72 resultados para radiation dose


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An investigation of hardening the buried oxides (BOX) in separation by implanted oxygen (SIMOX) silicon-on-insulator (SOI) wafers to total-dose irradiation has been made by implanting nitrogen into the BOX layers with a constant dose at different implantation energies. The total-dose radiation hardness of the BOX layers is characterized by the high frequency capacitance-voltage (C-V) technique. The experimental results show that the implantation of nitrogen into the BOX layers can increase the BOX hardness to total-dose irradiation. Particularly, the implantation energy of nitrogen ions plays an important role in improving the radiation hardness of the BOX layers. The optimized implantation energy being used for a nitrogen dose, the hardness of BOX can be considerably improved. In addition, the C-V results show that there are differences between the BOX capacitances due to the different nitrogen implantation energies.

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The effect of implanting nitrogen into buried oxide on the top gate oxide hardness against total irradiation does has been investigated with three nitrogen implantation doses (8 x 10(15), 2 x 10(16) and 1 x 10(17) cm(-2)) for partially depleted SOI PMOSFET. The experimental results reveal the trend of negative shift of the threshold voltages of the studied transistors with the increase of nitrogen implantation dose before irradiation. After the irradiation with a total dose of 5 x 10(5) rad(Si) under a positive gate voltage of 2V, the threshold voltage shift of the transistors corresponding to the nitrogen implantation dose 8 x 10(15) cm(-2) is smaller than that of the transistors without implantation. However, when the implantation dose reaches 2 x 10(16) and 1 x 10(17) cm(-2), for the majority of the tested transistors, their top gate oxide was badly damaged due to irradiation. In addition, the radiation also causes damage to the body-drain junctions of the transistors with the gate oxide damaged. All the results can be interpreted by tracing back to the nitrogen implantation damage to the crystal lattices in the top silicon.

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Charge trapping in the fluorinated SIMOX buried oxides before and after ionizing radiation has been investigated by means of C-V characteristics. Radiation-induced positive charge trapping which results in negative shift of C-V curves can be restrained by implanting fluorine ions into the SIMOX buried oxides. Pre-radiation charge trapping is suppressed in the fluorinated buried oxides. The fluorine dose and post-implantation anneal time play a very important role in the control of charge trapping.

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Radiation hardness of SIMOX(separation by implanted oxygen)/NMOSFET by implanting N and F ion has been carefully studied in this paper.Both N and F ion implantation can reduce hole traps in the buried oxide and the interfacial regions,which consequently improves the radiation hardness,especially under high dose radiation conditions.Moreover,experimental data show that the higher dose of the N and F ion implantation is,the better radiation hardness is achieved.In order to minimize the influence on the threshold voltage of devices,it is important to choose suitable implantation dose and energy of N or F implantation that have smaller impact on the preradiation device performance.

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A process for fabricating n channel JFET/SOS (junction field-effect transistors on silicon-on-sapphire) has been researched. The gate p(+)n junction was obtained by diffusion, and the conductive channel was gotten by a double ion implantation. Both enhancement and depletion mode transistors were fabricated in different processing conditions. From the results of the Co-50 gamma ray irradiation experimental we found that the devices had a good total dose radiation-hardness. When the tot;ll dose was 5Mrad(Si), their threshold voltages shift was less than 0.1V. The variation of transconductance and the channel leakage current were also little.

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摘要: In order to improve the total-dose radiation hardness of the buried oxide of separation by implanted oxygen silicon-on-insulator wafers, nitrogen ions were implanted into the buried oxide with a dose of 10(16)cm(-2), and subsequent annealing was performed at 1100 degrees C. The effect of annealing time on the radiation hardness of the nitrogen implanted wafers has been studied by the high frequency capacitance-voltage technique. The results suggest that the improvement of the radiation hardness of the wafers can be achieved through a shorter time annealing after nitrogen implantation. The nitrogen-implanted sample with the shortest annealing time 0.5 h shows the highest tolerance to total-dose radiation. In particular, for the 1.0 and 1.5 h annealing samples, both total dose responses were unusual. After 300-krad(Si) irradiation, both the shifts of capacitance-voltage curve reached a maximum, respectively, and then decreased with increasing total dose. In addition, the wafers were analysed by the Fourier transform infrared spectroscopy technique, and some useful results have been obtained.

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In the present study, we investigated the mechanisms of apoptosis resistance and the roles of the phosphorylation of BRCA1, p21, the Bax/Bcl-2 protein ratio and cell cycle arrest in IR-induced apoptosis in MCF-7 cells. X-irradiation, in particular at low dose (1 Gy), but not carbon ion irradiation, had a significant antiproliferative effect on the growth of MCF-7 cells. 1 Gy X-irradiation resulted in G1 and G2 phase arrest, but 4 Gy induced a significant G1 block. In contrast, carbon ion irradiation resulted in a significant accumulation in the G2 phase. Concomitant with the phosphorylation of H2AX induced by DNA damage,carbon ion irradiation resulted in an approximately 1.9–2.8-fold increase in the phosphorylation of BRCA1 on serine residue 1524, significantly greater than that detected for X-irradiation. Carbon ion irradiation caused a dramatic increase in p21 expression and drastic decrease in Bax expression compared with X-irradiation. The data implicated that phosphorylation of BRCA1 on serine residue 1524 might,at least partially, induce p21 expression but repress Bax expression. Together, our results suggested that the phosphorylation of BRCA1 at Ser-1524 might contribute to the G2 phase arrest and might be an upstream signal involved in preventing apoptosis signal via upregulation of p21 and downregulation of the Bax/Bcl-2 ratio.

