999 resultados para 1995_12130733 CTD-75 5401504
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由于Si/SiGe异质结构的带阶差主要发生在价带,为实现高效率的发光,本文从理论上设计了在硅基Si_(1-x) Ge_x虚衬底上外延应变补偿的Si/S_(1-y) Ge_y(y>x)量子阱的能带结构,将量子阱对电子的限制势垒提高到100meV以上.在实验上,采用300℃生长的Ge量子点插入层,制备出薄的SiGe驰豫缓冲层(虚衬底),表面Ge组份达到0.25,表面粗糙度小于2nm,驰豫度接近100%.在我们制备的SiGe缓冲层上外延了应变补偿SiGe/Si多量子阱结构,并初步研究了其发光特性.
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A novel InGaAs(LT-In0.25 Ga0.75 As) absorber grown by metal organic chemical vapor deposition at low temperature is presented.Using it as well as an output coupler,passive mode locking,which produces pulses as short as several hundred picoseconds for diode-end-pumped Nd∶YAG laser at 1.06μm,is realized.The pulse frequency is 150MHz.
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国科图
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研究了科尔沁沙地75种植物的结种量、种子形态、植物生活型关系。结果表明,灌木和半灌木(小半灌木)的结种量比草本植物的大;就草本植物而言,多年生植物的结种量较一、二年生植物的小;植物结种量和种子重量之间存在显著负相关;植物结种量和种子形状之间存在显著负相关,即种子越接近圆球形,结种量越大;占绝大多数的草甸植物结种量相对较小;而在物种数占总物种数的百分数相近时,草原植物的结种量最小,沙生植物的最大,杂草植物居中。
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A novel hard material of (W0.25Al75)C has been successfully prepared by the high-pressure sintering process without the addition of any binder phase. The high-pressure is a suitable and powerful technique for sintering the binderless hard material, the relative density of the hard material can reach 99.6% under high-pressure sintering. The density of the novel light hard material is only 6.2371 g cm(-3), which is much lighter than the normal hard material. The hardness of the light hard material can reach 18.89 GPa even the aluminum content get the astonished 75%.
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W1-xAlxC (x = 0.33, 0.50, 0.75, 0.86) solid solutions have been synthesized directly by ball-milling tungsten powder, aluminum powder and activated carbon. The structural development of W0.5Al0.5C phase with the milling times up to 160 h has been followed using X-ray diffraction. X-ray photoelectron spectra demonstrate that Al atom takes the place of W. High temperature annealing experiment reveals that Al is stable in hexagonal structure to 1873 K. Transmission electron microscopy image shows that the grain size of the prepared powders is about 5 nm.
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Model 75是一个先进的图象处理机,它大量采用了先进的硬件技术,从而使其具有一般通用机无法相比的强大处理能力。System 575是运行于Model 75上的图象处理软件系统。它有比较完善的图象处理能力,然而System 575却没有一种好的软件开发方法,致使我所购进Model 75以来没能充分利用它的强大能力。针对这种情况,本文探讨了一种能自由运用Model 75的软件开发方法。由于Model 75不同于一般的通用机,因而很好地使用Model 75必须建立在对它的结构有清楚的了解的基础上。本文在大量实验的基础上对Model 75的结构及功能特点做了分析。为验证本人对Model 75的理解和本文所述方法的正确性,本人做了两个较大的实验,一个是运动模糊图象的恢复,一个是道路寻找的可变此值方法。本文介绍了这两个实验。实验表明本文所述的开发方法是有效的,解决了在Model 75上开发软件的难题。
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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.
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info:eu-repo/semantics/submittedForPublication