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21.
本文采用三个边界元模型对巷道底板上锚杆的不同布置形式对防治底鼓的效果进行了模拟研究。根据研究结果,提出采用在巷道底板上分期安装锚杆的方法,可有效地防治巷道底鼓。本文对巷道底鼓产生机理和防治措施的研究结果,具有一定的理论价值和应用参考价值。 相似文献
22.
The new phenylpropanoid diglycoside ligusinenoside A ( 1 ), and the two new 8,4′‐oxyneolignan(‘8‐O‐4′‐neolignan’) diglycosides ligusinenosides B ( 2 ) and C ( 3 ), together with nine known compounds, were isolated from the rhizomes of Ligusticum sinensis Oliv. The structures of 1 – 3 were elucidated on the basis of spectroscopic analyses. 相似文献
23.
24.
建立一个描述低能电子在多元多层介质中散射的物理模型,运用MonteCarlo方法模拟低能电子在靶体胶衬底中的复杂散射过程,在此基础上通过大量计算研究入射束能、胶层厚度、衬底材料等不同曝光条件对抗蚀剂沉积能密度分布的影响,获得沉积能分布规律:适量的低束能、薄胶层、低原子序数衬底可以使前散射电子对胶中沉积能密度分布的贡献增大、背散射电子的贡献减小,从而提高曝光分辨率.
关键词:
电子束曝光
MonteCarlo方法
低能电子散射
能量沉积 相似文献
25.
It is well known that topology and dynamics are two major aspects to determine the function of a network. We study one of the dynamic properties of a network: trajectory convergence, i.e. how a system converges to its steady state. Using numerical and analytical methods, we show that in a logical-like dynamical model, the occurrence of convergent trajectory in a network depends mainly on the type of the fixed point and the ratio between activation and inhibition links. We analytically proof that this property is induced by the competition between two types of state transition structures in phase space: tree-like transition structure and star-like transition structure. We show that the biological networks, such as the cell cycle network in budding yeast, prefers the tree-like transition structures and suggest that this type of convergence trajectories may be universal. 相似文献
26.
Chirped fiber grating was used in dispersion compensator. We tried to use the same phase mask to write fiber grating of different wavelength with two methods to reduce the price of the fiber grating. 相似文献
27.
Using the theoretically calculated point-defect total-energy values of Baraff and Schlüter in GaAs, anamphoteric-defect model has been proposed by Walukiewicz to explain a large number of experimental results. The suggested amphoteric-defect system consists of two point-defect species capable of transforming into each other: the doubly negatively charged Ga vacancyV
Ga
2–
and the triply positively charged defect complex (ASGa+V
As)3+, with AsGa being the antisite defect of an As atom occupying a Ga site andV
As being an As vacancy. When present in sufficiently high concentrations, the amphoteric defect systemV
Ga
2–
/(AsGa+V
As)3+ is supposed to be able to pin the GaAs Fermi level at approximately theE
v
+0.6 eV level position, which requires that the net free energy of theV
Ga/(AsGa+V
As) defect system to be minimum at the same Fermi-level position. We have carried out a quantitative study of the net energy of this defect system in accordance with the individual point-defect total-energy results of Baraff and Schlüter, and found that the minimum net defect-system-energy position is located at about theE
v
+1.2 eV level position instead of the neededE
v
+0.6 eV position. Therefore, the validity of the amphoteric-defect model is in doubt. We have proposed a simple criterion for determining the Fermi-level pinning position in the deeper part of the GaAs band gap due to two oppositely charged point-defect species, which should be useful in the future. 相似文献
28.
29.
30.
A calcium sensor in the sodium channel modulates cardiac excitability. 总被引:11,自引:0,他引:11
Hanno L Tan Sabina Kupershmidt Rong Zhang Svetlana Stepanovic Dan M Roden Arthur A M Wilde Mark E Anderson Jeffrey R Balser 《Nature》2002,415(6870):442-447
Sodium channels are principal molecular determinants responsible for myocardial conduction and maintenance of the cardiac rhythm. Calcium ions (Ca2+) have a fundamental role in the coupling of cardiac myocyte excitation and contraction, yet mechanisms whereby intracellular Ca2+ may directly modulate Na channel function have yet to be identified. Here we show that calmodulin (CaM), a ubiquitous Ca2+-sensing protein, binds to the carboxy-terminal 'IQ' domain of the human cardiac Na channel (hH1) in a Ca2+-dependent manner. This binding interaction significantly enhances slow inactivation-a channel-gating process linked to life-threatening idiopathic ventricular arrhythmias. Mutations targeted to the IQ domain disrupted CaM binding and eliminated Ca2+/CaM-dependent slow inactivation, whereas the gating effects of Ca2+/CaM were restored by intracellular application of a peptide modelled after the IQ domain. A naturally occurring mutation (A1924T) in the IQ domain altered hH1 function in a manner characteristic of the Brugada arrhythmia syndrome, but at the same time inhibited slow inactivation induced by Ca2+/CaM, yielding a clinically benign (arrhythmia free) phenotype. 相似文献