广义逆A(2)T,S的体积

研究了广义逆A（T,S）^（2）是的体积，在不必首先计算出广义逆A（T,S）^（2）的前提下，导出了广义逆A（T,S）^（2）的体积表示，推广了文献[3]中的结果．由此分别给出了A的加权Moore-Penrose逆，Drazin逆Ad及群逆Ag的体积表示式．     

含有k次增生算子的方程x+Tx=f的具混合误差的Ishikawa迭代解

研究了一致光滑Banach空间中，k-次增生算子方程x Tx=f解的具混合误差的迭代过程．其中T不必是Lipschitz的，也不必是有界的．     

测度空间的拓扑序列熵

给定一个拓扑动力系统（X，T），记M（X）为X上Borel概率测度的全体，其上的拓扑由弱拓扑所诱导．如果系统（X，T）具有零拓扑序列熵，则它称为拓扑-null的．对于给定的一个伪度量空间以及其上的一个自映射（不必连续），引入并研究沿着给定序列的拓扑熵，包括由空间上连续实值函数所诱导的伪度量．作为应用可以证明，给定一个序列A包含于Z＋，如果X为零维的，那么，系统（X，T）沿着A具有零拓扑熵当且仅当（M（X），T）沿着A具有零拓扑熵．特别的，当X为一个零维空间时，系统（X，T）为拓扑-null的当且仅当（M（X），T）为拓扑-null的．     

含有κ—次增生算子T的方程x＋Tx=f的带误差的Ishikawa迭代解

建立了强收敛于方程x Tx=f的解的带误差的Ishikawa迭代过程，其中T是一致光滑Banach空间中的一个在D(T)既不必有界又不必连续(因而不必Lipschitz)的κ—次增生算子，推广了一些已有的结果。     

k次增生算子方程的Ishikawa迭代解

研究了一致光滑Banach空间中K—次增生算子的非线性方程解的迭代过程．其中K—增生算子T不必是Lip—ehitx的，也不必是有界的．改进和发展了一些文献中的结果。     

Fourier级数的极大Cesaro算子

讨论了Cesaro平均在Hardy空间Hp(T)上的有界性证明了当αp：＝1／p-1，0＜p≤时，极大Cesaro平均σ^α*是从Hp(T）到Lp（T）的有限界算子，而σ^α*（0＜p＜1）映Hp（T）到弱Lp（T）。其弱型估计是最好可能的，既不能扩以为p＝1的情形，也不能加强为强型估计，这些结论推广和完善了完善了已有结果。     

拓扑置成的LF拓扑空间

本又给出了由分明拓扑空间（X，T）置成的LF拓扑空间（LX，X（T）），研究了它的拓扑基结构，证明了（LX，X（T））是T2的，连通的空间，当且仅当（X，T）是T2的，连通的空间。     

关于k-次增生算子方程的具误差的Ishikawa迭代解

在任意Banach空间中,研究了非线性算子方程x+Tx=f的分别带2种误差的Ishikawa迭代序列的收敛性问题,其中T不必是增生的,也不必是Lipschitz的.     

线性赋范空间中不动点的逼近

在线性赋范空间中，应用Ishikawa迭代序列证明了3个不动点定理，这些定理也推广了Pathak HK和Kang SM等人的一些结果。设E是赋范线性空间X的凸子集，T是E到E的自映射，F（T）≠Ф，若对任意x1∈E，迭代序列M（x1，αn，βn，T）收敛于P，则P∈F（T）。又若X是一致凸的Banach空间，E是X的闭凸子集，T：E→E为自映射，对任意x0∈E，定义序列xn＋1=（1-cn）xn＋cnTxn，则迭代序列│xn│∞b=1若收敛于P，则P∈F（T）。     

