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修复/相互作用模型预测的细胞存活动力学。

Kinetics of cell survival as predicted by the repair/interaction model.

作者信息

Harder D, Virsik-Peuckert P

出版信息

Br J Cancer Suppl. 1984;6:243-7.

PMID:6582912
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2149156/
Abstract

A functional relationship determining the survival curve for reproductive cell death caused by low-LET radiation is derived on the basis of Lea's repair/interaction model. Radiation-induced primary lesions are assumed to interact pair-wise to form long-lived lethal lesions, simultaneously with the repair of the primary lesions. The formula derived for a short single irradiation gives a typical shouldered survival curve. At doses below the shoulder the interaction entirely occurs at low levels of primary lesion concentration, resulting in the parabolic shape of the logarithmic survival curve. At higher doses the interaction initially proceeds at high levels of primary lesion concentration, a state whose duration is determined by the dose and the finite speed of the first-order reaction of repair; this initial phase of the interaction results in the exponential tail of the survival curve. Survival after fractionated and protracted irradiation are also obtained. The dependence of cell survival on the irradiation conditions can be interpreted in terms of the basic parameters of the model.

摘要

基于利的修复/相互作用模型,推导了一个确定低传能线密度辐射导致生殖细胞死亡存活曲线的函数关系。假定辐射诱导的原初损伤两两相互作用形成长寿命致死性损伤,同时原初损伤进行修复。为单次短时间照射推导的公式给出了典型的具有肩区的存活曲线。在肩区以下剂量,相互作用完全发生在低水平的原初损伤浓度下,导致对数存活曲线呈抛物线形状。在较高剂量下,相互作用最初在高水平的原初损伤浓度下进行,该状态的持续时间由剂量和一级修复反应的有限速度决定;相互作用的这个初始阶段导致存活曲线的指数尾部。还得到了分次照射和持续照射后的存活情况。细胞存活对照射条件的依赖性可以根据模型的基本参数来解释。

相似文献

1
Kinetics of cell survival as predicted by the repair/interaction model.修复/相互作用模型预测的细胞存活动力学。
Br J Cancer Suppl. 1984;6:243-7.
2
Lethal and potentially lethal lesions induced by radiation--a unified repair model.辐射诱导的致死性和潜在致死性损伤——一种统一的修复模型。
Radiat Res. 1986 May;106(2):252-70.
3
A simple model of radiation action in cells based on a repair saturation mechanism.
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4
[Population kinetics of microcolonies causing "shouldered" survival curves at low LET].[低传能线密度下导致“肩部”存活曲线的微菌落的群体动力学]
Strahlentherapie. 1982 Jul;158(7):440-3.
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Induction and repair of DNA double-strand breaks in the same dose range as the shoulder of the survival curve.在与存活曲线肩部相同剂量范围内诱导和修复DNA双链断裂。
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Implications of repair models for LET effects and other radiobiological phenomena.修复模型对传能线密度(LET)效应及其他放射生物学现象的影响。
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Induction and disappearance of G2 chromatid breaks in lymphocytes after low doses of low-LET gamma-rays and high-LET fast neutrons.低剂量低传能线密度γ射线和高传能线密度快中子照射后淋巴细胞中G2期染色单体断裂的诱导与消失
Int J Radiat Biol. 2002 Apr;78(4):249-57. doi: 10.1080/09553000110102003.
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[Quantitative description of the process of radiation inactivation of cells. VII. Nature of primary radiation lesions leading to reproductive cell death].[细胞辐射失活过程的定量描述。VII. 导致生殖细胞死亡的初级辐射损伤的性质]
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Tests of the double-strand break, lethal-potentially lethal and repair-misrepair models for mammalian cell survival using data for survival as a function of delayed-plating interval for log-phase Chinese hamster V79 cells.利用对数生长期中国仓鼠V79细胞存活数据作为延迟接种间隔的函数,对哺乳动物细胞存活的双链断裂、潜在致死-致死和修复-错配修复模型进行测试。
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Recovery after exposure to high LET-radiation.暴露于高传能线密度辐射后的恢复情况。
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本文引用的文献

1
Numerical relationship between cells with radiation-induced chromosome aberrations and cells lethally injured by radiation.
Radiat Environ Biophys. 1980;18(1):73-7. doi: 10.1007/BF01324376.
2
The shape of dose-survival curves for mammalian cells and repair of potentially lethal damage analyzed by hypertonic treatment.通过高渗处理分析哺乳动物细胞的剂量-存活曲线形状及潜在致死损伤的修复。
Radiat Res. 1981 Sep;87(3):613-34.
3
Hypothesis. Elkind recovery and "sub-lethal damage": a misleading association?假设。埃尔金德恢复与“亚致死损伤”:一种误导性的关联?
Br J Radiol. 1977 Jul;50(595):459-67. doi: 10.1259/0007-1285-50-595-459.