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1)  Ataxia telangiectasia
共济失调性毛细血管扩张
2)  ataxia-telangiectasia
毛细血管扩张性共济失调症
1.
Objective To study the effects of ataxia-telangiectasia mutation ATM on cell cycle after irradiation.
方法采用流式细胞技术,以源于正常人皮肤的纤维细胞系GM0639(GM细胞)和毛细血管扩张性共济失调症(AT)患者皮肤的纤维细胞系AT5BIVA(AT细胞)为对照,检测比较AT细胞、GM细胞、AT-ATM+细胞经60Coγ射线照射0、1、3、5、7、9 Gy后细胞周期的差异。
2.
High radiosensitivity of fibroblast cells (AT5BIVA cells) from skin of Ataxia-telangiectasia (A-T) pa-tients were studied by comparing with GM0639 (GM cells) from the skin of healthy adult.
研究毛细血管扩张性共济失调症(AT)患者皮肤的成纤维细胞系AT5BIVA(AT细胞)的应对电离辐射导致细胞氧化损伤的能力。
3.
The study is to observe effects of exogenous ATM gene on mRNA expression of hTERT (human te- lomerase reverse transcriptase) in fibroblast cells (AT5BIVA cells) from skin of Ataxia-telangiectasia (AT) patients and to study the regulation of ATM to hTERT.
通过观察外源性毛细血管扩张性共济失调症突变基因(Ataxia-telangiectasiamutation,ATM)对毛细血管扩张性共济失调症(Ataxia-telangiectasia,AT)患者皮肤的成纤维细胞系AT5BIVA(AT细胞)端粒酶逆转录酶(humantelomerasereversetranscriptase,hTERT)mRNA表达的影响,探讨ATM对hTERT的调控作用。
3)  Ataxia telangiectasia mutated
毛细血管扩张性共济失调突变基因
4)  ataxia telangiectasia mutated gene
共济失调性毛细血管扩张症基因
5)  ataxia telangiectasia mutated(ATM)
毛细血管扩张性共济失调症突变蛋白(ATM)
6)  Ataxia telangiectasis
共济失调毛细血管扩张症
1.
Ataxia telangiectasis is caused by the mutation of AT gene (ATM) and it is characterized by hypersensitivity to the radiation.
共济失调毛细血管扩张症(ataxiatelangiectasis,AT)是由ATM(ataxiatelangiectasismutant)基因突变所致,其突出特点是对放射线敏感。
2.
The mutation of AT gene(ATM) leads to the AT disease(ataxia telangiectasis), the cancer incidence of AT patients and its carriers are significantly higer than the normal persons.
共济失调毛细血管扩张症基因的突变 (ataxiatelangiectasismutatedgene,ATM)导致AT疾病 (共济失调毛细血管扩张症 )。
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共济失调性毛细血管扩张症


  又称"运动性毛细血管扩张症""Louis-Barr综合征"。本病为涉及多个系统的遗传性变性疾病。多数呈常染色体隐性遗传,具有家族性。临床特征为:婴幼儿期起病,进行性的*共济失调和球结膜、皮肤的显著毛细血管扩张,胸腺发育不全或不存在。反复的呼吸系统感染为本病的突出症状之一,病儿几乎均有侏儒症与性功能发育障碍,通常不出现第二性征,近半数病例将发生肿瘤,血内IgA降低,迟发性过敏反应功能减退。目前尚无有效治疗措施。
  
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