标准算子代数的T-导子

设A为一代数，M为A－双模，线性映射，δ：A→M称为T－导子，是指对于任意，A，B∈A，使δ（AB）＝δ（A）T（B）＋T（A）δ（B）成立，该文研究了T－导子的性质，得出如下主要结论：（1）设A为标准算子代数，线性映射δ：A→A 满足δ（P）＝δ（P）T（P）＋T（P）δ（P），AP∈A，称为幂等元，则δ为T－导子；（2）设A是一个投影代数，M是一个BanachA一模，则A到M的任一范数连续的T－局部导子是T－导子。     

含有k-次增生算子T的方程x+Tx=f的带误差的Ishikawa迭代解

建立了强收敛于方程x Tx=f的解的带误差的Ishikawa迭代过程,其中T是一致光滑Banach空间中的一个在D(T)既不必有界又不必连续(因而不必Lipschitz)的k 次增生算子,推广了一些已有的结果.     

西北太平洋生成热带气旋的年代际变化

为了分析热带气旋年代际变化的特征和造成这种变化的原因,利用西北太平洋编号台风资料对1949～2003年55 a的西北太平洋热带气旋特点进行分析,发现西北太平洋生成的热带气旋不管是频数还是生成位置都存在明显的年代际变化,根据热带气旋频数的年代际变化,把研究的55 a分成低频时期(LFP)和高频时期(HFP)分别加以考察.结果发现:热带气旋生成的高低频时期海气条件存在明显的差异,HFP的海温、对流、涡散度和切变条件都有利于西北太平洋热带气旋的生成,而LFP则明显存在物理量场的相反异常.这表示HFP的海气环境相比LFP更有利于热带气旋生成,说明了变化的海气条件是引起热带气旋频数和生成位置年代际变化的主要原因.     

Mean-field cluster model for the critical behaviour of ferromagnets

Two separate theories are often used to characterize the paramagnetic properties of ferromagnetic materials. At temperatures T well above the Curie temperature, Tc (where the transition from paramagnetic to ferromagnetic behaviour occurs), classical mean-field theory yields the Curie-Weiss law for the magnetic susceptibility: X(T) infinity 1/(T - Weiss constant), where Weiss constant is the Weiss constant. Close to Tc, however, the standard mean-field approach breaks down so that better agreement with experimental data is provided by critical scaling theory: X(T) infinity 1/(T - Tc)gamma, where gamma is a scaling exponent. But there is no known model capable of predicting the measured values of gamma nor its variation among different substances. Here I use a mean-field cluster model based on finite-size thermostatistics to extend the range of mean-field theory, thereby eliminating the need for a separate scaling regime. The mean-field approximation is justified by using a kinetic-energy term to maintain the microcanonical ensembles. The model reproduces the Curie-Weiss law at high temperatures, but the classical Weiss transition at Tc = Weiss constant is suppressed by finite-size effects. Instead, the fraction of clusters with a specific amount of order diverges at Tc, yielding a transition that is mathematically similar to Bose-Einstein condensation. At all temperatures above Tc, the model matches the measured magnetic susceptibilities of crystalline EuO, Gd, Co and Ni, thus providing a unified picture for both the critical-scaling and Curie-Weiss regimes.     

哈茨木霉T23和3种土壤有益细菌的相互作用对白菜生长的影响

哈茨木霉T23对白菜生长的影响及叶绿素含量变化的影响不明显,也不能提高白菜硝酸还原酶的活性;3种供试细菌放线菌、光合细菌及乳酸杆菌均能促进植物的生长,提高白菜硝酸还原酶的活性,白菜叶绿素含量明显偏低;哈茨木霉T23与3种供试细菌两两混合使用对白菜的促生效果均比单独使用各供试细菌的效果明显,硝酸还原酶活性明显增加,白菜叶绿素含量明显偏低.哈茨木霉T23和3种供试细菌两两混合使用,4种供试菌的含量均比单独使用时显著增加.     

