Measurement of the inelastic branch of the O-14(alpha, p)F-17 reaction: Implications for explosive burning in novae and x-ray bursters

A measurement of the inelastic component of the key astrophysical resonance in the 14O(α,p)17F reaction for burning and breakout from hot carbon-nitrogen-oxygen (CNO) cycles is reported. The inelastic component is found to be comparable to the ground-state branch and will enhance the 14O(α,p)17F reaction rate. The current results for the reaction rate confirm that the 14O(α,p)17F reaction is unlikely to contribute substantially to burning and breakout from the CNO cycles under novae conditions. The reaction can, however, contribute strongly to the breakout from the hot CNO cycles under the more extreme conditions found in x-ray bursters.

NADPH oxidase-mediated generation of reactive oxygen species: A new mechanism for X-ray-induced HeLa cell death

Oxidative damage is an important mechanism in X-ray-induced cell death. Radiolysis of water molecules is a source of reactive oxygen species (ROS) that contribute to X-ray-induced cell death. In this study, we showed by ROS detection and a cell survival assay that NADPH oxidase has a very important role in X-ray-induced cell death. Under X-ray irradiation, the upregulation of the expression of NADPH oxidase membrane Subunit gp91(phox) was dose-dependent. Meanwhile, the cytoplasmic subunit p47(phox) was translocated to the cell membrane and localized with p22(phox) and gp91(phox) to form reactive NADPH oxidase. Our data Suggest, for the first time, that NADPH oxidase-mediated generation of ROS is an important contributor to X-ray-induced cell death. This suggests a new target for combined gene transfer and radiotherapy.

L-shell x-ray yields and production cross sections of Zr and Mo bombarded by slow highly charged Ar16+ ions

The L-shell x-ray yields of Zr and Mo bombarded by slow Ar16+ ions are measured. The energy of the Ar16+ ions ranges from about 150keV to 350keV. The L-shell x-ray production cross sections of Zr and Mo are extracted from these yields data. The explanation of these experimental results is in the framework of the adiabatic directionization and the binding energy modified BEA approximation. We consider, in the slow asymmetric collisions such as Ar and Mo/Zr, the transient united atoms (UA) are formed during the ion-surface interaction and the direct-ionization is the main mechanism for the inner-shell vacancy production. Generally, the theoretical results are in good agreement with the experimental data.

Kinetic energy and charge state effects in the X-ray emission of Mo surface induced by Xeq+ (q=25, 29) ions

L-shell X-ray spectra of Mo surface induced by Xe25+ and Xe29+ were measured. The X-ray intensity was obtained in the kinetic energy range of the incident ions from 350 to 600 keV. The relationship of X-ray intensity with kinetic energy of the projectile and its charge state were studied, and the simple explanation was given.

X-ray spectra induced by Xe-129(q+) impacting the metal surface

Using the slow highly charged ions Xe-129(q+) (q = 25, 26, 27; initial kinetic T-0 <= 4.65 keV/a.u.) to impact Au surface, the Au atomic M alpha characteristic X-ray spectrum is induced. The result shows that as long as the charge state of projectile is high enough, the heavy atomic characteristic X-ray can be effectively excited even though the incident beam is very weak (nA magnitude), and the X-ray yield per ion is in the order of 10(-8) and increases with the kinetic energy and potential energy of projectile. By measuring the Au M alpha-X-ray spectra, Au atomic N-level lifetime is estimated at about 1.33x10(-18) s based on Heisenberg uncertainty relation.

Antioxidant N-acetylcysteine attenuates the acute liver injury caused by X-ray in mice

The aim of this study was to evaluate the protective effects of different doses and administration modes of N-acetylcysteine (NAC) against X-ray-induced liver damage in mice. Kun-Ming mice were divided into four groups, each composed of six animals: two control groups and two NAC-treated groups. An acute study was carried out to determine alterations in lipid peroxidation (determined by measuring malondiadehyde (MDA) level), glutathione (GSH) content and superoxide dismutase (SOD) activity (assayed by colorimetric method), and DNA damage (characterized by DNA-single strand break using with comet assay) as well as cell apoptosis (measured by flow cytometry) at 12 h after irradiation. The results showed that there were dose-related decreases in MDA level, DNA damage and cell apoptosis, and dose-dependent increases in GSH content and SOD activity in all NAC-treated groups compared to control groups, indicating that pre-treatment or post-treatment with NAC significantly attenuates the acute liver damage caused by X-ray. In addition, significant positive correlations were observed between MDA level and DNA damage or cell apoptosis, implying that lipid peroxidation plays a major role in X-ray-induced liver injury. The data suggest that NAC exerts its radioprotective effect by counteracting accumulated reactive oxygen species in the liver through its properties as a direct antioxidant and a GSH precursor, when administered before or after X-ray irradiation.

