35MeV／u~(36)Ar+~(112,124)Sn反应中中等质量碎片关联函数的入射道依赖

测量了35MeV／u36Ar+112,124Sn反应中小角关联出射的中等质量碎片(IMF)约化速度关联函数．结果表明36Ar+124Sn反应系统中的约化速度关联函数在小约化速度处的反关联程度比36Ar+112Sn反应系统中的强,表现出明显的入射道依赖性．考察出射粒子对的单核子总动量时,发现这种差异主要来自于高动量粒子对的贡献．用三体弹道理论模型MENEKA分别计算了两个系统的IMF发射时标,在36Ar+112Sn反应系统中约为150fm／c,而在36Ar+124Sn反应系统中,约为120fm／c．同位旋相关的量子分子动力学计算表明,36Ar+124Sn系统中IMF的发射时间谱比36Ar+112Sn系统略有前移,相应地,其中心密度从最高点随时间的下降亦比36Ar+112Sn系统略快．

30MeV/u~(40)Ar+~(112,124)Sn反应中态布居核温度的同位旋效应

用 13单元望远镜探测器阵列测量了 30MeV u40 Ar +112 ,12 4Sn反应中小角关联粒子 ,由两体符合事件提取了α α关联函数 .用三体弹道理论模型MENEKA计算本底关联函数 ,用Monte Carlo方法计算探测效率函数 ,在扣除本底产额并考虑探测效率的修正后 ,对不同同位旋反应系统 40 Ar +112 Sn和 40 Ar+12 4Sn提取的相对态布居核温度分别是 4 .18±0 .2 50 .2 1MeV和 4 .10±0 .2 20 .2 0 MeV ;考察态布居核温度和粒子能量的关系时 ,观察到两个系统的发射温度均随着粒子能量的增加而降低 ,缺中子系统40 Ar +112 Sn中由低能时的 5 .13±0 .3 00 .2 6MeV降低到高能时的 3.87±0 .3 70 .2 9MeV ,丰中子系统 40 Ar +12 4Sn中由低能时的 5 .39±0 .3 00 .2 6MeV降低到高能时的 3.32±0 .2 80 .2 3 MeV .用激发热核衰变过程的同位旋选择性对这种同位旋相关性进行了解释

30MeV/u~(40)Ar+~(112,124)Sn反应中的同位素产额比与核温度

系统研究了 3 0MeV u40 Ar+ 1 1 2 ,1 2 4 Sn反应中的轻粒子同位素产额比随角度和初始激发能的变化关系 .对于两个反应体系 ,均观察到3He 4He和6Li 7Li的产额比随角度的增加而增加 ,6He 4He和8Li 7Li随角度的增加而减小 .统计发射的运动学效应不能完全符合实验结果 .各种单同位素产额比与靶核的N Z比有关 ,表现出同位旋效应 ,而由双同位素比提取的核温度几乎没有靶核相关性

30MeV/u~(40)Ar+~(112,124)Sn反应后角能谱温度的同位旋效应

在 30MeV/u4 0 Ar +112 ,12 4 Sn反应中用平行板雪崩计数器实现了前冲余核的测量 .在不同的线性动量转移下用运动源模型拟合了后角的3 He,α和6He能谱 ,发现3 He的能谱斜率温度在12 4 Sn系统中高于112 Sn系统 ,而6He的温度在112 Sn系统中更高 ,α粒子在两个系统中没有明显差别 .用热核粒子蒸发过程衰变道的选择性对这种同位旋相关性进行了解释 .GEMINI的计算不能重现实验结果

35MeV/u~(36,40)Ar+~(112,124)Sn反应中同位旋自由度的弛豫

35MeV/u 36 ,40　Ar+ 112 ,12 4Sn反应中 ,在前角 5°和 2 0°观测到丰中子核与稳定核的产额比随粒子出射动能的增加而减小 ,而缺中子核与稳定核的产额比随动能的增加而增加 .对于某种元素 ,随着动能的减小 ,其平均中质比逐渐由弹核N/Z向靶核N/Z过渡 .这些现象表明在这样的入射能量下 ,周边或近周边碰撞过程中同位旋自由度没有完全达到平衡 .这种行为对两个靶核系统是相似的 ,但是同位素产额比的绝对值在 5°没有靶核相关性 ,而在 2 0°处却表现出明显的靶核相关性 .

