1.23GeV Fe离子在C_(60)薄膜中形成潜径迹的Raman谱分析

用能量为1.23GeV的快Fe离子辐照了多层堆叠的C60薄膜。用Raman散射技术分析了快Fe离子在C60薄膜中由强电子激发引起的效应,主要包括辐照引起C60分子的聚合及其高温、高压相(HTHP)的形成,和在髙电子能损下C60晶体点阵位置上的C60分子向非晶碳的转变。由此演绎出了快Fe离子在C60薄膜中的损伤截面或潜径迹截面σ和潜径迹的半径Re,及其随沉积在电子系统中的能量密度的变化而变化的规律。

Ar~+和He~+离子与C_(60)碰撞后富勒希离子的激发机制

C60 在与重离子作用下的激发机制与入射离子能量、质量及电荷态有关。核阻止主要出现在低能重离子与C60 的碰撞中 ;而高能轻离子作用下 ,电子阻止迅速增强 ,成为主要的激发方式。本文中直接观察到由弹性碰撞引起的C+ 峰 ,及其丰度依赖于入射离子的质量。同时我们还发现电子阻止随入射离子能量 (7～ 2 0keV)增大相应增加 ,这与绝热量子分子动力学计算的结果一致。

60 MeV/u~(18)O离子同天然铀反应钡同位素截面的测定

通过60MeV/u18O离子照射天然铀靶产生Ba放射性同位素,使用BaCl2沉淀法从大量铀和其它反应产物混合物中分离出Ba.通过离线γ谱学方法测量了Ba样品的γ射线单谱,根据Ba同位素特征γ射线峰的强度及其它相关数据计算了Ba同位素的生成截面.发现在厚铀靶的情况下,缺中子Ba同位素仍有较高的截面.

快重离子辐照C_(60)薄膜的强电子激发效应研究

利用能量为 2 0GeV的13 6Xe和 2 7GeV的2 3 8U离子对C60 薄膜进行了辐照 ,并用傅立叶变换红外光谱、X射线衍射谱和拉曼散射技术分析了辐照过的C60 样品 ,在傅立叶变换红外光谱上 ,首次观察到一个位于 6 70cm-1处的 ,表征未知结构的新峰 ,研究了其强度随电子能损和辐照剂量的变化规律 .分析结果表明 ,电子能量转移主导了C60 薄膜的损伤过程 ;而损伤的部分恢复是由强电子激发的退火效应引起的 ;另外 ,离子的速度在损伤的建立过程中也起了一定的作用

Pollen record from red clay sequence in the central Loess Plateau between 8.10 and 2.60 Ma

IEECAS SKLLQG

重离子~(12)C对~(60)Coγ射线诱发人染色体畸变效应的比较研究

目的　重离子和高剂量率6 0 Coγ射线照射离体人血建立染色体畸变的剂量 效应曲线 ;比较重离子1 2 C照射与6 0 Coγ射线照射诱发染色体畸变的相对生物效能。方法　重离子1 2 C和6 0 Coγ射线照射离体人血 ,吸收剂量率为 3Gy min ,吸收剂量为 1 0～ 8 0Gy。主要记录染色体型畸变的非稳定性畸变 ,对双着丝粒体和着丝粒环做曲线拟合 ,并检验回归系数的显著性和曲线的拟合度。结果　重离子1 2 C和6 0 Coγ射线照射离体血诱发的染色体畸变 (双 +环 ) ,在 0～ 8Gy范围内 ,呈良好的剂量 效应关系。1 2 C离子诱发染色体畸变的RBE值是不恒定的 ,它随吸收剂量增加而减少 ,在 0 3～ 8 0Gy范围内 ,RBE值 (Dγ Dc)从 2 6 2到 1 0 0 ,平均 1 5 8。结论　1 2 C离子对6 0 Coγ射线照射诱发染色体畸变 ,在照射剂量较低时 ,有较高的生物效应。

重离子~(12)C~(6+)对~(60)Coγ射线诱发淋巴细胞微核效应的比较研究

目的　比较重离子束1 2 C6+对60 Coγ射线照射人离体血诱发淋巴细胞微核的效应。方法　用60 Coγ射线和地面加速器产生的重离子1 2 C6+(平均LET为 36 70keV μm) ,不同剂量照射离体人血 ,用CB微核法观察双核淋巴细胞的微核 ,计算重离子束1 2 C6+对60 Coγ射线的相对生物效能。结果　在 0～ 6Gy剂量范围内 ,重离子束1 2 C6+对60 Coγ射线的相对生物效能在 4 1 9～ 1 78之间 ,平均为 2 56。结论　重离子束1 2 C6+比60 Coγ射线有更高的生物效应

