粗糙极大算子交换子有界性的一个注记

本文给出一类粗糙核极大算子与ＢＭＯ函数产生的高阶交换子的加权（Ｌｐ，Ｌｑ）有界性     

住宅小区抹灰装饰工程质量预控

叙述了以往抹灰装饰工程中易发生的质量通病，并针对各病害产生原因，提出了施工方面的质量预控措施。     

交换压缩型映射的公共不动点定理

研究了交换压缩型映射不动点存在的问题，得到了四个映射公共不动点存在的条件和两类不动点存在的充分必要条件．     

加权Bergman空间的插值算子和乘子

用投影算子方法得了同了加权Ｂｅｒｍａｎ空间的一个插值算子定理，将此定理应用到Ｈａｒｄｙ空间和Ｂｅｒｇｍａｎ空间之间的乘子空间，得到一些在一定意义下为最好的充分条件。     

Gene product expression of cyclin D<Subscript>2</Subscript> and p16 during the transition from cardiac myocyte hyperplasia to hypertrophy

The current study was to investigate mRNA expression of cyclin D₂ and p16 during the transition from cardiac myocyte hyperplasia to hypertrophy. Cultured cardiac myocytes (CM) and fibroblasts (FC) obtained from 1-day-old Sparague-Dawley rats were used in this study. We have determined (1) hyperplasia by cell growth curve and fluorescence activated cell sorting (FACS); and (2) ultrastructure by electron microscope observation; and (3) expresions of cyclin D₂ mRNA and p16 mRNA by using in situ hybridization and image analysis. The results were shown (1) Results of cell growth curve and FACS analysis showed CM could proliferate in the first 3 cultured days (4 days in postnatal development). But the ability decreased quickly, concomitant with the differentiation. (2) The ultrastructure of CM showed the large amount of myofilaments and mitochondrion and FC showed moderate amount of rough endoplasmic reticulum. (3) The expression of cyclin D₂ mRNA in 3−, 4−, 5−day CM group was 0.89 times (p<0.05), 0.80 times (p<0.05) and 0.56 times (p<0.01) of that in 1-day group respectively. P16 mRNA in 2−, 3−, 4−, 5−day CM group were 1.63 times (p<0.01), 1.72 times (p<0.01), 1.99 times (p<0.01) and 2.84 times (p<0.01) of that in 1−day group respectively. It can be concluded that cultured neonatal rat cardiac myocytes could proliferate during the first 3 cultured days, but the ability of proliferation decreased, from the fourth day, concomitant with differentiation. Cyclin D₂ and p16 have the key roles during the transition from myocyte hyperplasia to hypertrophy. Biography: Zhang Yu-xia (1974-), female, Master, research direction: cardiovascular pathology.     

关于p-adic变量函数的微分

给出了p-adic变量p-adic值函数及p-adic变量实值函数的导数定义,将黎曼积分中下列公式推广到p-adic积分中去(1)有限增量公式;(2)积分变量替换公式;(3)微分链导法则.     

序列空间l_(p)的两个提升性质

证明了Banach空间序列{E_n}的l_(p)乘积l_(p)(E_n)的连续对偶空间为m_(p)(E_n~*),l_(p)(E_n)为r-凸空间当且仅当l_(p)为r-凸空间(0相似文献   

数坛怪杰爱尔特希

匈牙利数学家爱尔特希(Erdos,P.)是世界沃尔夫数学大奖得主之一.本文仅从几个侧面,介绍其数学生涯,评述其数学思想、工作特色.     

变p值二叉树形冲突分解算法分析

 提出了一种二叉树形冲突分解的改进算法,通过对随机争用多址访问系统中的信息分组冲突分解的研究,给出了冲突信息分组平均分解次数的解析式和系统吞吐量的解析式,仿真实验表明,仿真实现结果与理论值相吻合.     

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