35CrMo结构钢热塑性变形流动应力模型

采用Gleeble 1500热模拟实验机对35CrMo结构钢进行实验研究，根据经典应力一位错关系和动态再结晶动力学方程分别对加工硬化一动态回复和动态再结晶两阶段建立流动应力模型，并统一表示为完整的35CrMo结构钢高温流动应力模型；根据实验结果计算拟合了模型中的各参数．采用建立的流动应力模型计算实验条件下的流动应力，计算结果与实验结果吻合较好．所建立的流动应力模型可以直接用于35CrMo结构钢热成形过程的数值模拟分析．     

SO42-/ZrO2系列固体超强酸的制备与应用

本文对采用不同方法制备了两种SO4^2-/ZrO2系列的SO4^2-/ZrO2-TiO2和SO4^2-/ZrO2-Al2O3固体超强酸催化剂，并以顺丁烯二酸酐和正丁醇的酯化反应为探针反应，考察了Zr：A1，Zr：Ti的原于配比，焙烧温度，焙烧时间以及浸渍液硫酸的浓度对催化剂活性的影响。     

RAPD鉴定远缘杂交牧草蔗新品系94-42

应用RAPD技术对远缘杂交牧草蔗新品系94—42，父本PT43—52及母本甘蔗栽培良种C0419进行分子鉴定．67个引物共扩增出284条带，其中l16条为多态性带，占40．85％．计算相似性系数，并对3个品种进行亲缘关系的分析，结果分别为：新品系和母本：0．9138；新品系和父本：0．8009；父本和母本：0．7658．RAPD结果证明，牧草蔗94—42基因组出现多态性，具有父、母本特异DNA带，是两者远缘杂交的后代．提示RAPD技术是一种适合远缘杂交物种分子鉴定的有效方法．     

纳米固体超强酸SO42-/Fe2O3催化合成柠檬酸三丁酯

合成了纳米固体超强酸，考察了该催化剂在柠檬酸三丁酯合成中的催化活性，并与非纳米的SO4^2-/TiO2,SO4^2-/ZrO2,SO4^2-/Fe2O3，浓H2SO4催化剂进行了比较，同时对酯化反应的几种影响因素进行了研究。     

42CrMo钢回火方程的建立

通过回归分析给出了４２ＣｒＭｏ钢的回火硬度、回火温度及回火时间的函数关系式。该关系式具有精度高，使用方便。同时分析了回火参量Ｐ＝ｆ［Ｔ（Ｃ＋ｌｇτ）］的算法，指出了其存在较大误差的原因     

Targeting of the Akt/PKB kinase to the actin skeleton

Serine/threonine kinase Akt/PKB intracellular distribution undergoes rapid changes in response to agonists such as Platelet-derived growth factor (PDGF) or Insulin-like growth factor (IGF). The concept has recently emerged that Akt subcellular movements are facilitated by interaction with nonsubstrate ligands. Here we show that Akt is bound to the actin skeleton in in situ cytoskeletal matrix preparations from PDGF-treated Saos2 cells, suggesting an interaction between the two proteins. Indeed, by immunoprecipitation and subcellular fractioning, we demonstrate that endogenous Akt and actin physically interact. Using recombinant proteins in in vitro binding and overlay assays, we further demonstrate that Akt interacts with actin directly. Expression of Akt mutants strongly indicates that the N-terminal PH domain of Akt mediates this interaction. More important, we show that the partition between actin bound and unbound Akt is not constant, but is modulated by growth factor stimulation. In fact, PDGF treatment of serum-starved cells triggers an increase in the amount of Akt associated with the actin skeleton, concomitant with an increase in Akt phosphorylation. Conversely, expression of an Akt mutant in which both Ser473 and Thr308 have been mutated to alanine completely abrogates PDGF-induced binding. The small GTPases Rac1 and Cdc42 seem to facilitate actin binding, possibly increasing Akt phosphorylation.Received 10 September 2003; accepted 25 September 2003     

[CrMo_6O_(24)H_6]~(3-)掺杂聚苯胺材料的制备及荧光性质

在盐酸介质中,以(NH4)2S2O8为氧化剂,杂多阴离子[CrMo6O24H6]3-为掺杂剂合成出了聚苯胺掺杂材料,用FT-IR,XRD进行了表征,测定了该材料的电导率、常见溶剂中的溶解度及其荧光性质.该材料的电导率为1.4×10-2S·cm-1,最高溶解度可达到0.60mg·mL-1,在以260nm和332nm为激发波长,可分别在425nm和567nm处得到荧光发射峰。     

Monogenetic determinants of Alzheimer's disease: APP mutations

Mutations within exons 16 and 17 of the β-amyloid precursor protein (APP) gene were the first known cause of familial Alzheimer's disease. These mutations are rare and have been reported in a handful of families exhibiting autosomal dominant inheritance of Alzheimer's disease with age of onset around 50 years. In vitro and in vivo studies have demonstrated that each of these mutations alters proteolytic processing of APP, resulting in an increase in the production of Aβ42, a highly fibrillogenic peptide, that spontaneously aggregates and deposits in the brain. Transgenic mice carrying a mutant human APP gene also show age-dependent β-amyloid (Aβ) deposition in the brain. The rate of deposition in these mice can be modified by apolipoprotein E expression.     

基于元胞自动机的30CrMo钢动态再结晶组织演变规律研究

根据30CrMo钢的热模拟实验数据,建立了基于动态再结晶物理机制的位错密度、形核率及晶粒长大模型,并采用元胞自动机(CA)方法模拟了30CrMo钢在不同温度及应变速率下的微观组织演变规律。结果显示,通过CA方法模拟得到30CrMo钢的流变应力曲线及平均晶粒尺寸均与实验值吻合较好,所建模型的有效性和准确性得到验证。当应变速率一定时,变形温度越高越利于动态再结晶的充分进行,稳态下晶粒尺寸相对较大;而当变形温度一定时,高应变速率条件下材料的形核率较大,再结晶晶粒较细小。     

Emodin inhibits tumor cell migration through suppression of the phosphatidylinositol 3-kinase-Cdc42/Rac1 pathway

Enhanced cell migration is one of the underlying mechanisms in cancer invasion and metastasis. Therefore, inhibition of cell migration is considered to be an effective strategy for prevention of cancer metastasis. We found that emodin (3-methyl-1,6,8-trihydroxyanthraquinone), an active component from the rhizome of Rheum palmatum, significantly inhibited epidermal growth factor (EGF)- induced migration in various human cancer cell lines. In the search for the underlying molecular mechanisms, we demonstrated that phosphatidylinositol 3-kinase (PI3K) serves as the molecular target for emodin. In addition, emodin markedly suppressed EGF-induced activation of Cdc42 and Rac1 and the corresponding cytoskeleton changes. Moreover, emodin, but not LY294002, was able to block cell migration in cells transfected with constitutively active (CA)-Cdc42 and CA-Rac1 by interference with the formation of Cdc42/Rac1 and the p21-activated kinase complex. Taken together, data from this study suggest that emodin inhibits human cancer cell migration by suppressing the PI3K-Cdc42/Rac1 signaling pathway.Received 7 February 2005; received after revision 11 March 2005; accepted 18 March 2005