~(125)Cs的能级结构

通过116Cd(14N,5n),Ebeam=65MeV的核反应布居了125Cs的高自旋态.利用在束γ谱学实验方法,进行了γ γ符合测量,使已知的125Cs核能级纲图得到了扩展,并且修正了某些组态的带头激发能.

质量数A≈125的热核GDR特性的研究

简单介绍了利用LNS的回旋加速器产生的116Sn束轰击12C和24Mg靶的实验装置以及实验过程.该实验通过MEDEA探测器测量了由全熔合与非全熔合反应产生的较低激发能区(160—300MeV)质量数A≈125的热核的巨偶极共振特性,比较了不同靶子、不同束流能量时巨偶极共振的γ产额的变化.

~(125)Sb高自旋态:粒子-核芯激发耦合

利用在束γ谱学方法,通过~(124)Sn(~7Li,α2n)反应研究了~(125)Sb的激发态,首次建立了~(125)Sb的高自旋能级纲图,其中包括21条新γ跃迁和14个新能级。发现1970,2110和2470 keV3个能级为同质异能态,基于延迟符合测量确定了它们的寿命范围,并确定其自旋、宇称分别为15/2~-,19/2~-和23/2~+。根据粒子-核芯耦合图像和经验壳模型计算解释了~(125)Sb的能级结构,3个同质异能态的组态分别被指定为πg_(7/2)(×)V(h_(11/2)s_(1/2))_(5~-),πg_(7/2)(×)V(h_(11/2)d_(3/2))_(7~-)和πg_(7/2)(×)V(h_(11/2)~2)_(10~+),

丰中子核~(125)Sb的高自旋态(英文)

利用在束γ谱学方法 ,通过1 2 4 Sn( 7Li,α2n)反应首次研究了丰中子核1 2 5Sb的高自旋态 .建立了自旋达 2 3 2 +、激发能至 2 63 7keV的能级纲图 ,其中包括 2 1条新γ跃迁和 1 4个新能级 .在 1 970 ,2 1 1 0和 2 471keV识别出了 3个同质异能态 ,估计了它们的寿命范围 ,并建议分别具有πg7 2 ν(h1 1 2 s1 2 ) ,πg7 2 ν(h1 1 2 d3 2 ) ,πg7 2 ν(h21 1 2 )三准粒子组态 .根据价质子与1 2 4 Sn核芯激发态的耦合讨论了1 2 5Sb的能级结构 .

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.

Elevated CA-125 and ascites: not always malignancy

Abstract
BACKGROUND: We present two clinical cases from a single institution where a final diagnosis of cardiac failure was made following the initial finding of ascites and an elevated CA 125 level. In both cases gynaecological malignancy was initially suspected.