The structures and transformations on Si(113) surface

The surface structures of the Si(113)-(1 X 1), Si(113)-(3 X 1) and Si(113)-(3 X 2) have been studied theoretically by means of an ab initio quantum chemical CNDO method. We address not only the importance of the surface energy but also the energy minimization and the barrier height in the different structural conversion. We found that (1) the relaxed Si(113)-(1 X 1) structure. (2) the Si(113)-(3 X 1) close to the Si(113) Ranke (3 X 1)-2 model; (3) the atomic positions of Si(113)-(3 X 2) corrugated arrangement. (C) 1997 Elsevier Science B.V.

Kinetics of dissociative water adsorption on stepped Si(001), on Si(115), Si(113), Si(5,5,12) and Si(112)

We present photoelectron spectroscopic and low energy electron diffraction measurements of water adsorption on flat Si samples of the orientations (001), (115), (113), (5,5,12) and (112) as well as on curved samples covering continuously the ranges (001)-(117) and (113)-(5,5,12)-(112). On all orientations, water adsorption is dissociative (OH and H) and non-destructive. On Si(001) the sticking coefficient S and the saturation coverage Theta(sat) are largest. On Si(001) and for small miscuts in the [110]-azimuth, S is constant nearly up to saturation which proves that the kinetics involves a weakly bound mobile precursor state. For (001)-vicinals with high miscut angles (9-13 degrees), the step structure breaks down, the precursor mobility is affected and the adsorption kinetics changed. On (115), (113), (5,5,12) and (112), the values of S and Theta(sat) are smaller which indicates that not all sites are able to dissociate and bind water. For (113) the shape of the adsorption curves Theta versus exposure shows the existence of two adsorption processes, one with mobile precursor kinetics and one with Langmuir-like kinetics. On (5,5,12), two processes with mobile precursor kinetics are observed which are ascribed to adsorption on different surface regions within the large surface unit cell. From the corresponding values of S and Theta(sat), data for structure models are deduced. (C) 1997 Elsevier Science B.V.

Hydrogen adsorption induced surface reconstructions on Si(113) studied by LEED

Surface reconstructions on Si(113) induced by dissociated hydrogen adsorption have been studied using low energy electron diffraction (LEED). It has been found that: (1) at 300 K and 80 K temperatures, with the increase of hydrogen coverage on the surface, the (3 x 1) phase transferred continuously into a hydrogen saturated (1 x 1)-2H phase; (2) flashing of the (1 x 1)-2H surface at about 1100 degrees C resulted in a complete new phase of(1 x 3) and further annealing of the sample at 1250 degrees C gave back the starting surface of (3 x 1); (3) saturated hydrogen adsorption at a sample temperature of 700 degrees C resulted in a stable new phase of(1 x 2)-H and further saturation doses of hydrogen at other temperatures below 700 degrees C did not change the (1 x 2) LEED pattern; (4) annealing of the (I x 2)-H surface in the same manner as (2) gave similar results.

（113）面硅衬底上自组织生长的GeSi量子点及其光荧光

用透射电子显微镜观察了Si(113)衬底上由固态源分子束外延生长的自组织量子点的形貌，测量了其原生及退火后低温下的荧光光谱。对所得结果进行了分析。

（113）B-GaAs/As（0.3）Ga（0.7）As单量子阱结构的光致发光谱研究

于2010-11-23批量导入

H原子吸附对Si（113）表面的影响

采用半经验分子轨道理论方法AM1研究用Si_(16)H_(21)模拟的Si(113)高指数表面及其吸附H原子的体系,得到生成热和表面原子上受力随吸附的变化。从生成热分析得知,Si(113)表面上形成Si─H_2吸附比Si─H容易,且为放热吸附;受力分析指出了表面原子再构发生的趋向,而吸附则引起趋向改变。

Si（113）表面原子结构的低能电子衍射研究

于2010-11-23批量导入

Si（113）表面的原子结构

于2010-11-23批量导入

Si（113）表面电子结构的研究

于2010-11-23批量导入

Half-Lives of Superheavy Nuclei in Z=113 Alpha Decay Chain

The generalized liquid drop model (GLDM), including the proximity effects and centrifugal potential, and the cluster model with Cosh potential are used to study the half-lives of some Z=113 isotopes and their alpha-decay products.The experimental half-lives of (284)113, (283)113, (282)113and their alpha-decay products are well reproduced by the two models when zero angular momenta transfer is assumed. For (278)113 and its alpha-decay products, both the GLDM andthe cluster model could provide satisfactory results if we assume the alpha particle carry five units of angular momenta, which indicates that possible non zero angular momenta transfer and need further experimental measurements with high precision. Finally, we show that half-lives of alpha-decay are quite sensitive to the angular momentum transfers, and a formula could be used to describe the correlation between alpha-decay half-life and angular momentum transfer successfully.

Yeast screens identify the RNA polymerase II CTD and SPT5 as relevant targets of BRCA1 interaction.

BRCA1 has been implicated in numerous DNA repair pathways that maintain genome integrity, however the function responsible for its tumor suppressor activity in breast cancer remains obscure. To identify the most highly conserved of the many BRCA1 functions, we screened the evolutionarily distant eukaryote Saccharomyces cerevisiae for mutants that suppressed the G1 checkpoint arrest and lethality induced following heterologous BRCA1 expression. A genome-wide screen in the diploid deletion collection combined with a screen of ionizing radiation sensitive gene deletions identified mutants that permit growth in the presence of BRCA1. These genes delineate a metabolic mRNA pathway that temporally links transcription elongation (SPT4, SPT5, CTK1, DEF1) to nucleopore-mediated mRNA export (ASM4, MLP1, MLP2, NUP2, NUP53, NUP120, NUP133, NUP170, NUP188, POM34) and cytoplasmic mRNA decay at P-bodies (CCR4, DHH1). Strikingly, BRCA1 interacted with the phosphorylated RNA polymerase II (RNAPII) carboxy terminal domain (P-CTD), phosphorylated in the pattern specified by the CTDK-I kinase, to induce DEF1-dependent cleavage and accumulation of a RNAPII fragment containing the P-CTD. Significantly, breast cancer associated BRCT domain defects in BRCA1 that suppressed P-CTD cleavage and lethality in yeast also suppressed the physical interaction of BRCA1 with human SPT5 in breast epithelial cells, thus confirming SPT5 as a relevant target of BRCA1 interaction. Furthermore, enhanced P-CTD cleavage was observed in both yeast and human breast cells following UV-irradiation indicating a conserved eukaryotic damage response. Moreover, P-CTD cleavage in breast epithelial cells was BRCA1-dependent since damage-induced P-CTD cleavage was only observed in the mutant BRCA1 cell line HCC1937 following ectopic expression of wild type BRCA1. Finally, BRCA1, SPT5 and hyperphosphorylated RPB1 form a complex that was rapidly degraded following MMS treatment in wild type but not BRCA1 mutant breast cells. These results extend the mechanistic links between BRCA1 and transcriptional consequences in response to DNA damage and suggest an important role for RNAPII P-CTD cleavage in BRCA1-mediated cancer suppression.