24 resultados para DOSES
em Chinese Academy of Sciences Institutional Repositories Grid Portal
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Carbon ions with concentration of (0.6-1.5)% were implanted into silicon crystals at room temperature and Si1-xCx alloys were grown by solid phase epitaxy with high temperature annealing. The formation and characteristics of Si1-xCx alloys under different implanted carbon doses were studied. If the implanted carbon atom concentration was less than 0.6%, carbon atoms would tend to combine with the defects produced during implantation and it was difficult for Si1-xCx alloys to form during annealing at 850-950 degreesC. With the increase of implanted C concentration, almost all implanted carbon atoms would occupy substitution positions to form Si1-xCx alloys, but only part of implanted carbon atoms would occupy the substitution position to form Si1-xCx alloys as the implanted dose increased to 1.5 %. Most Si1-xCx alloy phases would vanish as the annealing temperature was increased higher.
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In order to improve the total-dose radiation hardness of the buried oxides(BOX) in the structure of separa tion-by-implanted-oxygen(SIMOX) silicon-on-insulator(SOI), nitrogen ions are implanted into the buried oxides with two different doses,2 × 1015 and 3 × 1015 cm-2 , respectively. The experimental results show that the radiation hardness of the buried oxides is very sensitive to the doses of nitrogen implantation for a lower dose of irradiation with a Co-60 source. Despite the small difference between the doses of nitrogen implantation, the nitrogen-implanted 2 × 1015 cm-2 BOX has a much higher hardness than the control sample (i. e. the buried oxide without receiving nitrogen implantation) for a total-dose irradiation of 5 × 104rad(Si), whereas the nitrogen-implanted 3 × 1015 cm-2 BOX has a lower hardness than the control sample. However,this sensitivity of radiation hardness to the doses of nitrogen implantation reduces with the increasing total-dose of irradiation (from 5 × 104 to 5 × 105 rad (Si)). The radiation hardness of BOX is characterized by MOS high-frequency (HF) capacitance-voltage (C-V) technique after the top silicon layers are removed. In addition, the abnormal HF C-V curve of the metal-silicon-BOX-silicon(MSOS) structure is observed and explained.
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Up to now, clinical trials of heavy-ion radiotherapy for superficially placed tumors have been carried out for six times and over 60 selected patients have been treated with 80—100 MeV/u carbon ions supplied by the Heavy Ion Research Facility in Lanzhou (HIRFL) at the Institute of Modern Physics, Chinese Academy of Sciences since November, 2006. A passive irradiation system and a dose optimization method for radiotherapy with carbon-ion beams have been developed. Experimental verification of longitudinally ...
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IEECAS SKLLQG
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This study provides a useful biodosimetry protocol for radiation accidents that involve high doses of heavy particle radiation. Human peripheral blood lymphocytes (PBLs) were irradiated in vitro with high doses (5–50 Gy) of charged heavy-ion particles (carbon ions, at an effective linear-energy-transfer (LET) of 34.6 keV/ m), and were then stimulated to obtain dividing cells. PBLs were treated with 100nMcalyculin A to force chromosomes to condense prematurely, and chromosome spreads were obtained and stained with Giemsa. The G2 prematurely condensed chromosome (G2-PCC) index and the number of G2-PCC including fragments (G2-PCC-Fs) per cell for each radiation dose point were scored. Dose-effect relationships were obtained by plotting the G2-PCC indices or G2-PCC-Fs numbers against radiation doses. The G2-PCC index was greater than 5% up to doses of 15 Gy; even after a 30Gy radiation dose, the index was 1 to 2%. At doses higher than 30 Gy, however, the G2-PCC indices were close to zero. The number of G2-PCC-Fs increased steeply for radiation doses up to 30 Gy at a rate of 1.07 Gy−1. At doses higher than 30 Gy, the numbers of G2-PCC-Fs could not be accurately indexed because of the limited numbers of cells for analysis. Therefore, the number of G2-PCC-Fs could be used to estimate radiation doses up to 30 Gy. In addition, a G2-PCC index close to zero could be used as an indicator for radiation doses greater than 40 Gy.
