Construction of heteroduplex DNA and in vitro model for functional analysis of mismatch repair

Functional deficiency of mismatch repair (MMR) system is one of the mechanisms of tumorigenesis. With the development of the investigation and the requirement from the clinical diagnosis and treatment it is necessary to build up a method to evaluate the functional status of the whole MMR system in the concerned tumors. The original ssDNA and dsDNA from wild type (wt) bacteriophage M13mp2 and its three derivates with mutation points in the     

Functional and physical communication between oncoproteins and tumor suppressors

The discovery of oncogenes (c-onc’s) and tumor suppressors (TS’s) has led to the concept that cancer arises from defects in each of these classes of genes or their products. More recently, it has been appreciated that c-onc and TS proteins often affect one another’s functions. Within this context, I review the two classical TS’s, p53 and the retinoblastoma protein, and the consequences of their inactivation. The various forms of genomic instability (GI) that underly the high mutation rates of transformed cells are then discussed. Particular emphasis is placed upon the concept that GI is not only an integral part of the transformed state but is a prerequisite. Increased oxidative DNA damage, and/or an inabiliy to repair it, can lead to GI. The review then discusses recent observations showing that loss of the TS protein peroxiredoxin 1 (prdx1) and increased expression of the c-onc protein c-Myc, each leads to increased oxidative DNA damage. The critical nature of the c-onc-TS interaction is underscored by that occurring between prdx1 and c-Myc, with the former protein regulating the production of DNA-damaging reactive oxygen species by the latter. The intimate association between these proteins and others serves as a paradigm for the exquisite balancing act that c-onc’s and TS’s must maintain in order to properly control normal DNA replication and cellular proliferation while simultaneously minimizing the acquisition of potentially neoplastic mutations. Received 10 May 2005; received after revision 3 July 2005; accepted 19 July 2005     

AZ31镁合金的热变形加工图及其应用

为了确定AZ31镁合金轧制工艺参数,利用Gleeble--3500热模拟试验机进行热压缩试验以测试其热变形行为,并根据动态材料模型理论得到其热加工图.当变形温度为380～400℃、应变速率为3～12 s-1时,功率耗散效率大于30%,属于动态再结晶峰区;在该区域进行异步轧制变形退火处理后得到平均晶粒直径为2.3μm的细晶组织,抗拉强度为322.7MPa,延伸率为19.6%.当应变速率大于15 s-1时,属于流变失稳区,250～300℃低温加工时合金的塑性显著降低,350～400℃高温加工时合金出现混晶组织.     

基于一阶二次矩阵的寒区土质高切坡稳定可靠度分析

以寒区土质高切坡为研究对象,构建了寒区土质高切坡浅层滑动失稳模型,基于极限平衡原理和可靠性原理,建立了寒区土质高切坡的可靠指标和失稳概率计算方法。以G580线和田至康西瓦公路段K86+780～K86+840土质高切坡为例进行了寒区土质高切坡可靠度计算,并分析了各种因素对寒区土质高切坡失稳概率的影响规律。结果表明,该方法建立的可靠指标与失稳概率计算方法可以用于寒区土质高切坡稳定性分析,并且当融化深度大于1.4 m时高切坡失效概率迅速升高,1.4～2.1 m失效概率增长74.4 %,当融化深度大于2.1 m时坡体处于不稳定的状态;当土质高切坡粘聚力从8 kPa增长到14 kPa的时候,失稳概率降低约88.4 %,稳定系数增长0.45;当土质高切坡内摩擦角从15 °增长到23 °时,失稳概率降低约15 %,稳定系数增加约0.07;当土质高切坡坡率由0.5增加到0.8时,边坡失稳概率由26.5 %增长到61.4 1%,坡率到0.8时为峰值,大于0.8之后失稳概率逐渐减小,到1.5时失稳概率降低至25.2 %,降低约36.21 %。     

基于GPC的环肋耐压圆柱壳结构失稳概率分析

为评估具有小失效概率特性的深潜环肋耐压圆柱壳结构的失稳概率，提出了一种新的基于高斯过程分类和重要抽样的自适应分析方法.该方法通过引入马尔科夫链蒙特卡洛法和欧式距离，开发了一种新的考虑预测不确定性和取样均匀性的自适应试验设计策略，以便更高效地构造高斯过程分类器；采用核密度估计构造准最优重要抽样密度函数；基于失效概率估计的稳定性，提出了一种更精确的迭代停止准则.通过某一分段函数验证了所提分析方法的准确性及高效性.应用所提方法得到某深潜环肋耐压圆柱壳结构的失稳概率约为8.242×10^-5.     

参数族λ（e^2z＋e^z）的动力学

在Ｂａｋｅｒ,Ｄｅｖａｎｅｙ研究族ｅλｚ动力系统的基础上讨论族ｆλ（ｚ）＝λ（ｅ２ｚ＋ｅｚ）的动力学问题．     

三维反应扩散系统中的螺旋波和失稳控制

三维螺旋波(卷轴波)的运动和失稳的研究在心颤等高发心脏病中扮演重要角色,对三维螺旋波的运动和失稳过程以及控制的研究对于心颤等心脏病的防治具有指导意义.本文主要对我们过去几年在梯度系统中螺旋波的研究结果做一个总结.我们以反应扩散系统为研究对象,对于具有参数梯度的螺旋波的失稳过程和控制进行了探讨.在实验和数值模拟研究中,我们发现在三维梯度系统中,梯度大小的改变可以促使三维螺旋波发展产生线缺陷或者引起二维螺旋波运动的相位差的积累而产生漫游,两者都可使螺旋波的运动失去稳定性.对于螺旋波失稳的控制,我们研究了外力周期驱动和噪声对螺旋波失稳的影响,对控制的机制进行了分析.     

规则波致剪切波的时空变化

基于物理模型试验、小波变换理论及剪切不稳定理论等,研究入射波为规则波、地形为平直斜坡情况下的剪切波时空变化特性。通过对15个不同波况下的剪切波流速时间历程的小波谱进行分析,得出如下结论:入射波为规则波、地形为平直斜坡情况下可以观测到剪切波,但是时空变化不明显;剪切波产生后随时间的变化呈现连续性;剪切波在沿岸方向的能量谱中比在垂直岸线方向能量谱中占优势;地形坡度增加会使剪切波产生的区域减小;无论是1∶40坡还是1∶100坡,由剪切不稳定引起的剪切波频率都在约0.015 Hz左右变化。