1000 resultados para 09132300 CTD-174


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Eudiaptomus vulgaris Schmeil is the most abundant copepod in Lake Maggiore and forms also, in respect to other entomostraca, the most important element, through its average biomass and because it is fairly numerous throughout the year. Plankton samples collected in a systematic and quantitative way, gave the opportunity to study some aspects of the dynamics of the population of this copepod, in safety in view of the uncertainty which in this kind of study can ensue when samples are taken only at a single station - in consequence of the changes in size of population between different water masses. The results of the biometrical observations are of the population of Eudiaptomus vulgaris is presented.

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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.

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对双奇核174Re的在束γ谱学实验数据作了仔细分析,提取出了带间与带内E2γ跃迁分支比,并导出了其约化跃迁概率的比值。用带混合理论对约化跃迁概率的比值进行了分析,得到带间相互作用强度及转动带形变的信息。发现不同组态的转动带其跃迁电四极矩具有明显的差异。与相邻奇A核的结构特征类似,这种跃迁电四极矩的差异很可能是由于1/2-[541]准质子或1/2-[521]准中子对原子核的形状驱动效应造成的。

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利用重离子熔合蒸发反应~ (159)Tb(~(20)Ne,5n)~(174)Re,并通过激发函数、KX- γ和γ-γ符合测量,研究了~(174)Re核的高自旋态.鉴别并指定了~(174)Re核的一个 基于л1/2-[541]v1/2~ -[521]准粒子组态上的双退耦带.还发现了两个分别具 有半退耦特征和强耦合特征的转动带,定性地讨论了它们的粒子组态.

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High spin states in Re-174 are investigated via the Sm-152(Al-27, 5n gamma)Re-174 reaction and gamma-gamma coincidence relationships are analysed carefully. A new band is identified due to its spectroscopic connection with the known pi 1/2(-)[541] circle times nu 1/2(-)[521] band. This band is proposed to be the ground-state band built on the pi 1/2(-)[541] circle times nu 5/2(-)[512] configuration in view of the low-lying intrinsic states in the neighbouring odd-mass nuclei. It is of particular interesting that the new band exhibits a phenomenon of low-spin signature inversion, providing a new situation for theoretical investigations.

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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.