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find Keyword "黄斑变性/病因学" 22 results
  • 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
  • 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
  • Serum vitamin B12 and folic acid in exudative age-related macular degeneration patients

    Objective To investigate the serum levels of vitamin B12 and folic acid (FA) of exudative agerelated macular degeneration (AMD).Methods A total of 84 patients with exudative AMD(AMD group)and 78 patients with non-exudative AMD (control group) diagnosed at Xijing Hospital between June 2008 and September 2009 were assessed in this study. Serum vitamin B12 and FA levels were measured by chemiluminescence immunoassay. The statistical information of epidemiology and risk factors exposure histories were collected and compared.Results AMD group had significantly lower serum vitamin B12 levels [(247.51plusmn;93.92)ng/ml] compared with the control group [(312.52plusmn;143.08) ng/ml],the difference was statistical significance (t=5.013, P<0.001). Serum FA levels in AMD group [(5.64plusmn;3.72)ng/ml] were slightly lower than the control group [(10.14plusmn;4.48) ng/ml], the difference was not statistical significance (t=0.780, P=0.437).Conclusion People with lower serum vitamin B12have higher risk of exudative AMD. Low levels of serum vitamin B12 may relate with the occurrence of exudative AMD.

    Release date:2016-09-02 05:41 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
  • 老年性黄斑变性的危险因素研究进展

    老年性黄斑变性(AMD) 是引起老年人视力损害的主要原因,对其危险因素的识别和干预有助于筛选高危人群并指导早期治疗。其流行病学危险因素主要包括可改变的危险因素以及遗传危险因素。现就近年来心脑血管疾病危险因素、膳食、AMD候选基因等遗传标记物的研究进展等作一综述。

    Release date:2016-09-02 05:43 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
  • 老年性黄斑变性发病机制的研究进展

    老年性黄斑变性(AMD)是老年人视力丧失的主要原因。近年来,许多学者对AMD发病机制作了大量深入研究,发现老化与代谢失调、循环障碍、光损害与氧化损伤、炎症反应及相关的分子遗传学改变等,均与AMD发病有关。现就AMD发病机制研究进展综述如下。 (中华眼底病杂志, 2006, 22:283-285)

    Release date:2016-09-02 05:51 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
  • 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
  • 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
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