977 resultados para HL-60


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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

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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。

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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.

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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.

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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.

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A thick natural uranium target was bombarded with a 60 MeV/u O-18 beam. The neutron-rich isotope Ra-230 as the target residue was produced through the multinucleon transfer reaction (U-238-4p-4n). The barium and radium fraction as BaCl2 precipitate were radiochemically separated first from the mixture of uranium and reaction products. Then, the radium fraction was separated from BaCl2 precipitate by using cation exchange technique. The gamma-ray spectra of the Ra fraction were measured using an HPGe detector. The production cross sections of Ra-230 were obtained by a combination of the radiochemical separation technique and off-line gamma-ray spectroscopy. The cross section of Ra-230 has been determined to be 66 +/- 20 mu b.

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The neutron-rich target-like isotope Th-236 has been produced in the U-238-2p multinucleon transfer reaction between a 60 MeV/u O-18 beam and natural U-238 targets. The activities of thorium were determined after radiochemical separation of Th from the mixture of uranium and reaction products. The Th-236 isotope was identified by the characteristic gamma-rays of 642.2, 687.6 and 229.6 keV. The production cross section of Th-236 was determined to be 250 +/- 50 mu b.

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The brain of the Kun-Ming strain 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 of 12C6+ ion or Co-60 gamma-ray as challenging irradiation dose at 4 h after per-exposure. Body weight and serum growth hormone (GH) concentration were measured at 35th day after irradiation. The results showed that irradiation of mouse brain with 2 Gy of C-12(6+) ion or Co-60 gamma-ray significantly diminished mouse body weight and level of serum GH. The relative biological effectiveness values of a 2 Gy dose of C-12(6+) ion calculated with respect to Co-60 gamma-ray were 1.47 and 1.34 for body weight and serum GH concentration, respectively. Pre-exposure with a low-dose (0.05 Gy) of C-12(6+) ion or Co-60 gamma-ray significantly alleviated reductions of mouse body weight and level of serum GH induced by a subsequent high-dose (2 Gy) irradiation. The data suggested that low-dose ionizing irradiation can induce adaptive hormetic responses to the harmful effects of pituitary by subsequent high-dose exposure.

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为了研究低速高电荷态离子在C60薄膜中引起的势效应,用能量为200keV的高电荷态Xen+(n=3,10,13,15,17,20,22,23)离子辐照了C60薄膜。用原子力显微镜(AFM)和Raman散射技术分析了辐照过程中高电荷态Xen+离子所储存势能在C60薄膜中引起的效应,即势效应。AFM分析结果表明,辐照C60薄膜的表面粗糙度随辐照Xen+离子电荷态(即势能)的增加而减小,揭示了势效应的存在。而Raman分析结果表明,由于Xe离子的动能远大于其所储存的势能,因此,尽管有表面势效应的影响,但在Raman分析的深度范围内,弹性碰撞还是主导了C60薄膜的损伤过程。

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Irradiation effect in C-60 films induced by 170 keV B ion was investigated by means of Fourier transform infrared (FTIR) and Raman spectroscopies. The damage cross section sigma and the effective damage radius R are deduced from the experimental data of all four IR active modes and evident four Raman active modes of C-60 molecule. The differences on irradiation sensitivity and structural stability of the different active modes of C-60 molecule are compared. The results indicate that T-1u (4) of infrared active mode and A(g) (1) of Raman active mode are most sensitive for B ion irradiation. On the other hand T-1u (2) of infrared active mode and H-g (3) of Raman active mode are comparatively stable under B ion irradiation. (C) 2010 American Institute of Physics. [doi:10.1063/1.3512968]

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The structural stability of C-60 films under the bombardment of 1.95 GeV Kr ions is investigated. The irradiated C-60 films were analyzed by Fourier Transform Infrared (FTIR) spectroscopy and Raman scattering technique. The analytical results indicate that the irradiation induced a decrease of icosahedral symmetry of C-60 molecule and damage of C-60 films; different vibration modes of C-60 molecule have different irradiation sensitivities; the mean efficient damage radius obtained from experimental data is about 1.47 nm, which is in good agreement with thermal spike model prediction.

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近年来,放射治疗在肿瘤治疗中的作用受到了越来越多的重视,放疗技术和手段的迅速发展为人们选择放疗创造了更多的机会[1]。放疗是利用电离辐射对细胞,特别是细胞中的遗传物质DNA的损伤作用,诱发病灶部位不正常细胞的凋亡和坏死来治疗肿瘤的。即使制定了周密的放疗方案和计划,放疗过程中难免也会对正常组织和细胞造成一定程度的损伤,而且辐射的远后效应和旁效应的发现,也使得放射治疗肿瘤的安全性受到了很大的关注。要想充分发挥放疗的优势,而又使其对人体正常组织的毒副作用尽可能降低,就必须搞清楚电离辐射对细胞造成的各种损伤的类型及其分子机理。自从电离辐射的远后效应和旁效应被发现以来就一直是辐射生物医学领域的研究热点,国内外的科研人员进行了大量的实验试图解释它们的本质,可是几十年来相关领域的研究一直局限于细胞学的水平,在向分子水平前进的道路上遇到了巨大的困难[2,3]。目前对于电离辐射远后效应和旁效应的研究是相对独立进行的,很少有探讨二者相互关系的论文发表。本文试图在总结前人科研成果并结合对自己所取得的实验数据进行分析的基础上对电离辐射的远后效应、旁效应、基因不稳定性与电离辐射所产生的活性氧自由基的关系进行初步的探讨。实验方法与结果: 1.用X射线辐照人正常肝细胞系HL-7702细胞,运用胞质分离阻滞微核实验检测细胞微核率,AnnexinV-FITC细胞凋亡检测试剂盒检测细胞凋亡率,细胞微核率和凋亡率随着辐照剂量的增加而显著增加。X射线照射后细胞继续传代培养,第七代时不同剂量辐照后子代细胞微核率和凋亡率同未辐照细胞的微核率和凋亡率相比已经没有明显区别。对不同剂量辐照后传代七代的细胞再次照射2.5Gy相同的剂量,发现受初次不同剂量辐照的细胞其微核率和凋亡率再次出现明显差异,初次辐照剂量高的细胞再次相同剂量辐照后的微核率和凋亡率也高。 2.对不同剂量X射线辐照后的细胞继续传代到第十五代时用H2O2浓度为1ul/ml的培养基处理15min,发现受初次不同剂量辐照的细胞其微核率再次出现比较明显差异,初次辐照剂量高的细胞H2O2处理后的微核率也高。 3.对受到不同剂量X射线辐照的人正常肝细胞存活后代进行二次辐照,分两组分别给予1.5GyX射线和1Gy碳离子束辐照,并检测二次辐照后细胞的微核率,发现重离子束二次辐照后并不像X射线一样可以诱发初次X射线辐照造成的损伤信息的表达,而只是表现出二次重离子辐照所造成的损伤。结论: 1.X射线辐照导致了HL-7702细胞基因组不稳定性这一辐射远后效应,X射线二次辐照辐照存活细胞的子代细胞可以诱发辐射的远后效应(如基因组不稳定性)明显的表现; 2.X射线辐照导致的HL-7702细胞后代基因组不稳定性,可以通过H2O2处理而得以诱发,揭示电离辐射过程中产生的氧自由基可能与辐射的远后效应存在密切的联系; 3.电离辐射产生的ROS在诱发细胞产生微核中具有重要的作用,但是并非唯一的影响因素。 4.X射线和12C6+重离子束辐照后存活细胞的后代中的细胞损伤类型可能存在着本质上的区别