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find Keyword "黄斑变性/病因学" 22 results
  • 补体在渗出型老年性黄斑变性中的作用研究进展

    补体系统是机体免疫系统的重要组成部分,广泛参与机体抗微生物防御反应,清除凋亡细胞和免疫复合物以及维持组织稳态,进行免疫调节。补体系统与老年性黄斑变性(AMD)发生也密切相关。在玻璃膜疣中,含有多种选择激活途径中的蛋白;补体成分基因变异也使AMD的发病风险大大增加。补体系统多种分子与AMD CNV形成关系密切,针对补体系统异常激活的治疗可能为渗出型AMD的治疗带来新的曙光。

    Release date:2016-09-02 05:26 Export PDF Favorites Scan
  • The role of 7-ketocholesterol in age-related macular degeneration

    The hallmark lesions of age-related macular degeneration (AMD) are drusen and basal linear deposit which are lipid substances deposited in Bruch membrane or the compartment on the Bruch membrane. There is a prevailing hypothesis that lipid and its oxidized derivant deposited in retina may have important roles in the pathogenesis of AMD. Lipid oxidation products are toxic, may affect the adjacent cells, induce inflammation, and trigger neovascularization.7-ketocholestoral (7KCh), a naturally occurring oxidized form of cholesterol, had been found to be toxic to retinal cells and able to induce chronic inflammation, which may play a critical role in the development of AMD. However the precise mechanism remains to be elucidated. Thus we will make a brief review of 7KCh and its association with AMD.

    Release date:2017-11-20 02:25 Export PDF Favorites Scan
  • 补体系统在老年性黄斑变性发病机制中的作用

    补体系统是机体固有免疫的重要组成部分,包含分布于血浆中或细胞表面的40多种物质,可通过经典途径、凝集素途径或替代途径激活。补体系统通过炎症免疫、血管内皮生长因子表达上调、氧化应激等途径参与和影响老年性黄斑变性(AMD)的发生发展过程;其相关分子的基因多态性与AMD的易感性息息相关;靶向补体系统的治疗对AMD也有一定的疗效。补体系统与AMD相互关系的研究将有助于进一步阐明AMD的发病机制并为其治疗提供新的方向。

    Release date:2016-09-02 05:26 Export PDF Favorites Scan
  • Stargardt病的研究现状

    Stargardt病(STGD)系一种遗传性疾病,眼底表现为黄斑部外侧对称的萎缩性改变,呈ldquo;靶心rdquo;状外观,可伴有眼底黄色斑点,荧光素眼底血管造影显示 特异的暗脉络膜征,吲哚青绿眼底血管造影证实有黄斑区的脉络膜毛细血管萎缩或充盈迟缓。近年来,分子遗传学研究已初步揭示了该病的致病相关基因位点。就有关该病的临床表现、发病机制和遗传学研究现状作一介绍。 (中华眼底病杂志,2000,16:213-284)

    Release date:2016-09-02 06:05 Export PDF Favorites Scan
  • The analysis of mitochondrial DNA point mutation at position 3243 in age-related macular degeneration

    Purpose To detect whether a 3243 point mutation existed in age-related macular degeneration (AMD). MethodsTwenty-six cases of wet form AMD patients, ten cases of dry form AMD patients were selected,and compared with twenty nomal controls. After collecting anti-coagulated blood samples, total cellular DNA were extracted and purified. Using polymerase chain reaction and restriction fragment long polymorphism techniques, the mtDNA Ararr;G point mutation at position 3243 were detected. Results After cleaveded by restriction endonuclease Apa I, a 294 bp fragment remained only in all detected DNA samples including twenty-six wet form AMD, and ten dry form AMD. No any other fragment appeared. The result showed that there was no Ararr;G mutation at position 3243 found in AMD. Conclusion It is suggested that mtDNA 3243 point mutation due to maternal inheritance might be not concerned with both wet form AMD and dry form AMD. (Chin J Ocul Fundus Dis,2000,16:231-232)

    Release date:2016-09-02 06:05 Export PDF Favorites Scan
  • 补体因子H与老年性黄斑变性

    Release date:2016-09-02 05:48 Export PDF Favorites Scan
  • 先天性视盘小窝合并黄斑病变三例

    Release date:2016-09-02 06:03 Export PDF Favorites Scan
  • β淀粉样蛋白在玻璃膜疣形成中的作用

    beta;淀粉样蛋白(Abeta;)是由淀粉样前体蛋白在体内经过一系列酶水解后形成的。生理情况下,Abeta;的生成和降解处于动态平衡中;当机体应激或众多因素刺激使这一平衡破坏时,Abeta;会在眼内大量聚集,成为玻璃膜疣的主要致病成分之一。Abeta;能与I因子和H因子等免疫因子相互作用,参与补体旁路途径的激活;还能与C1相互作用,参与补体经典途径的激活,产生级联放大效应,激活下游的免疫分子和炎症分子,参与老年性黄斑变性(AMD)的形成过程。敲除表达Abeta;降解酶的基因,能成功建立AMD模型;通过抑制Abeta;生成及其作用,有可能成为治疗AMD的新靶点。

    Release date:2016-09-02 05:41 Export PDF Favorites Scan
  • 老年性黄斑变性姐妹二例

    Release date:2016-09-02 06:07 Export PDF Favorites Scan
  • The regulation of miRNA in age-related macular degeneration

    MiRNAs are stable small RNAs that are expressed abundantly in animals and plants. They can bind to the 3'-untranslated region of the target mRNA, and regulate its expression at the post-transcriptional level. The miRNAs’ abnormal expression and its following abnormal biological regulation are closely related to the occurrence and development of age-related macular degeneration (AMD), including inflammatory response, oxidative stress injury, phagocytosis dysfunction and abnormal angiogenesis. Since the dysregulation of miR-155, miR-125b and miR-34a seems to play a more important role in AMD, these microRNAs may be expected to become the new biomarkers and therapeutic targets for AMD.

    Release date:2020-08-18 06:26 Export PDF Favorites Scan
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