江汉平原47号钻孔中化石硅藻的新种类

在江汉平原47号钻孔中的46.60—2.20m层位上(上更新统到全新统),含有丰富的化石硅藻,经鉴定有4个新种类,即Cymbella jianghanensis sp.nov.,C.tenuistriata sp.nov.,C.cistula(Hempr.) Grun.var.retcta var.nov.,Gomphonema tropicale Brun var.nonpunctatum var.nov..同时,对一个变种进行了重新命名和特征修改,即Eunotia clevei Grun.var.ob

In_(0.53)Ga_(0.47)As/In_(0.52)Al_(0.48)As量子阱中的正磁电阻效应

在低温强磁场条件下,对In_(0.53)Ga_(0.47)As/In_(0.52)Al_(0.48)As量子阱中的二维电子气进行了磁输运测试.在低磁场范围内观察到正磁电阻效应,在高磁场下这一正磁电阻趋于饱和,分析表明这一现象与二维电子气中的电子占据两个子带有关.在考虑了两个子带之间的散射效应后,通过分析低磁场下的正磁电阻,得到了每个子带电子的迁移率,结果表明第二子带电子的迁移率高于第一子带电子的迁移率.进一步分析表明,这主要是由两个子带之间的散射引起的.

两个子带占据的In_(0.53)Ga_(0.47)As/In_(0.52)Al_(0.48)As量子阱中填充因子的变化规律

研究了低温(1.5K)和强磁场(0-13T)条件下,InP基In_(0.53)Ga_(0.47)As/In_(0.52)A_(l0.48)As量子阱中电子占据两个子带时填充因子随磁场的变化规律.结果表明,在电子自旋分裂能远小于朗道能级展宽的情况下,如果两个子带分裂能是朗道分裂能的整数倍时,即⊿E_(21)=κ*ω_c(其中κ为整数),填充因子为偶数;当两个子带分裂能为朗道分裂能的半奇数倍时,即⊿E_(21)=(2κ+1*ω/2,填充因子出现奇数.

In_(0.53)Ga_(0.47)As/In_(0.52)Al_(0.48)As量子阱中双子带占据的二维电子气的输运特性

研究了不同沟道厚度的In_(0.53) Ga_(0.47)As/In_(0.52)Al_(0.48)As量子阱中双子带占据的二维电子气的输运特性.在考虑了两个子带电子之间的磁致子带间散射效应后,通过分析Shubnikov-de Haas振荡一阶微分的快速傅里叶变换结果,获得了每个子带电子的浓度、输运散射时间、量子散射时间以及子带之间的散射时间.结果表明,对于所研究的样品,第一子带电子受到的小角散射更强,这与第一子带电子受到了更强的电离杂质散射有关.

匹配In（0.53）Ga（0.47）As/InP量子阱材料的GSMBE生长及特性分析

于2010-11-23批量导入

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。

Quasi-Elastic Scattering of C-16 from C-12 at 47.5 MeV/Nucleon

Differential cross sections for the quasi-elastic scattering of C-16 at 47.5 MeV/nucleon from C-12 target are measured. Coupled-channels calculations are carried out and the optical potential parameters are obtained by fitting the experimental angular distribution.

~(12)C与~(209)Bi反应中Au同位素的产额与Q_(gg)的关系；Q_(gg)-Yield Dependence of Au Isotopes in Interaction of 47 MeV/u ~(12)C With ~(209)Bi

用47MeV/u12C离子轰击天然铋靶,通过炮弹和靶核之间的核子转移反应产生Au同位素。使用放射化学方法从大量Bi和复杂反应产物中分离、纯化Au,并制备Au的γ射线测量源。使用HPGe探测器测量放射性Au同位素的γ活性。根据照射结束时Au同位素的活度和其他相关数据,确定每个Au同位素的产生截面。分析发现,缺中子Au同位素的产生截面与Qgg值之间不遵从指数依赖关系,这可用重离子碰撞中的次级过程加以解释。

Practice Links [Issue 47, April 2012]

Practice Links is a free e-publication for practitioners working in Irish social services, voluntary and nongovernmental sectors. Practice Links was created to enable practitioners to keep up-to-date with new publications, electronic resources and conference opportunities. issue 47 includes research into the follow-up treatment of women in the aftermath of miscarriage and effects upon employment outcomes for those suffering Autism Spectrum Disorders.

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.