非线性尘埃声波在含有2种不同温度离子的尘埃等离子体中的稳定性问题

在无磁场的尘埃等离子体中 ,由冷的尘埃颗粒和热的电子和离子组成的尘埃等离子体 ,对于有限的小振幅的非线性波的运动可以用KdV方程描述 .对由 2种不同温度离子的尘埃等离子体中的弱二维尘埃声波 ,得到了它所满足的KP方程 .并且发现 ,在横向扰动下 ,弱的非线性孤立波在尘埃等离子体中是稳定的 .在这个系统中既存在压缩孤立波又存在稀疏孤立波     

氮化硅陶瓷表面的融盐热还原反应法锆金属化的研究

以Al粉、K2ZrF6为原料，在KCl LiCl的融盐介质中，利用高温融盐热还原法在氮化硅陶瓷基体表面镀锆金属化膜；以XRD分析镀膜物相成分，并用SEM对试样表面、断面进行显微结构分析。结果表明：氮化硅陶瓷镀件表面镀膜外观呈银白色，并有有金属光泽；镀膜物质成分为Zr5Si3；镀层中无铝元素存在。     

耦合非线性波动方程组的约化摄动分析

基于远方场理论的思想,应用约化摄动分析方法对耦合KdV方程和耦合mKdV方程进行了近似求解,并得到了它们的几组孤立波解,与已有结论相比,其振幅的物理意义更加丰富.在特殊情况下,所得到的近似解与精确解具有完全相同的形式.分析表明,所应用的约化摄动方法在研究小振幅扰动问题方面有一定的普适性.     

等离子体中(3+1)维弱非线性离子声波的摄动分析

通过约化摄动法,获得了等离子体中离子声波的(3 1)维KP(Kadomtsev Petviashvili)方程.结果表明,离子声波沿轴方向的速度分量、密度和电位势,在垂直方向有色散的情况下,仍然有孤立波解出现,但其它2个垂直方向的速度分量不会出现孤波结构.     

Habitat-induced reciprocal transformation in the root phenotype of Oriental ginseng is associated with alteration in DNA methylation

Oriental ginseng is an important medicinal plant that grows in 2 major forms or ecotypes, wild and domesticated. Each form differs conspicuously in root phenotype, but can be converted from one type to another by habitat. Here we show that the habitat-induced transformation of ginseng root phenotype was accompanied by alteration in cytosine methylation at a large number of 5′-CCGG-3′ sites detected by the methylation-sensitive polymorphism (MSAP) marker. The collective CG and CHG methylation levels of all 4 landraces of the domesticated form were significantly lower than those of the wild form. Interestingly, artificially transplanted ginseng plants recreated in both directions the methylation levels (at least in CHG) of their natural counterparts. The methylation differences between the 2 ginseng ecotypes were validated at 2 isolated MSAP loci bearing homology to a 5S rRNA gene or a copia retrotransposon. Our results implicate a link between epigenetic variation and habitat-induced phenotypic flexibility in Oriental ginseng.     

Role of Tip60 tumor suppressor in DNA repair pathway

To prevent the damage caused by DNA strand breaks, eukaryotic cells have evolved a series of highly conserved DNA repair mechanisms. The ubiquitously expressed acetyltransferase, Tip60, plays a central role in ATM (ataxia-telangiectasia mutated) activation which is involved in DNA repair. Recent work uncovered a new mechanism of ATM activation mediated by Tip60 and demonstrated that histone methylation, specifically, trimethylation of histone H3, is a key factor in the process. Here, we review the current understanding of how Tip60 is activated and how it activates ATM in response to DNA damage.     

亚硝胺类化合物诱导小鼠食管病变与基因组甲基化的关系研究

研究亚硝胺类化合物诱导小鼠食管发生病变与基因甲基化的关系,在亚硝酸钠（NaNO2）和N,N-二甲基苄胺（N,N-Dimethylbenzylamine）混合物诱导小鼠食管病变过程中,定期取小鼠食管,一部分做病理切片观察组织学变化;另一部分提取组织DNA做变性高效液相色谱（Denaturing High Performance Liquid Chromatography,DHPLC）,检测基因组甲基化修饰的改变。结果在亚苄混合物诱导的小鼠食管癌变过程中,全基因组甲基化修饰是逐渐降低的,在达到一定程度后即保持一种稳态。此时组织病理学才发生光镜下可见的改变。说明全基因组甲基化修饰的逐渐降低可能是亚硝胺类化合物诱导食管发生病变的途径之一．这种基因修饰的变化有助于进一步研究食管鳞癌发生的分子机制。     

Histone methylation and ubiquitination with their cross-talk and roles in gene expression and stability

Methylation of lysine residues of histones is associated with functionally distinct regions of chromatin, and, therefore, is an important epigenetic mark. Over the past few years, several enzymes that catalyze this covalent modification on different lysine residues of histones have been discovered. Intriguingly, histone lysine methylation has also been shown to be cross-regulated by histone ubiquitination or the enzymes that catalyze this modification. These covalent modifications and their cross-talks play important roles in regulation of gene expression, heterochromatin formation, genome stability, and cancer. Thus, there has been a very rapid progress within past several years towards elucidating the molecular basis of histone lysine methylation and ubiquitination, and their aberrations in human diseases. Here, we discuss these covalent modifications with their cross-regulation and roles in controlling gene expression and stability. Received 24 September 2008; received after revision 21 November 2008; accepted 28 November 2008