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婴幼儿血管瘤的发病机制及γ-干扰素治疗作用的研究

The Pathogenesis of Infantile Hemangioma and an Experimental Study on the Therapy for Infancy Hemangiomas with Recombinant Interferon-γ

【作者】 彭强

【导师】 刘文英;

【作者基本信息】 四川大学 , 外科学, 2006, 博士

【摘要】 第一部分 血管内皮祖细胞在血管瘤中的表达和作用 目的:婴幼儿血管瘤的具体发病机制目前仍不明确。近年来,有研究证实血管瘤中存在血管内皮祖细胞,提示血管瘤的发生可能与血管内皮祖细胞的表达和生长有关。本研究目的在于了解血管内皮祖细胞在血管瘤、血管畸形、正常皮肤组织和胎盘绒毛膜中的表达情况。探讨血管内皮祖细胞在血管瘤发病和生长中的作用。 方法:应用逆转录多聚酶链反应技术(RT—PCR)荧光探针法定量检测CD133mRNA在28例血管瘤(增生期13例、消退期15例)、11例血管畸形、12例正常皮肤组织和10例胎盘绒毛膜标本中的表达。比较不同组织间CD133mRNA的阳性率和含量差别。 同时,应用免疫组化方法检测血管内皮祖细胞标志抗原CD133、成熟血管内皮细胞标志抗原CD31、端粒逆转录酶(TERT)和细胞增殖核抗原(Ki-67)在血管瘤、血管畸形及正常皮肤组织中的表达。观察血管内皮祖细胞在血管瘤的血管形成中的形态学和组织学特征。 用Image pro plus 4.10版本的专业图像分析软件进行图像分析。每张切片在200倍光学显微镜下选取10个视野,每个视野统计100个细胞中的阳性细胞数、总数除以10,乘以100%,得到该免疫组化标记物的阳性细胞表达指数。 所有统计数据以百分率或均数±标准差((?)±s)的方式表示,在SPSS13.0统计软件下,阳性率计数资料行Fisher确切概率法卡方检验,计量资料行样本均数t检验、t′检验或方差分析,P<0.05为有统计学差别。

【Abstract】 Background/Purpose: Infantile hemangioma is one of the most common benign tumors in children. A important pathological character of hemangioma is that it could appear the excess proliferation of endothelial cells . It could grow rapidly during life early but regresses spontaneously beyond 1 age. The pathogenesis of hemangioma is still unclear. Recently, there were researches confirmed that endothelial progenitor cells(EPCs) were existed in hemangioma and EPCs contributed to the early growth of hemangioma. However, the role of EPCs in the growth of hemangioma and the way of EPCs proliferating remained unknown. The aim of this study was to investigate the expression of EPCs in hemangioma and to discuss the relations of the EPCs and pathogenesis in hemangioma.Methods: CD133mRNA expressed in 13 proliferating hemangioma specimens, 15 involuting hemangioma specimens, 11 vascular malformation specimens, 12 normal skin (foreskin)tissues and 10 placental chorion specimens were detected by reverse transcription-polymerase chain reaction(RT-PCR). Simultaneously, hemangiomas, vascular malformations and normal skin tissues were subjected to assay with immunohistochemistry for CD133, CD31, TERT and Ki-67.The process of EPCs proliferation was

  • 【网络出版投稿人】 四川大学
  • 【网络出版年期】2007年 03期
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