MICROBEAM INITIATED SINGLE CELL DAMAGE & IN SITU HYBRIDIZATION

H001电离产生的能量在细胞内的沉积 辐射引发了一系列分子事件， 在细胞周期的这个阶段中，直到后来的细胞世代。 了解这些分子事件可以帮助我们理解 致癌过程，并最终规避或控制。 微束的独特之处在于它可以将辐射损伤传递到 其中已知细胞或许多细胞中的亚细胞区室。 另外，可以将精确地1个颗粒[或更多个]递送至 特定位点，并且已经发现1个α粒子导致 更少的细胞从G1期进入S期，从而导致细胞 周期延迟响应 然而，更多的细胞延迟而不是显示p53 p53应答组p21表达明显高于非p53应答组 细胞 很明显， 反应细胞的百分比，但有强烈的迹象表明， 对α粒子存在非随机的核内灵敏度 侮辱。 压力反应的开始似乎并不像 仅限于核扰动，但可以表现出以下邻居 或细胞质照射。 这对推断有影响 风险评估。

H001 The intracellular deposition of energy from ionizing radiations initiates a cascade of molecular events which can express within that phase of the cell cycle through to later cell generations. Understanding these molecular events can lead to an understanding of the carcinogenic process and ultimately to circumvention or control. The microbeam is unique in that it can deliver a radiation insult to a known cell amongst others or subcellular compartments in many cells. Additionally precisely 1 particle [or more] can be delivered to a specific site, and it has been found that 1 alpha particle results in fewer cells progressing from G1 into S phase, thereby causing a cell cycle delay response. However more cells are delayed than show a p53 response while p21 expression can be found in non p53 responding cells. Clearly there is a fluence dependent increase in the percentage of cells responding, with however a strong indication that there is a non-random intra-nuclear sensitivity to alpha particle insult. The initiation of a stress response does not appear to be confined to nuclear perturbation, but can manifest following neighbor or cytoplasmic irradiation. This has implications for extrapolations in risk estimation.