血清中微量镉的离心光度法测定研究

研究一种超高灵敏直接测定血清中微克级钢的新分析方法──离心光度法．在Ｃｄ－Ｂｒ－ＲＢ体系中缔合物表观摩尔吸光系数ε５６０＝５．０６×１０８Ｌ·ｍ－１·Ｃｍ－１，Ｃｄ２＋的浓度在１．０×１０－９～１０．０×１０－９ｍｏｌ·Ｌ－１范围服从Ｂｅｅｒ定律．本法用于分析测定人体血清样品中Ｃｄ２＋，得其含量为１．８７×１０－１１ｍｏｌ·Ｌ－１，变异系数为４．２％（ｎ＝５）．     

主次波长新光度法测定环境水中微量硼

在浓硫酸中,硼与胭脂红生成蓝色络合物。本文在此显色基础上,依据主次双波长光度理论,研究了环境水体中微量硼测定的新方法。该方法提高了分析精密度及灵敏度,且计算曲线稳定性好。在对环境水体的测定中,方法的检出限为0.3mg/L,相对标准偏差RSD≤2.2％,回收率96.2～103.0％。     

基于B^＋树的关系数据库性能评价

本文提出了一种关系数据库性能评价的方法。对采用B~+树索引结构的关系数据库存储开销、响应时间和系统维护开销作了分析讨论,并在此基础上提出了4个评价关系数据库性能的参数,即存储开销n_(total)、平均响应时间T。、系统维护开销C_m和性能代价差R。     

北京鸭腔上囊的研究：Ⅶ,B淋巴细胞分化的免疫球蛋白表达

应用兔抗鸭IgM和5.7S IgG血清,以间接免疫荧光法研究北京鸭腔上囊中B淋巴细胞的分化,得到以下结果:(1)B淋巴细胞表面和胞质免疫球蛋白出现的时间:胚胎11天,CIgM;胚胎15天SIgM;胚胎18天 SIgG;胚胎21天CIgG。(2)B淋巴细胞分化可分为3个阶段.第1阶段(胚胎11～15天),CIgM~+淋巴干细胞分化为SIgM~+前淋巴母细胞;第2阶段(胚胎15～21天),SIgM~+前淋巴母细胞分化为SIgM~+、SIgG~+淋巴母细胞;第3阶段(胚胎21～28天孵出),SIgG~+淋巴母细胞分化为中、小淋巴细胞,并开始从腔上囊迁出。(3)北京鸭腔囊中B淋巴细胞分化过程与鸡具有平行的时间关系。     

河北省丝孢菌研究Ⅴ.节簇孢属、小枝双孢属和斯佩霉属

本文报道了作者近年来采自河北省的丝孢菌纲的3个国内新记录种,它们分别是节簇孢属(Gonatobotrys Cda)的简单节簇孢(G.simplex Cda),小枝双孢属(Diplocladiella Arnaud apud M.B.Ellis)的拟梯孢小枝双孢(D.scalarioides Arnaud apud M.B.Ellis)和斯佩霉属(Spegazzinia Sacc.)的四方斯佩霉(S.tessarthra(Berk.& Curt.)Sacc.)。节簇孢属和斯佩霉属系国内新纪录属,小枝双孢属在中国大陆首次报道。     