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In order to investigate the biological effects of heavy ion radiation at low closes and the different radiosensitivities of growing and non-growing plants. rice at different lift stages (dry seed, wet seed and seedling) were exposed to carbon ions at closes of 0 02, 0.2, 2 and 20 Gy. Radiobiological effects on survival, root growth and mitotic activity, as well as the induction of chromosome aberrations in root meristem. were observed The results show that radiation exposure induces a stimulatory response at lower close and an inhibitory response at higher dose on the mitotic activity of wet seeds and seedlings Cytogenetic damages are induced in both seeds and seedlings by carbon ion radiation at doses as low as 0.02 Gy Compared with seedlings. seeds are more resistant to the lethal damage and the growth rate damage by high doses of carbon ions, but are more sensitive to cytogenetic damage by low closes of irradiation Different types of radiation induced chromosome aberrations are observed between seeds and seedlings. Based on these results, the relationships between low close heavy ion-induced biological effects and the biological materials are discussed.
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In this work. an alpha-Al2O3:C crystal was directly grown by the temperature gradient technique (TGT) using Al2O3 and graphite powders as the raw materials. The optical, optically stimulated luminescence (OSL) properties and dosimetric characteristics of as-grown crystal were investigated. As-grown alpha-Al2O3:C crystal shows strong absorption band at 205, 230 and 256 nm. Three-dimensional thermoluminescence (TL) emission spectrum of the crystal shows a single emission peak at similar to 415 nm. The OSL decay curve can be fitted to two exponentials, the faster component and the slower component. The OSL response of the crystal shows a linear-sublinear-saturation characteristic. As-grown alpha-Al2O3:C crystal shows excellent linearity in the dose range from 5 x 10(-6) to 50 Gy. For doses higher than the saturation dose (100 Gy). the OSL sensitivity decreases as the dose increases. Crown Copyright (C) 2008 Published by Elsevier B.V. All rights reserved.
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The effects of ketamine, an N-methyl-D-aspartate (NMDA) antagonist, on memory in animals have been limited to the sub-anesthetic dose given prior to training in previous studies. We evaluated the effects of post-training anesthetic doses of ketamine to se
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The aim of the present Study was to investigate if different levels of circulating corticosterone (CORT) modulate the effect of nicotine on prepulse inhibition (PPI), a measure of sensorimotor gating that is disrupted in schizophrenia and other mental illnesses. Four groups of mice were investigated: sham-operated, adrenalectomized (ADX) and implanted with a cholesterol pellet, ADX and implanted with a 10 mg CORT pellet, or ADX and 50 mg, of CORT. Different CORT levels or doses of nicotine did not significantly affect startle responses. Baseline PPI was significantly reduced in mice implanted with the highest dose of CORT. In ADX mice implanted with cholesterol, nicotine treatment influenced PPI depending on the prepulse intensity. In ADX mice implanted with 50 mg of CORT, treatment with 10 mg/kg of nicotine caused a significant increase in PPI at all prepulse intensities. Binding studies showed that corticosterone treatment had significantly affected nicotinic acetylcholine receptor (nAChR) density in the mouse brain. Treatment with 50 mg CORT decreased I-125-epibatidine binding in the globus pallidus and I-125-alpha-bungarotoxin binding in the claustrum. These results suggest a possible interaction of corticosterone and nicotine at the level of the alpha4- and alpha7-type nAChR in the regulation of PPI. In situations of high circulating levels of corticosterone, nicotine may be beneficial to restore disruption of PPI. (C) 2004 Elsevier Ltd. All rights reserved.
