Nutrient Enhanced Coastal Ocean Productivity (NECOP). Data report: CTD and hydrographic data, R/V Pelican cruise, April 3-11, 1993

The Nutrient Enhanced Coastal Ocean Productivity (NECOP) Program is a component of NOAA's Coastal Ocean Program. The central hypothesis of this research is: Anthropogenic nutrient inputs have enhanced coastal ocean productivity with subsequent impacts on coastal ocean water quality, living resource yields, and the global marine carbon cycle. The initial study area for this program is the Mississippi/Atchafalaya River Outflow and adjacent Louisiana shelf region.

Zero biased Ge-on-Si photodetector with a bandwidth of 4.72 GHz at 1550 nm

High quality Ge was epitaxially grown on Si using ultrahigh vacuum/chemical vapor deposition (UHV/CVD). This paper demonstrates efficient germanium-on-silicon p-i-n photodetectors with 0.8 mu m Ge, with responsivities as high as 0.38 and 0.21 A/W at 1.31 and 1.55 mu m, respectively. The dark current density is 0.37 mA/cm(2) and 29.4 mA/cm(2) at 0 V and a reverse bias of 0.5 V. The detector with a diameter of 30 mu m, a 3 dB-bandwidth of 4.72 GHz at an incident wavelength of 1550 nm and zero external bias has been measured. At a reverse bias of 3 V, the bandwidth is 6.28 GHz.

A Novel 0.72-6.2GHz Continuously-Tunable Delta Sigma Fractional-N Frequency Synthesizer

This paper presents a wideband Delta Sigma-based fractional-N synthesizer with three integrated quadrature VCOs for multiple-input multiple-output (MIMO) wireless communication applications. It continuously covers a wide range frequency from 0.72GHz to 6.2GHz that is suitable for multiple communication standards. The synthesizer is designed in 0.13-um RE CMOS process. The dual clock full differential multi-modulus divide (MMD) with low power consumption can operate over 9GHz under the worst condition. In the whole range frequency from 0.72GHz to 6.2GHz, the maximal tuning range of the QVCOs reaches 33.09% and their phase noise is -119d8/Hz similar to 124d8/Hz @1MHz. Its current is less than 12mA at a 1.2V voltage supply when it operates at the highest frequency of 6.2GHz.

In_(0.28)Ga_(0.72)As/GaAs量子点超晶格的生长

于2010-11-23批量导入

72型分光光度计的改装

为满足多元素分析的需要,对一台72型分光光度计进行了改装,增加了数显、打印等功能.本文介绍改装后的光学系统、信号放大电路、数显和打印电路.改装后的仪器,测量速度比原来提高约10倍,可作批量样品的连续测定.

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.