46.7 MeV/u~(12)C轰击~(58)Ni、~(115)In、~(197)Au反应中粒子发射研究中子皮及中子分布弥散度对核势的影响

用能量密度公式及小液滴模型给出的费米密度分布，并引入中子皮及中子分布弥散度随中子过剩自由度增加而增加这一因素，计算了重离子反应在相互作用势及熔合位垒。熔合位垒的计算值和实验值符合很好，特别是在中重核区域，改善了以前的计算结果。详细研究了亲近势标度，发现用中子皮及中子分布弥散度的变化能较好地解释中子过剩自由度对新近势标度偏离的影响。本工作对奇异核结构与核反应性质的研究无疑是有用的。我们利用HIRFL提供的46.7MeV/u ~(12)C束轰击~(58)Ni、~(115)In、~(197)Au研究了反应中发射的α粒子角分布和能谱。从速度表象中洛仑兹不变截面等高图中明显看到发射α粒子的三个源。用这三个源的运动模型成功拟合了α粒子能谱，所提取的参数符合费米气体模型计算结果，并讨论了能谱及拟合参数对靶的依赖关系。认为快速源实质上来自弹核碎裂或类弹核碎裂

内蒙古翁牛特旗46年气候变化规律分析

本文分析了翁牛特旗46年(1957-2002年)逐月降水量和平均气温。结果表明:气温呈非连续增暖趋势,其中年平均气温线性变化率为0.39℃.(10a)-1,年平均最高气温线性变化率为0.19℃.(10a)-1,年平均最低气温线性变化率为0.93℃.(10a)-1;最低气温上升速率是最高气温的1-4倍,气温日较差显著减小。上世纪60年代较50年代有所增暖,80年代后期开始明显升温,90年代是近50年来最暖的10年。1987年开始转暖,其后呈连续性增暖趋势,1998年为1957年以来的最暖年,年平均气温7.7℃,高于1957年2.9℃。降水以平均5-7年的周期变化,并从50年代到90年代呈连续性递减趋势,线性变化率为-11.7mm.(10a)-1,90年代较50年代年降水减少了39.4mm。

Isothermal and nonisothermal crystallization kinetics of nylon-46

Isothermal and nonisothermal crystallization kinetics of nylon-46 were investigated with differential scanning calorimetry. The equilibrium melting enthalpy and the equilibrium melting temperature of nylon-46 were determined to be 155.58 J/g and 307.10 degreesC, respectively. The isothermal crystallization process was described by the Avrami equation. The lateral surface free energy and the end surface free energy of nylon-46 were calculated to be 8.28 and 138.54 erg/cm(2), respectively. The work of chain folding was determined to be 7.12 kcal/mol. The activation energies were determined to be 568.25 and 337.80 kJ/mol for isothermal and nonisothermal crystallization, respectively. A convenient method was applied to describe the nonisothermal crystallization kinetics of nylon-46 by a combination of the Avrami and Ozawa equations.

Practice Links [Issue 46, February 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 46 features information regarding databases to support practice as well as the latest research being conducted in the fields of youth empowerment programs and relevant podcasts.

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.

Truncated estrogen receptor alpha 46-kDa isoform in human endothelial cells: relationship to acute activation of nitric oxide synthase.

Background Estrogen acutely activates endothelial nitric oxide synthase (eNOS). However, the identity of the receptors involved in this rapid response remains unclear. Methods and Results We detected an estrogen receptor (ER) transcript in human endothelial cells that encodes a truncated 46-kDa ER (1a-hER-46). A corresponding 46-kDa ER protein was identified in endothelial cell lysates. Transfection of cDNAs encoding the full-length ER (ER-66) and 1a-hER-46 resulted in appropriately sized recombinant proteins identified by anti-ER antibodies. Confocal microscopy revealed that a proportion of both ER-66 and hER-46 was localized outside the nucleus and mediated specific cell-surface binding of estrogen as assessed by FITC-conjugated, BSA-estrogen binding studies. Both ER isoforms colocalized with eNOS and mediated acute activation of eNOS in response to estrogen stimulation. However, estrogen-stimulated transcriptional activation mediated by 1a-hER-46 was much less than with ER-66. Furthermore, 1a-hER-46 inhibited classical hER-66 mediated transcriptional activation in a dominant-negative fashion. Conclusions These findings suggest that expression of an alternatively spliced, truncated ER isoform in human endothelial cells confers a unique ability to mediate acute but not transcriptional responses to estrogen.