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。     

茶刺蛾[Darna trima(more)]颗粒体病毒鉴定及核酸与蛋白质特性的初步研究

1985年从四川珙县分离到的茶刺蛾病原物,经感染试验,组织病理研究,包涵体及病毒粒子超微结构研究,核酸类型鉴别等,定名该病原物为茶刺蛾颗粒体病毒.另对该病毒核酸作了限制性内切酶分析和热变性试验,测得该病毒核酸为双链DNA分子,分子量为64.11×10~6d,93.87kb,Tm值为67.3℃,(G+C)含量为32.7％,包涵体蛋白的氨基酸组分中Asp、Glu和Arg含量高,占氨基酸总量的34.12％,His,Cys和Met含量很少。该病毒对茶刺蛾幼虫有很强的感染力,氨基酸在生物防治上有潜在应用前景.     

（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．     

B位元素掺杂对Y-Ba-Cu-O系ABO_3化合物超导电性影响的研究

自高T_c氧化物超导陶瓷出现以来,已提出了许多可能与超导电性相关的因素。为探讨这些因素对超导性的影响,对元素掺杂的研究有着重要的意义。按照容许因子公式的要求,我们选择了满足ABO_3化合物中B位要求条件下的过渡族元素,将它们掺入(YBa)CuO_3中时,能部分取代Cu的位置而处于B位上。这样利用B位元素的少量掺杂,可以作为“结构探针”引出与周围O的2P电子、氧缺位及Cu、稀土离子等相互作用信息的变化,有助于对超导微观机理的了解;又因为ABO_3化合物     

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