RADIATION CYTOGENETICS

在高等真核细胞中，染色体畸变是 主要参与了所有重要的生物效应 电离辐射，包括细胞生殖性死亡 通过放射治疗癌症的中心，以及肿瘤的发生 低水平对人类人口的主要危害 电离辐射暴露。该项目的目标是 更好地理解像差的机制 形成；识别和表征影响类型的因素 和辐射产生的像差的频率；以及 探索和开发量化的新方法 低水平辐射暴露遗传效应的测量。 具体地说，我们的目标是研究病变的性质 这导致了像差的形成，包括对 过早表达的间期染色体断裂 浓缩染色体(PCCs)以及有丝分裂染色体。 将在与其他药物治疗后进行比较 比也能产生DNA双链的电离辐射 休息一下。将进行进一步的具体研究，以 确定是否发生间期染色体断裂 优先于常染色质或异染色质，以及 紫外线和X射线引起的中期像差主要发生在 田鼠细胞中的一种或另一种具有巨型 异染色性染色体。抑菌作用的研究进展 X射线诱导的PCC断裂重新连接或表达增加 使用等渗盐、Ara-A和咖啡因治疗也可以 要强调影响之间的关系 观察对PLD和SLD的“修复”。此外，研究将是 在杂交细胞中进行缺陷的互补 来自共济失调-毛细血管扩张症患者的细胞；首先，看看 缺陷是否会导致染色单体产生像差 来自G1x-射线的辐射可以通过互补在 第二，确定一个人的染色体位置 纠正导致过敏的缺陷的人类基因 在对X射线敏感的CHO细胞突变体中。最后，我们会 尝试测量X射线诱发的染色体异常 比以前更高的分辨率和更高的灵敏度 使用EM制备联会膜复合体是可能的 早期粗线期小鼠精母细胞。 该项目的目标和目的对于 癌症放射治疗的科学基础和更全面的 评价低水平的遗传和致癌危害 电离辐射暴露。

In higher eukaryotic cells, chromosomal aberrations are principally involved in all of the important biological effects of ionizing radiations, including cell reproductive death that is central to cancer therapy by radiation, and oncogenesis that is the principal hazard to the human population from low level ionizing radiation exposure. The goals of this project are to gain a better understanding of the mechanisms of aberration formation; to identify and characterize factors influencing types and frequencies of aberrations produced by radiation; and to explore and develop new approaches to the quantitative measurement of genetic effects of low level radiation exposure. Specifically our aims focus on studies of the nature of lesions that lead to aberration formation including an investigation of interphase chromosome breakage as expressed in prematurely condensed chromosomes (PCCs) as well as mitotic chromosomes. Comparisons would be made following treatment with agents other than ionizing radiation that also produce DNA double strand breaks. Further specific studies would be carried out to determine whether interphase chromosome breakage occurs preferentially in euchromatin or heterochromatin and whether metaphase aberrations from U.V. and x-rays occur predominantly in one or the other in Microtus agrestus cells with giant heterochromatic sex chromosomes. Studies on the inhibition of rejoining or increased expression of x-ray induced PCC breaks using anisotonic salt, ara-A, and caffeine treatments would also be undertaken with emphasis on the relationship of the effects observed to PLD and SLD "repair". In addition, studies would be undertaken on the complementation in hybrid cells of a defect in cells from patients with Ataxia-Telangiectasia; first, to see whether the defect resulting in chromatid aberration production from G1 x-irradiation can be corrected by complementation in hybrids, and second to determine the chromosomal location of a human gene that corrects the defect leading to hypersensitivity in an x-ray sensitive mutant of CHO cells. Lastly, we would attempt to measure x-ray induced chromosomal abnormalities with higher resolution and greater sensitivity than has previously been possible, using EM preparations of synaptonemal complexes of early pachytene mouse spermatocytes. The goals and aims of this project are important for the scientific underpinning of cancer radiotherapy and for a fuller appreciation of genetic and oncogenic hazards of low level ionizing radiation exposure.