133-W pulsed fiber amplifier with large-mode-area fiber

A master-oscillator fiber power amplifier (MOPA) system with a 4-m-long Yb3+-doped homemade large mode area (LMA) double-clad fiber is reported. The system emits up to 133.8 W of amplified radiation at a wavelength of 1064 nm and a repetition rate of 100 kHz, limited only by the available pump power. Peak power of 300 kW at 20 kHz with a pulse duration of 15 ns is obtained. (c) 2006 Society of Photo-Optical Instrumentation Engineers.

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.

47 MeV/u ~(12)C与~(133)Cs反应中碘同位素产生截面的Q_(gg)依赖关系

用47 MeV/u 12C离子轰击133Cs靶,应用放射化学分离技术和离线γ射线谱学,得到碘同位素的产生截面。丰中子碘同位素的独立产生截面指数地依赖于Qgg值,而缺中子碘同位素的独立产生截面则偏离这一直线关系。这一事实可对在深部非弹转移过程中产生丰中子碘同位素予以解释。

~(12)C与~(133)Cs反应中Ba同位素的Q_(gg)产额依赖

使用47MeV/u12C离子轰击133Cs靶,由多核子转移反应产生Ba同位素。使用放射化学方法,从133Cs和反应产物中分离出产物Ba,再使用高纯Ge探测器测量Ba放射性同位素的γ活性,根据Ba同位素的活度和其他相关数据,确定Ba同位素的产生截面。通过分析测得的Ba同位素的厚靶平均产生截面,发现缺中子Ba同位素的独立截面不遵从规则的Qgg系统性。该结果可用重离子碰撞中的次级过程加以解释。

~(133)Sm和~(149)Yb的β缓发质子衰变

利用40Ca+96Ru融合蒸发反应产生了近质子滴线核133Sm,配合氦喷嘴带传输系统采用“质子-γ”符合方法观测了它们的β缓发质子衰变,其中包括半衰期、质子能谱、第二代子核低位态之间的γ跃迁,并估计出衰变到第二代子核不同低位态的分支比．通过统计理论拟合上述实验数据,指认了133Sm的自旋宇称的可能范围．并用Woods-Saxon Strutinsky方法计算了限制组态的133Sm的核势能面,通过对比发现133Sm的自旋宇称可能有两种成分:5／2+和1／2-．这一结果与2001年发表的133Sm(EC+β+)衰变的简单衰变纲图是相容的．此外用同一方法分析了2001年Eur．Phys．J．A12: 1-4中发表的有关149Yb的β缓发质子衰变实验数据,由此指认了149Yb的基态自旋宇称为1／2-．

~(133)Sm的(EC+β~+)衰变和~(133)Pr的1.1s同质异能态

通过96 Ru( 4 0 Ca ,ln2p)反应 ,采用氦喷嘴带传输系统和X γ与γ γ符合测量方法 ,首次建议了133Sm的简单的 (EC + β+)衰变纲图 .由于Ru靶中含有98— 10 2 Ru的成分 ,同时产生了133Pr,并首次测定了133Pr的 1 1 / 2 - 同质异能态的寿命为( 1 .1± 0 .2 )s.用单粒子模型提取了131,133,135 ,137Pr的 1 1 / 2 - 同质异能态的约化跃迁几率的实验值 ,并与Weisscopf近似估计进行了比较 .

beta-delayed proton decays of Sm-133 and Yb-149

Sm-133 was produced via fusion evaporation in the reaction Ca-40+Ru-96. Its P-delayed proton decay was studied by means of "p-gamma" coincidence in combination with a He-jet tape transport system, including half-lives, proton energy spectra, gamma-transitions following the proton emissions, and the branching ratios to the low-lying states in the grand-daughter nuclei. The possible spins and parities of 133Sm were extracted by fitting the experimental data with a statistical model calculation. The configuration-constrained nuclear potential energy surfaces of Sm-133 were calculated by using the Woods-Saxon Strutinsky method. Comparing the experimental and calculated results, the spins and parities Of Sm-133 were assigned to be 5/2(+) and 1/2(-), which is reconciled with our published simple (EC+beta(+)) decay scheme Of Sm-113 in 2001. In addition, our experimental data on the beta-delayed proton decay of Yb-149 reported in Eur. Phys. J., 2001, A12: 1-4 was also analyzed by using the same method. The spin and parity of Yb-149 was assigned to be 1/2-.

beta-delayed proton decays and spin assignments for Sm-133 and Yb-149

The proton-rich isotope Sm-133 was produced via the fusion evaporation reaction Ca-40 + Ru-96. Its beta-delayed proton decay was studied by p-gamma coincidence in combination with a He-jet tape transport system, and half-lives, proton energy spectra, gamma-transitions following the proton emission, as well as beta-delayed proton branching ratios to the low-lying states in the grand-daughter nucleus were determined. Comparing the observed beta-delayed proton branching ratios with statistical model calculations, the best agreement is found assuming that only one level with the spin of 3/2 in Sm-133 decays or two levels with the spins of 1/2 and 5/2 decay with similar half-lives. The configuration-constrained nuclear potential energy surfaces of Sm-133 were calculated using the Woods-Saxon-Strutinsky method, which suggests a 1/2-ground state and a 5/2(+) isomer with an excitation energy of 120 keV. Therefore, the simple(EC+beta(+)) decay scheme of Sm-133 in Eur. Phys. J.A 11,277(2001) has been revised. In addition, our previous experimental data on the beta-delayed proton decay of Yb-149 reported in Eur. Phys. J. A 12,1 ( 2 0 0 1) was also analyzed using the same method. The spin-parity of Yb-149 is suggested to be 1/2(-).

稀土离子与红细胞作用的~(133)Cs NMR研究

随着稀土资源的不断开发利用,它们不可避免地通过多种途径进入生物体内,因而从分子和细胞水平上研究稀土的生物效应具有非常重要的理论和实际意义.关于稀土与细胞作用的研究已有诸多报道,本文报道用~(133)Cs NMR方法研究La~(3+)对Cs~+跨膜进入红细胞的影响.对于物质跨膜传输的研究,首先需要合适的手段将被传输物质在膜两侧的分布区分开.在碱金属离子中,仅~(133)Cs~+在不引入顺磁位移试剂情况下,细胞内外NMR信号能确切区分,并且在体系中无K~+时,Cs~+有类似于K~+的功能,故~(133)Cs是研究稀土离子与细胞作用

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.