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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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Survivin is a member of the inhibitors of apoptosis (IAP) protein family that interferes with post-mitochondrial events including activation of caspases. To examine the regulation of survivin expression in response to irradiation with different linear energy transfer (LET), human hepatoma HepG2 cells were irradiated in vitro with X-rays and carbon ions. Cellular sensitivities to low- and high-LET radiation were determined by colony formation. Survivin expression at mRNA and protein level were measured with RT-PCR and Western blot analyses, respectively. Radiation-induced cell cycle arrest and apoptosis were investigated with flow cytometry. We found that low-LET X-rays induced dose-dependent increases in survivin expression. After exposure to high-LET carbon ions, survivin expression gradually increased from 0 to 4 Gy, and then declined at 6 Gy. More pronounced survivin expression, stronger G(2)/M phase arrest was observed after exposure to carbon ions in comparison with X-rays at doses from 0 to 4 Gy. These observations indicate that there is a differential survivin expression in response to different LET radiations and the cycle arrest mechanism may be associated with it. In addition, our data on induction of apoptosis are compatible with the assumption that survivin expression induced by low-LET X-rays radiation may play a critical role in inhibiting apoptosis. However, after irradiation with ions, an anti-apoptotic function of survivin is not evident, possibly because of the serious damage produced by densely ionizing radiation.

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Three human malignancy cell lines were irradiated with Co-60 gamma-rays. Initial chromatid breaks were measured by using the chemically induced premature chromosome condensation technique. Survival curves of cells exposed to gamma rays was linear-quadratic while the efficiency of Calyculin A in inducing PCC of G(2) PCC was about five times more than G(1) PCC. A dose-dependent increase in radiation-induced chromatid/isochromatid breaks was observed in G(1) and G(2) phase PCC and a nearly positive linear correlation was found between cell survival and chromatin breaks. This study implies that low LET radiation-induced chromatid/isochromatid breaks can potentially be used to predict the radiosensitivity of tumor cells either in in vitro experimentation or in in vivo clinical radiotherapy.

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The combination of ionizing radiation and gene therapy has been investigated. However, there are very few reports about the combination of heavy-ion irradiation and gene therapy. To determine if the pre-exposure to low-dose heavy ion beam enhances the suppression of AdCMV-p53 on non-small lung cancer (NSLC), the cells pre-irradiated or non-irradiated were infected with 20, 40 MOI of AdCMV-p53. Survival fraction and the relative biology effect (RBE) were determined by clonogenic assay. The results showed that the proportions of p53 positive cells in C-12(6+) beam induced AdCMV-p53 infected cells were more than 90%, which were significantly more than those in gamma-ray induced AdCMV-p53 infected cells. The pre-exposure to low-dose 12C6+ beam significantly prevented the G(0)/G(1) arrest and activated G(2)/M checkpoints. The pre-exposure to C-12(6+) beam significantly improved cell to apoptosis. RBEs for the C-12(6+)+ AdCMV-p53 infection groups were 30%-60%,20% -130% and 30%-70% more than those for the C-12(6+)_irradiated only, AdCMV-p53 infected only, and gamma-irradiation induced AdCMVp53 infected groups, respectively. The data suggested that the pre-exposure to low-dose C-12(6+) beam significantly promotes exogenous p53 expression in NSLC, and the suppression of AdCMV-p53 gene therapy on NSLC.

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Hypersensitive response of mammalian cells in cell killing to X- and gamma-rays has been reported at doses below 1 Gy. The purpose of this study was to examine the low dose sensitivity of human hepatoma SMMC-7721 cells irradiated with Co-60 gamma-rays and 50 MeV/u C-12 ions. Experiments using gamma-rays and charged particle irradiation were performed, particularly in the low dose range from 0 to 2 Gy. The survival effect of SMMC-7721 cells was measured by means of standard clonogenic assay in conjunction with a cell sorter. The result indicates SMMC-7721 cells showed hyper-radiosensitive response at low doses and increased radio-resistance at larger single doses for the carbon ions (LET = 45.2 keV/mu m) and the gamma-rays. However, the HRS/IRR effect caused by high-LET irradiation is different from that by low-LET radiation. This might possibly be due to the difference in the mode of energy deposition by particle beam and low-LET irradiation.

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The aim of this study was to estimate the acute effects of low dose C-12(6+) ions or X-ray radiation on human immune function. The human peripheral blood lymphocytes (HPBL) of seven healthy donors were exposed to 0.05 Gy C-12(6+) ions or X-ray radiation and cell responses were measured at 24 h after exposure. The cytotoxic activities of HPBL were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT); the percentages of T and NK cells subsets were detected by flow cytometry; mRNA expression of interleukin (IL)-2, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma were examined by real time quantitative RT-PCR (qRT-PCR); and these cytokines protein levels in supematant of cultured cells were assayed by enzyme-linked immunosorbent assays (ELISA). The results showed that the cytotoxic activity of HPBL, mRNA expression of IL-2, IFN-gamma and TNF-alpha in HPBL and their protein levels in supernatant were significantly increased at 24 h after exposure to 0.05 Gy C-12(6+) ions radiation and the effects were stronger than observed for X-ray exposure. However, there was no significant change in the percentage of T and NK cells subsets of HPBL. These results suggested that 0.05 Gy high linear energy transfer (LET) C-12(6+) radiation was a more effective approach to host immune enhancement than that of low LET X-ray. We conclude that cytokines production might be used as sensitive indicators of acute response to LDL (C) 2009 COSPAR. Published by Elsevier Ltd. All rights reserved.