200 resultados para X-ray computed tomography


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The characteristic Ll, Lα, Lβ and Lγx-rays of Au and energy shifts produced by 20–50MeV 16O5+ beams on a thick Au ilm are measured with a Si (Li) detector. Cross-section ratios of σ(Ll)/σ(Lα), σ(Lβ)/σ(Lα) andσ(Lγ)/σ(Lα) versus O5+ energy show that consistent calculations yield considerably better agreements. Energy shifts Ll, Lα, Lβ and Lγ x-rays of Au target increase with more incidence energy. The main application for these measurements is multi-element trace analysis through particle induced x-ray emission.

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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.

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We consider electron capture in fast collisions between a proton and hydrogen in the presence of an intense x-ray laser whose angular frequency omega is close to v(2)/2, where v is the collision velocity. We show that in such a case laser-induced capture becomes possible and that the latter proceeds via both induced photon emission and photon absorption channels and can, in principle, compete with kinematic and radiative electron capture.

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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.

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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.

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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.

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The X-ray spectra of Nb surface induced by Arq+ (q = 16,17) ions with the energy range from 10 to 20 keV/q were studied by the optical spectrum technology. The experimental results indicate that the multi-electron excitation occurred as a highly charged Ar16+ ion was neutralized below the metal surface. The K shell electron of Ar16+ was excited and then de-excited cascadly to emit K X-ray. The intensity of the X-ray emitted from K shell of the hollow Ar atom decreased with the increase of projectile kinetic energy. The intensity of the X-ray emitted from L shell of the target atom Nb increased with the increase of projectile kinetic energy. The X-ray yield of Ar17+ is three magnitude orders larger than that of Ar16+.

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The 10-20 qkeV Ar16+ and Ar17+ ions produced by SECRAL enter on metallic surface of Zr. In this interaction, the multi-electron excitation possibly occurred in the neutralization of the highly charged Ar16+ ions, which produced vacancy in the K shell. Electron of the high n state de-excited to K vacancy gives off X-ray. The experimental results show that X-ray intensities for the Ar hollow atom decrease with increase of incidence energy, and L beta X-ray intensities of target atom Zr increase with increasing incidence energy. K alpha X-ray yield per ion for Ar17+ was five orders of magnitude greater than that for Ar16+

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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.

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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.