在40MeV/u时~(112)Sn+~(112)Sn和~(124)Sn+~(124)Sn中多重碎裂的同位旋效应

利用同位旋相关的量子分子动力学模型，研究了~(１１２)Ｓｎ＋~(１１２)Ｓｎ和~(１２４)Ｓｎ＋ ~(１２４)Ｓｎ两个反应系统在入射能量 Ｅ＝４０ＭｅＶ／ｕ时的多重碎裂。计算结果能与 实验值定性符合。观察到两个反应系统中，中等质量碎片多重性、中子多重性、 荷电粒子多重性与轻荷电粒子多重性之间的关联存在着明显的差别。另外，通 过与膨胀蒸发源模型及同位旋相关的渗透模型分析结果的比较，发现这种差别 主要是由同位旋相关的反应动力学所造成的。

Entrance channel dependence of the correlation function of IMFs in Ar-36+Sn-112,Sn-124 at 35MeV/u

The reduced velocity correlation functions of the Intermediate Mass Fragments (IMFs) were measured in the reactions of Ar-36+ Sn-112,Sn-124 at 35MeV/u. The anti-correlation at small reduced velocities is more pronounced in Ar-36+ Sn-124 system than that in Ar-36+ Sn-112 system. The difference of the correlation functions between the two reactions is mainly contributed by the particle pairs with high momenta. A three-body Coulomb repulsive trajectory code (MENEKA) is employed to calculate the emission time scale of IMFs for-the both systems. The time scale is 150fm/c in the Ar-36+ Sn-112 system and 120fm/c in the Ar-36+ Sn-124 system, respectively. A calculation based on an Isospin dependence Quantum Molecular Dynamics code (IQMD) reveals that the emission time spectrum of IMFs is shifted slightly leftwards in Ar-36+ Sn-124 compared with that in the Ar-16+ Sn-112 system, indicating a shorter emission time scale. Correspondingly, the central density of the hot nuclei decreases faster in Ar-36+ Sn-124 than in Ar-36+ Sn-112

30,35MeV/u 36,40Ar＋112,124Sn反应中热核性质同位旋效应的实验研究

针对①中能反应中同位旋自由度是否达到平衡，②同位旋自由度对几中不同方法测量的核温度是否有影响 这两个基本问题，设计了用30和35MeV/u ~(36,40)Ar轰击~(112,124)Sn反应的实验方案。得到如下结果：对于前角5°处的耗散弹核碎裂产物，丰中子同位素与稳定核的产额比随产物出射动能的增加而减小，而丰质子子同位素与稳定核的产额比随动能的增加而增加，呈现明显的剪刀差分布特性。随耗散时间的增大，产物的平均中质比逐渐由弹核的平均中质比向系统的平均中质比过渡。这个结果说明在该反应中，同位旋自由度没有达到完全平衡。而对于20°处的DIC产物，上述剪刀差分布特性变得更不明显，这是同位旋自由度由非平衡向平衡过渡的表现。后角轻粒子的能谱分析表明，初始热核的同位旋会影响斜率核温度的提取，由于丰中子轻粒子~6He在~(40)Ar + ~(112)Sn系统中的蒸发被抑制，相比~(40)Ar + ~(112)Sn而言，其蒸发比较容易发生在衰变链早期，因此提取的温度偏高，同样，丰质子轻粒子~3He的温度在~(40)Ar + ~(112)Sn中略高。但中后角的同位素产额分析表明，反应系统的同位旋对双同位素比核温度几乎没有影响。核温度作为热核的热力学量，是独立于测量方法的，这种不同的方法得出的差异主要来源于同位旋对衰变机制的影响。作为一个尝试，将中高能反应中的熵的提取推广到这个能区，发现两个系统的熵几乎一致。在量子统计模型框架下，考察核温度与熵的关系发现，~(40)Ar + ~(112)Sn反应的挤出时刻密度略高于~(40)Ar + ~(112)Sn。

John Adcock, In place of schools, New Education Press Ltd, Londyn 1994, ss. 112.

Recenzje i sprawozdania z książek

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.