R0-代数上的滤子拓扑空间

在R0-代数M上以全体MP滤子之集为拓扑基建立了一个滤子拓扑空间(M,TM),给出了导集、闭包以及内部的计算公式。证明了(M,TM)是连通的、覆盖紧的且满足第一可数性公理;(M,TM)满足第二可数性公理当且仅当主滤子之集是可数集,(M,TM)不是T1的,不是T2的,也不是正则的或正规的;(M,TM)是T0空间当且仅当M是Boole代数。最后讨论了积R0-代数上的积空间。     

关于BCK代数的模型论性质

研究BCK代数的逻辑性质,对于形式化的BCK代数理论T,证明了在子模型和链连接下T是保存的;T既不具有完备性也不具有模型完备性,因此存在非构建的Skolem函数.另外,通过使用超滤子的概念以及所讨论的模糊理想的相应的性质,提出了超积BCK代数和BCK代数模糊子集的模糊超积.     

Phytohaemagglutinin activation of T cells through the sheep red blood cell receptor

Expression of receptors for sheep red blood cells and the ability to proliferate in response to phytohaemagglutinin (PHA) are the traditional properties of human T cells, but the function of the sheep red cell receptor (the T11 antigen) is controversial and the mechanism of PHA-induced mitogenesis unclear. Mitogenesis involves a complex series of cell-mediated and factor-dependent interactions, but a rise in intracellular free calcium concentration, [Ca2+]i, seems to be an important primary event in T-cell activation. We have now investigated the effects of three monoclonal antibodies, previously shown to inhibit mitogen-induced proliferation, on T-cell [Ca2+]i. We find that anti-LFA-2 and OKT11, which react with the sheep red cell receptor, have no effect on [Ca2+]i, nor do they inhibit the rise in [Ca2+]i induced by concanavalin A (Con A) or the mitogenic anti-T3 monoclonal antibody UCHT1 (ref. 11). They do, however, block PHA-induced Ca2+ mobilization. Anti-LFA-1, which reacts with the lymphocyte function-associated antigen, has no effect on intracellular Ca2+. These studies suggest that the sheep red blood cell receptor is an activation pathway for T cells and that the effects of PHA are mediated through this pathway.     

Assembly and function of the two ABC transporter proteins encoded in the human major histocompatibility complex.

Presentation of cytoplasmic antigens to class I-restricted cytotoxic T cells implied the existence of a specialized peptide transporter. For most class I heavy chains, association with peptides of the appropriate length is required for stable assembly with beta 2-microglobulin. Mutant cells RMA-S and .174/T2 neither assemble stable class I molecules nor present intracellular antigens, and we have suggested that they have lost a function required for the transport of short peptides from the cytosol to the endoplasmic reticulum. The genetic defect in .174 has been localized to a large deletion in the class II region of the major histocompatibility complex, within which two genes (RING4 and RING11) have been identified that code for 'ABC' (ATP-binding cassette) transporters. We report here that the protein products of these two genes assemble to form a complex. Defects in either protein result in the formation of unstable class I molecules and loss of presentation of intracellular antigens. The molecular defect in a new mutant, BM36.1, is shown to be in the ATP-binding domain of the RING11/PSF2 protein. This is in contrast to the mutant .134, which lacks the RING4/PSF1 protein.     

A novel family of human major histocompatibility complex-related genes not mapping to chromosome 6

Thymocyte antigens CD1 [Thy,gp45,12] are thought to be the human counterparts of mouse thymus leukaemia (TL) antigens. Serological and biochemical analyses indicate that at least three subsets exist, the first of which (HTA 1/T6) was initially identified by the monoclonal antibody NA1/34. Like TL, CD1 are expressed on cortical thymocytes as well as on some lymphoid neoplasias, and resemble in structure major histocompatibility complex (MHC) class I antigens. However HTA 1/T6 is loosely associated with beta 2-microglobulin and is also found linked by a disulphide bridge to CD8(T8). A molecular genetic approach is needed to investigate the CD1 system, to clarify its relationship to TL antigens and to understand its regulation. We report the isolation of complementary DNA (cDNA) clones encoding a CD1 antigen. These clones reveal a novel family of genes which are MHC-related but are neither equivalent to mouse TL antigens nor linked to the MHC.