荷能离子在C_(60)薄膜中引起的辐照效应

用 Raman散射和 XPS技术分析了能量为几百 ke V到几百 Me V的多种离子在 C60 薄膜中引起的辐照效应 .分析结果表明 ,在低能重离子辐照的 C60 薄膜中 ,其晶态向非晶态的转变过程是由核碰撞主导的 .在快离子 (1 2 0 ke V的 H离子和 1 71 .2 Me V的 S离子 )辐照的情况下 ,电子能损起主导作用 .发现在 H离子辐照过程中 ,电子能损有明显的退火效应 ,致使 C60 由晶态向非晶态转变的过程中 ,经历了一个石墨化的中间过程 ;而在 S离子辐照的情况下 ,电子能损的破坏作用超过了退火效应 ,因此 ,在 C60 由晶态向非晶态转变的过程中 ,无石墨化的中间过程

低能离子在C_(60)薄膜中引起的辐照效应

用 Ｒａｍａｎ（拉曼）散射技术分析了 １２０ｋｅＶ的 Ｈ， Ａｒ和 Ｆｅ离子在 Ｃ６０薄膜中引起的辐照效应，主要指由晶态向非晶态的转变．分析结果表明，在Ｆｅ和Ａｒ离子辐照的Ｃ６０薄膜中，核碰撞主导了由晶态向非晶态的转变过程．而在Ｈ离子辐照的情况下，电子能损起主导作用，并发现在Ｈ离子辐照过程中，电子能损有明显的退火效应，致使由晶态向非晶态转变的过程中，经历了一个石墨化的中间过程。

Kinetic energies of C-n(+) (n <= 58) fragment ions produced by nanosecond laser impact on C-60

Laser-induced fragmentation of C-60 has been studied using a time-of-flight mass spectrometric technique. The average kinetic energies of fragment ions C-n(+) (n <= 58) have been extracted from the measured full width at half maximum (FWHM) of ion beam profiles. The primary formation mechanism of small fragment ion C-n(+) (n < 30) is assumed to be a two-step fragmentation process: C60 sequential decay to unstable C-30(+) ion and the binary fission of C-30(+). Considering a second photo absorption process in the later part of laser pulse duration, good agreement is achieved between experiment and theoretical description of photoion formation. (C) 2009 Elsevier B. V. All rights reserved.

Alleviation of pre-exposure of mouse brain with low-dose C-12(6+) ion or Co-60 gamma-ray on male reproductive endocrine damages induced by subsequent high-dose irradiation

Irradiation has been widely reported to damage organisms by attacking on proteins, nucleic acid and lipids in cells. However, radiation hormesis after low-dose irradiation has become the focus of research in radiobiology in recent years. To investigate the effects of pre-exposure of mouse brain with low-dose C-12(6+) ion or Co-60 gamma (gamma)-ray on male reproductive endocrine capacity induced by subsequent high-dose irradiation, the brains of the B6C3F(1) hybrid strain male mice were irradiated with 0.05 Gy of C-12(6+) ion or Co-60 gamma-ray as the pre-exposure dose, and were then irradiated with 2 Gy as challenging irradiation dose at 4 h after pre-exposure. Serum pituitary gonadotropin hormones, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), testosterone, testis weight, sperm count and shape were measured on the 35th day after irradiation. The results showed that there was a significant reduction in the levels of serum FSH, LH, testosterone, testis weight and sperm count, and a significant increase in sperm abnormalities by irradiation of the mouse brain with 2 Gy of C-12(6+) ion or Co-60 gamma-ray. Moreover, the effects were more obvious in the group irradiated by C-12(6+) ion than in that irradiated by Co-60 gamma-ray. Pre-exposure with low-dose C-12(6+) ion or Co-60 gamma-ray significantly alleviated the harmful effects induced by a subsequent high-dose irradiation.

Chromosomal aberrations induced by C-12(6+) ions and Co-60 gamma-rays in mouse immature oocytes

The ovaries of Kun-Ming strain mice (3 weeks) were irradiated with different doses of C-12(6+) ion or Co-60 gamma-ray. Chromosomal aberrations were analyzed in metaphase II oocytes at 7 weeks after irradiation. The relative biological effectiveness (RBE) of C C-12(6+) ion was calculated with respect to Co-60 gamma-ray for the induction of chromosornal aberrations. The C-12(6+) ion and Co-60 gamma-ray dose-response relationships for chromosomal aberrations were plotted by linear quadratic models. The data showed that there was a dose-related increase in frequency of chromosomal aberrations in all the treated groups compared to controls. The RBE values for C-12(6+) ions relative to (CO)-C-60 gamma-rays were 2.49, 2.29, 1.57, 1.42 or 1.32 for the doses of 0.5, 1.0, 2.07 4.0 or 6.0 Gy, respectively. Moreover, a different distribution of the various types of aberrations has been found for C-12(6+) ion and Co-60 gamma-ray irradiations. The dose-response relationships for C-12(6+) ion and (CO)-C-60 gamma-ray exhibited positive correlations. The results from the present study may be helpful for assessing genetic damage following exposure of immature oocytes to ionizing radiation.