（Nd，Dy）－（Fe，Co，Tm）－B稀土永磁体的磁性能与显微组织（Tm＝Al，Nb，Mo，V）

研究了含钴ＮｄＦｅＢ系列稀土永磁体的磁性能与显微组织，Ｃｏ加入到三元ＮｄＦｅＢ磁体中显著提高磁体的居里温度Ｔｃ，因而大大改善了可逆温度系数α（Ｂｒ）．对实验数据的计算机拟合表明二者间符合指数函数关系，且在单对数坐标中表现为两阶段曲线．在多组元ＮｄＦｅＢ合金系列中，Ａｌ是提高含Ｃｏ磁体矫顽力最有效的元素，其次是Ｍｏ，而Ｎｂ和Ｖ则不能改善Ｃｏ对矫顽力的有害影响．高Ｃｏ磁体中，Ａｌ恶化α（Ｂｒ）的作用已非主要，这是由于Ｃｏ提高Ｔｃ的作用大于Ａｌ对Ｔｃ的降低作用，但含Ａｌ磁体的β（ｆＨＣ）较大，导致ｆＨｃ随温度上升而迅速下降．含Ｎｂ、Ｍｏ、Ｖ磁体的β（ｆＨｃ）则显著优于含Ａｌ磁体．     

无穷维随机微分方程的稳定性

本文主要考察确定性ｋ值随机微分方程（Ⅰ）ｄｘｔ＝Ａｘｔｄｔ和关于Ｈ值Ｃ．Ｂ．ｍ的随机微分方程（Ⅱ）ｄｘｔ＝ＡＸｔｄｔ＋Ｇ（Ｘｔ）ｄＢｔ及（Ⅲ）ｄｘｔ＝ＡＸｔｄｔ＋Ｇ（Ｘｔ－Ｘｔ－τ）ｄＢｔ（其中τ为充分小常量）的几种稳定性之间的关系     

B90催化剂上丁烯氧化脱氢的反应动力学─一一种简便的建立化学动力学方程的方法

采用简便的建立化学反应动力学方程的方法，研究了Ｂ９０催化剂上丁烯氧化脱氢制丁二烯反应的动力学，即先在一较低温度下，用微分法拟合得到化学反应动力学方程中的浓度项，然后改变反应温度，求算不同温度下的反应速率常数。采用这个简便方法，只需较少的实验，即可求得该反应体系中的丁烯转化速率方程式。     

Peptide aptamers: exchange of the thioredoxin-A scaffold by alternative platform proteins and its influence on target protein binding

Peptide aptamers have emerged as powerful new tools for molecular medicine. They can specifically bind to and functionally inactivate a given target molecule under intracellular conditions. Typically, peptide aptamers are generated by screening a randomized peptide expression library, displayed from the Escherichia coli thioredoxin A (TrxA) protein. Here, we transferred peptide moieties from defined TrxA-based peptide aptamers to alternative scaffold proteins, such as the green fluorescent protein and staphylococcal nuclease. Yeast and mammalian two-hybrid assays as well as in vitro binding analyses show that the TrxA scaffold can be a major determinant for the binding of peptide aptamers. In addition, we demonstrate that TrxA can correctly display peptide sequences that correspond to the binding domains of natural interaction partners. Therefore, sequence analyses of TrxA-based peptide aptamers, isolated by two-hybrid screening from randomized expression libraries, should also be useful to find cellular binding partners for a given target protein, by homology. Received 1 August 2002; received after revision 17 September 2002; accepted 19 September 2002 RID="*" ID="*"Corresponding author.     

The Ror receptor tyrosine kinase family

Receptor tyrosine kinases (RTKs) participate in numerous developmental decisions. Ror RTKs are a family of orphan receptors that are related to muscle specific kinase (MuSK) and Trk neurotrophin receptors. MuSK assembles acetylcholine receptors at the neuromuscular junction [1, 2], and Trk receptors function in the developing nervous system (reviewed in [3-5]). Rors have been identified in nematodes, insects and mammals. Recent studies have begun to shed light on Ror function during development. In most species, Rors are expressed in many tissue types during development. Analyses of mutants that are defective in the single nematode Ror demonstrate a role in cell migration and in orienting cell polarity. Mice lacking one of the two Ror gene products display defects in bone and heart formation. Similarly, two different human bone development disorders, dominant brachydactyly B and recessive Robinow syndrome, result from mutations in one of the human Ror genes. Received 17 April 2001; received after revision 2 July 2001; accepted 4 July 2001