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作 者:郭蕊萌[1] 尹利荣[1] 王宇全[1] 马洪达[1]
出 处:《天津医科大学学报》2013年第3期206-208,F0003,共4页Journal of Tianjin Medical University
基 金:天津医科大学科学基金资助项目(2010ky49)
摘 要:目的:探讨子宫内膜异位症(EMs)患者在位及异位内膜中CD146的过表达在EMs发病机制中的作用。方法:免疫组化方法检测50例EMs患者(EMs组)在位内膜(增殖期26例,分泌期24例)、异位内膜及50例非EMs患者(对照组)子宫内膜(增殖期22例,分泌期28例)中CD146表达情况及微血管密度(MVD),结合临床资料进行比较分析。结果:EMs组在位、异位内膜中CD146阳性率、MVD值均高于对照组(P<0.05),但EMs组在位、异位内膜之间相比无统计学差异(P>0.05);EMs组在位分泌期内膜CD146阳性率、MVD值均高于增殖期内膜(P<0.05),而对照组内此差异无统计学意义(P>0.05);EMs组在位、异位内膜CD146阳性率、MVD值均与美国生育协会修正标准(R-AFS)评分成正相关(P<0.05);EMs组在位、异位内膜和对照组内膜CD146阳性率与MVD值呈正相关(P<0.05)。结论:CD146在EMs患者在位、异位内膜中的过表达可能通过促血管形成机制参与了EMs的发生、发展。Objective: To discuss the relationship of pathogenesis and overexpression of CD146 in ectopic and eutopic endometrium of patients with endometriosis (EMs). Methods: Immunohistochemical staining was used to detect the expression of microvessel density (MVD) and CD146 in 50 eutopic (26 proliferative phase, 24 secretory phase), ectopic endometrium of EMs patients (EMs group) and 50 normal endometrium (control group)(22 proliferative phase, 28 secretory phase) .Combined with clinical material, results were analysed comparatively. Results: The expression of CD146 and MVD in eutopic, ectopic endometrium in EMs group were higher than those in con- trol group (P〈0.05), while there was no statistical differences between eutopic and ectopic endometrium in EMs group (P〉0.05);In EMs group, the expression of CD146 and MVD in eutopic secretory phase endometrium were higher than those in eutopic proliferative phase endomerium(P〈0.05),while this differents had no statistical significance in control group(P〉0.05); The expression of CD146 and MVD in eutopic and ectopic endometrium of EMs group were positively correlated with clinical stage (R-AFS)(P〈0.05); In eutopic, ectopic en- dometrium of EMs group and endometrium of control group, the expression of CD146 were positively correlated with MVD(P〈0.05). Con- clusion: The overexpression of CD146 in eutopic, ectopic endometrium of patients with EMs may be involves in the occurrence and de- velopment of the EMs through promoting angiogenesis.
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