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Drug addiction is increasingly viewed as the expression of abnormal associative learning following repeated exposures to the drugs of abuse Previous I studies have demonstrated that the patterns of repetition such as frequency and spacing are important to many kinds of learning and memory retention We hypothesized that drug repetition pattern might affect the reward-related learning although the total doses of the drug were the same. In the present study, we tested morphine-induced place preference following either regular or irregular pattern of morphine pairing in rats Regular morphine group received morphine administration daily at a regular time with the same dose Irregular morphine groups received morphine administration either at the same time but irregular doses, irregular time but same dose, or irregular time and irregular doses. We found that rats, who received irregular morphine pairing, exhibited similar acquisition of peace preference but different preference retentions compared with regular morphine-treated rats after the same total dose of morphine Rats, who received morphine administration at the same time but irregular doses and at irregular time and irregular doses, showed rapid disruption of place preference than the regular morphine group. Rats, who received morphine at irregular time but the same dose, showed similar retention of place preference to regular morphine group Our results suggest that the pattern of drug pairing plays an important role in the retention of reward-related memory This study may provide new evidence to broaden our understanding of the development and maintenance of drug craving (C) 2009 Elsevier B V. All rights reserved
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Chronic exposure to opiates impairs hippocampal long-term potentiation (LTP) and spatial memory, but the underlying mechanisms remain to be elucidated. Given the well known effects of adenosine, an important neuromodulator, on hippocampal neuronal excitability and synaptic plasticity, we investigated the potential effect of changes in adenosine concentrations on chronic morphine treatment-induced impairment of hippocampal CA1 LTP and spatial memory. We found that chronic treatment in mice with either increasing doses (20-100 mg/kg) of morphine for 7 d or equal daily dose (20 mg/kg) of morphine for 12 d led to a significant increase of hippocampal extracellular adenosine concentrations. Importantly, we found that accumulated adenosine contributed to the inhibition of the hippocampal CA1 LTP and impairment of spatial memory retrieval measured in the Morris water maze. Adenosine A(1) receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine significantly reversed chronic morphine-induced impairment of hippocampal CA1 LTP and spatial memory. Likewise, adenosine deaminase, which converts adenosine into the inactive metabolite inosine, restored impaired hippocampal CA1 LTP. We further found that adenosine accumulation was attributable to the alteration of adenosine uptake but not adenosine metabolisms. Bidirectional nucleoside transporters (ENT2) appeared to play a key role in the reduction of adenosine uptake. Changes in PKC-alpha/beta activity were correlated with the attenuation of the ENT2 function in the short-term (2 h) but not in the long-term (7 d) period after the termination of morphine treatment. This study reveals a potential mechanism by which chronic exposure to morphine leads to impairment of both hippocampal LTP and spatial memory.
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Very low doses (0.00001 mg/kg) of the alpha-2 adrenergic antagonist, yohimbine, improved working memory performance in a subset of aged monkeys. Improvement appeared to result from increased norepinephrine (NE) release onto postsynaptic alpha-2 adrenoceptors, as the response was blocked by the ''postsynaptic'' alpha-2 antagonist, SKF104078. Cognitive-enhancing effects of low dose yohimbine treatment may depend on aged animals retaining an intact, endogenous NE system. In contrast to yohimbine, the alpha-2 agonist, clonidine, has improved working memory in air aged animals examined. In the present study, clonidine's beneficial effects were also blocked by the postsynaptic antagonists SKF104078 and SKF104856, suggesting that clonidine acts by directly stimulating postsynaptic alpha-2 adrenoceptors. Beneficial doses of clonidine (0.01 mg/kg) and yohimbine (0.00001 mg/kg) were combined to see if they would produce additive effects on memory enhancement. This strategy was successful in young monkeys with intact NE systems but was not effective in the aged monkeys. These findings demonstrate that drugs that indirectly stimulate postsynaptic alpha-2 receptors by increasing NE release are not as reliable in aged monkeys as directly acting agonists that can replace NE at postsynaptic alpha-2 receptors.
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Dopamine (DA) D-1 receptor compounds were examined in monkeys for effects on the working memory functions of the prefrontal cortex and on the fine motor abilities of the primary motor cortex. The D-1 antagonist, SCH23390, the partial D-1 agonist, SKF38393, and the full D-1 agonist, dihydrexidine, were characterized in young control monkeys, and in aged monkeys with naturally occurring catecholamine depletion. In addition, SKF38393 was tested in young monkeys experimentally depleted of catecholamines with chronic reserpine treatment. Injections of SCH23390 significantly impaired the memory performance of young control monkeys, but did not impair aged monkeys with presumed catecholamine depletion. Conversely, the partial agonist, SKF38393, improved the depleted monkeys (aged or reserpine-treated) but did not improve young control animals. The full agonist, dihydrexidine, did improve memory performance in young control monkeys, as well as in a subset of aged monkeys. Consistent with D, receptor mechanisms, agonist-induced improvements were blocked by SCH23390. Drug effects on memory performance occurred independently of effects on fine motor performance. These results underscore the importance of DA D-1 mechanisms in cognitive function, and provide functional evidence of DA system degeneration in aged monkeys. Finally, high doses of D-1 agonists impaired memory performance in aged monkeys, suggesting that excessive D-1 stimulation may be deleterious to cognitive function.