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作 者:王军[1] 赵雪莲[2] 冯建飞[2] 张利[2] 王伟[2] 胡豫[1] 王宏[2]
机构地区:[1]华中科技大学同济医学院附属协和医院血液科,武汉430022 [2]郑州大学第三附属医院儿内科,郑州450052
出 处:《郑州大学学报(医学版)》2005年第4期623-625,共3页Journal of Zhengzhou University(Medical Sciences)
基 金:河南省医学科技创新人才工程计划项目豫卫科(2001)9号
摘 要:目的:观察再生障碍性贫血(AA)患儿骨髓单个核细胞(BMMNC)c-kit受体的表达。方法:采用SABC免疫细胞化学方法对58例AA患儿(慢性再生障碍性贫血(CAA)38例,重型再生障碍性贫血(SAA)20例)和29例正常儿童BMMNC上c-kit受体蛋白(CD117)进行检测,结果观察采用计算机病理图像分析系统进行分析处理,测定阳性细胞内产物平均光密度值(A值),对表达产物进行半定量分析;采用逆转录-聚合酶链反应方法(RT-PCR)对AA患儿和正常儿童BMMNC中c-kitmRNA进行检测,紫外照相并扫描后,进行半定量分析。结果:CAA组、SAA组和正常对照组CD117阳性细胞表达值(A值)分别为0.52±8.81、0.46±2.18、0.58±7.94,CAA组、SAA组与正常对照组比较差异无统计学意义(P均>0.05);CAA、SAA组与正常对照组c-kitmRNA的半定量表达值分别为0.85±0.10、0.79±0.09、0.86±0.12。CAA、SAA组与正常对照组比较差异亦无统计学意义(P均>0.05)。结论:AA患儿造血衰竭并非c-kit受体蛋白及mRNA低表达所致。Aim: To explore the expression of c-kit receptor in bone marrow mononuclear cells (BMMNC) in the children with aplastic anemia and its role in the pathogenesis of pediatric aplastic anemia. Methods: Immunocytochemistry and RT-PCR were employed to determine c-kit protein and c-kit mRNA expressions in the BMMNC of 38 cases of chronic aplastic anemia(CAA),20 cases of severe aplastic anemia(SAA) and 29 normal controls. Positive cells were identified by the presence of buffy granules.The staining was determined by computerized pathology image analyzing system.The relative amount of c GAAB2 kit mRNA was compared with the amount of β-actin mRNA by densitometrical scanning preformed on photomicrographs of ethidium-stained agarose gel. Results: The values of c-kit protein expression in CAA,SAA and controls were 0.52± 8.81,0.46±2.18,0.58±7.94, respectively, and there was no significant difference among them(P>0.05). The values of c-kit mRNA expression in CAA,SAA and control groups were 0.85±0.10,0.79± 0.09, 0.86±0.12, and there was no significant difference among them(P>0.05). Conclusion: Hematopoiesis failure of pediatric aplastic anemia is not attributed to lower expression of c-kit receptor on the BMMNC.
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