages of RPE in different cell circle phase was assayed by FCM; the changes of phenotypical properities were observed with SCM; the protein expression of cx43 was studied through immunocytochemistry stain and Weston blot; the communication intercellular was calculated with FRAP; and the ability of recovery was assessed by using an in vitro wound healing model.4、The total proteins of siRNA1 and RPE were seperated by two-dimensional gel electrophoresis and visualized by silver staining. Proteins with significant expression alterations were selected and their peptide mass fingerprints (PMFs were obtained by matrix-assisted laser desorption/ionization time of flying mass spectrometry (MALDI-TOF-MS).The PMFs were used to search NCBInr database by Auto MS-Fit software.

实验方法：1、培养原代的人RPE细胞，经过细胞角蛋白、S-100和神经胶质原纤维酸性蛋白免疫细胞化学鉴定后，通过AO/PI染色技术确定培养细胞的存活率，描记其生长曲线，第3-5代用于以下细胞实验2、生物合成针对人cx43基因的三条小干扰RNA和一条阴性RNA通过脂质体转染RPE细胞后，通过RT-PCR的方法确定抑制效率最高的干扰片断3、将该片段以不同浓度通过阳离子脂质体转染培养的人RPE细胞后，采用MTT法观察其对细胞的增殖力的作用；通过流式细胞仪观察其对细胞周期的影响；通过扫描电镜观察其对细胞形态的影响；通过免疫细胞化学和Weston blot观察其对cx43蛋白表达的作用；采用激光共聚焦和荧光淬灭恢复技术观察荧光恢复速率平均百分率，评价其对细胞间通讯功能的影响；通过制作RPE细胞损伤模型，观察其对损伤修复能力的作用4、分离纯化转染siRNA的RPE组和正常对照组RPE细胞的全部蛋白质，应用等电聚焦电泳和SDS-PAGE双向电泳技术，银染显示分离出的蛋白质斑点，经凝胶图像分析软件对两个样本进行胶图分析，寻找差异蛋白点。

Using 11C--PK11195 positron emission tomography, we investigated microglial activation in HD presymptomatic gene carriers, its relationship with striatal neuronal dysfunction measured with 11C-raclopride PET, and the role of PK PET as a possible marker of subclinical disease progression in PGCs. Eleven HD PGCs underwent PK and RAC PET. Their results were compared with those of healthy controls.

利用11C--PK11195电子发射断层扫描，我们研究了HD的基因携带者症状发生前小神经胶质细胞的活化情况，它与纹状体的神经元的机能障碍的关系，以及PET可能作为PGCs亚临床症状进展的指标。11位HDPGCs接受了PK和RACPET检查，其结果与健康对照人群进行比较。

Using an in itro bioassay, we demonstrated that cytokine-actiated microglia release cytotoxins that kill retinal neurons.

应用体外生物测定技术，我们证明细胞因子活化的小神经胶质细胞释放杀死视网膜神经元的细胞毒素。

Minocycline represses diabetes-induced inflammatory cytokine production, reduces the release of cytotoxins from actiated microglia, and significantly reduces measurable caspase-3 actiity within the retina.

二甲胺四环素抑制糖尿病诱导的炎性细胞因子的产生，降低来自于活化的小神经胶质细胞的细胞因子的释放，同时显著降低视网膜内可检测的caspase-3的活性。

Furthermore, we provide evidence that the CD36 scavenger receptor and downstream kinases are involved in SYN-mediated microglial activation.

此外，CD36受体和下游的激酶参与SYN介导的小神经胶质的活化。

Breath, muscle contraction of the buttocks; arch body, as far as possible to hold his head, right leg straight towards the ceiling (peg-leg knee in order to avoid muscle tension).

呼气，收缩臀部肌肉；拱起身体，尽量抬起头来，右腿伸直朝向天花板（膝微屈，以避免肌肉紧张）。

The cost of moving grain food products was unchanged from May, but year over year are up 8%.

粮食产品的运输费用与5月份相比没有变化，但却比去年同期高8％。