一种求解非线性方程组的单纯形算法(algorithm)——同伦算法的分析及其收敛性

本文介绍了一种求解非线性方程组的单纯形算法——同伦算法 ,并对算法进行了分析 ,证明了其收敛性定理     

一类对称不定线性方程组的叠代求解(Ⅰ)

本文对于对称不定线性方程组■非奇异构造二步叠代格式求解,得到了较为完整的结果。     

试析调和级数的两个互补子级数的收敛性

本文在调和级数收敛性的基础上,通过对其两个互补子级数收敛性进行分析,以期说明在调和级数中去掉若干项后所构成的子级数,其收敛性是不同的。其根本原因就在于:调和级数去掉若干项后剩余下的项数相对于原调和级数的项数是否为一个低阶的无穷大。     

分布尾等价与极值的矩收敛

设（Ｘｎ，ｎ≥）是公共分布为Ｆ（ｘ）的独立同分布序列（简称ｉｉｄ序列，下同），（Ｘ１，Ｘ２，…Ｘｎ）的第ｋ个（１≤ｋ≤ｎ）最大值为Ｍｎ＾ｋ，（Ｙｎ，ｎ≥）是公共分布为Ｇ（ｘ）的ｉｉｄ序列，（Ｙ１，Ｙ２…Ｙｎ）的第ｋ个（１≤ｋ≤ｎ）最大值为Ｍｎ＾ｋ，在Ｆ（ｘ）与Ｇ（ｘ）尾等价的条件下，讨论了Ｍｎ＾ｋ的ｌ（ｌ∈Ｎ）阶矩与Ｍｎ＾ｋ的ｌ（ｌ∈Ｎ）阶矩之间的收敛关系。得到定理 设Ｆ（ｘ）∈Ｄ（Ｈ），ｌ∈Ｎ（     

The Convergence Rate of Ergodic Limits for Regularized Resolvent Families

This paper is concerned with the convergence rates of ergodic limits and approximation for regularized resolvent families for a linear Volterra integral equation. The results contain C0-semigroups, cosine operator functions and α-times integrated resolvent family as special cases.     

关于微积分学中的极限概念

本文详细分析了数学分析中各种主要类型的极限概念的区别与联系，就有关数学内容的处理提出一点参考意见．     

Carbon tetrachloride modulates the rat hepatic microsomal UDP-glucuronyl transferase activity and membrane fluidity

Summary Modulations in rat hepatic microsomal UDP-glucuronyl transferase activity have been observed during carbon tetrachloride (CCl₄) poisoning, with a large decrease in the enzyme cooperativity and increase in the membrane fluidity, occurring 30 min after administration. The results strengthen the possibility that an increase in microsomal membrane fluidity may be an early key event in liver injury induced by CCl₄.Acknowledgments. This work was supported by funds of the University of Athens.     

函数在无穷级数有关计算中的应用

将函数应用于无穷级数之中.欲求一个无穷级数的和,构造一个辅助幂级数,先求出这个幂级数的和函数,再将其结论应用于原问题之中,求出常数项无穷级数的和,从而给出了一个利用函数及其幂级数计算常数项级数之和的方法.     

Luteolytic potency of 16-phenoxy-derivatives of prostaglandin F2α

Summary The binding of 16-phenoxy derivatives of prostaglandin (PG) F₂ to rat luteal membranes, and also their abortifacient potency in pregnant rats, have been studied. Competitive binding studies with various PG-analogues were performed in ovaries of juvenile rats pretreated with PMSG and HCG, and in parallel studies the abortifacient potency of these substances was tested, in pregnant rats. It was observed that this class of derivatives bound to the PGF₂ receptor as well as, or even better than the parent compound PGF₂. Modifications in the carboxyl group at C-1 yielded derivatives with a higher affinity for the receptor, in decreasing order of effectiveness as follows:-COOR>COOH>OH. The data obtained from the binding studies also compared well with data on the abortifacient potency in pregnant rats. It is concluded that the addition of a phenoxy group to either the lower or upper side chain of PGF₂ may augment the binding to the receptor as well as the biological responses induced by the post receptor effect.     

Expression of the mutant gene for L-gulono-γ-lactone oxidase in scurvy-prone rats

A mutant strain of Wistar rats with L-gulono--lactone oxidase deficiency has recently been established. To investigate this deficiency by DNA and RNA blot hybridization analyses, a fragment of a previously cloned cDNA encoding rat L-gulono--lactone oxidase was used as a probe. When genomic DNA of the mutant rat was digested with several restriction enzymes, the probe hybridized to fragments of the same sizes as those produced from DNA of normal rats. Poly(A)⁺RNA from the liver of the mutant rat was found to contain an L-gulono--lactone oxidase-specific mRNA of a normal size at a comparable level to that of normal rats. An in vitro translation experiment revealed that the mRNA programmed the synthesis of an enzyme protein which had the same molecular weight as that of the translational product of the normal mRNA, although the amount synthesized was markedly reduced as compared with that synthesized with the normal mRNA. In accordance with this observation, a very low but definite degree of L-gulono--lactone oxidase activity was detected in the microsomes of the mutant rat by a newly developed, highly sensitive method.Acknowledgments. The authors thank Dr Susumu Makino, Shionogi Research Laboratories, Shionogi & Co., Ltd, Japan, for his kind donation of normal (ODS- +/+) and ODS (ODS-od/od) rats. This work was supported in part by Grant-in-Aid (59570103) for Scientific Research from the Ministry of Education, Science and Culture of Japan.