Study on the apoptosis and Bcl-2/Bax expression of human hepatoma SMMC-7721 cells after exposure to heavy-ion and X-ray irradiations

This study is aimed at observing the apoptosis and Bcl-2/Bax gene expression of mammalian cells following heavy-ion and X-ray irradiations. Exponentially growing human hepatoma SMMC-7721 cells cultured in vitro were irradiated with a C-12 ion beam of 50 MeV/u (corresponding to a LET value of 44.56 keV/mu m) from Heavy Ion Research Facility in Lanzhou (HIRFL) at doses varying from 0 to 3 Gy. The X-ray irradiation (8 MV) was performed in the therapy unit of the General Hospital of the Lanzhou Military Area. Survival fractions of irradiated cells at various doses were measured by means of MTT assay. Apoptotic cells after irradiation were analyzed with fluorescence microscope and flow cytometer (FCM). Immuno-histological assay were applied to detect the expression of Bcl-2/Bax genes in the irradiated cells. The survival fraction of SMMC-7721 cells decreased gradually (vs. control p<0.05) with increasing the dose of the carbon ion beam more obviously than X-ray irradiation, and the carbon ion irradiation efficiently induced cell apoptosis and significantly promoted the expression of Bax gene while Bcl-2 gene expression was restrained. High-LET heavy ion beam would induce cell apoptosis effectively than low-LET X-ray, and the apoptosis rate is correlated with the transcription of Bcl-2/Bax and the ratio of Bcl-2/Bax in human hepatoma SMMC-7721 cells after irradiation to heavy ion beam.

Potentiality of phosphorylation of BRCA1 at Ser 1524 to activate p21 in response to X-ray irradiation

The breast and ovarian cancer susceptibility gene BRCA1 encodes a nuclear phosphoprotein, which functions as a tumor suppressor gene. Many studies suggested that multiple functions of BRCA1 may contribute to its tumor suppressor activity, including roles in cell cycle checkpoints, apoptosis and transcription. It is postulated that phosphorylation of BRCA1 is an important means by which its cellular functions are regulated. In this study, we employed phospho-Ser-specific antibody recognizing Ser-1524 to study BRCA1 phosphorylation under conditions of DNA damage and the effects of phosphorylation on BRCA1 functions. The results showed that 10 Gy X-ray treatment significantly induced phosphorylation of Ser-1524 but not total BRCA1 protein levels. The expression both of p53 and p21 increased after irradiation, but ionizing radiation (IR) -induced activation of p21 was prior to that of p53. The percentages of G0/G1 phase remarkably increased after IR. In addition, no detectable levels of 89 kDa fragment of PARP, a marker of apoptotic cells, were observed. Data implied that IR-induced phosphorylation of BRCA1 at Ser-1524 might activatep21 protein, by which BRCA1 regulated cell cycle, but play no role in apoptosis.

X-ray photoelectron spectroscopy study on GaN crystal irradiated by slow highly charged ions

We utilize slow highly charged ions of Xeq+ and Pbq+ to irradiate GaN crystal films grown on sapphire substrate, and use X-ray photoelectron spectroscopy to analyze its surface chemical composition and chemical state of the elements. The results show that highly charged ions can etch the sample surface obviously, and the GaN sample irradiated by highly charged ions has N depletion or is Ga rich on its surface. Besides, the relative content of Ga-Ga bond increases as the dose and charge state of the incident ions increase. In addition, the binding energy of Ga 3d(5/2) electrons corresponding to Ga-Ga bond of the irradiated GaN sample is smaller compared with that of the Ga bulk material. This can be attributed to the lattice damage, which shifts the binding energy of inner orbital electrons to the lower end.

低速高电荷态重离子辐照的GaN晶体表面X射线光电子能谱研究；X-ray photoelectron spectroscopy study on GaN crystal irradiated by slow highly charged ions

利用低速高电荷态Xeq+和Pbq+离子对在蓝宝石衬底上生长的GaN晶体膜样品进行辐照,并利用X射线光电子能谱(XPS)对样品表面化学组成和元素化合态进行了分析.结果表明,高电荷态离子对样品表面有显著的刻蚀作用;经高电荷态离子辐照的GaN样品表面氮元素贫乏而镓元素富集;随着入射离子剂量和所携带电荷数的增大,Ga—Ga键相对含量增大;辐照后,GaN样品中Ga—Ga键对应的Ga3d5/2电子的束缚能偏小,晶格损伤使内层轨道电子束缚能向低端方向偏移.

低速~(40)Ar~(17+)离子入射金属Be表面发射的近红外光谱线和X射线谱；Infrared Light and X-ray Emissions of ~(40)Ar~(17+) Impacting on Be Surface ；

用速度不同的(动能EK=272和357keV,速度v=1.14×106和1.72×106m/s)的高电荷态离子40Ar17+分别入射金属Be表面,同时测量这种相互作用过程中产生的近红外光谱线和X射线谱。实验结果表明,在低速范围内(速度小于玻尔速度vBohr=2.19×106m/s),速度较小的40Ar17+离子在到达金属的表面临界距离Rc到进入表面(2—3原子层)的进程中,形成了较多的高激发态Ar原子,其退激辐射较强的光谱线,进而验证了经典过垒模型。