钒模拟超氧化物歧化酶的活性中心计算

借助Fe-SOD的晶体结构模型，运用Gaussian 94程序包，采用HF下的LznL2DZ基组对钒辅基模拟超氧化物歧化酶的活性中心进行了量子化学计算，由其分子轨道能量，电荷分布和前线轨道的贡献可以理论预测，V－SOD具有较高的结构稳定性和催化超氧阴离子的活性。     

一种新型超氧化物歧化酶的活性中心量子化学计算

借助Fe-SOD的晶体模型，运用Gaussian94程序包，采用HF下的LanL2DZ基组对一种新型的超氧化物歧化酶Ni-SOD的还原型Ni(Ⅱ）－SOD的活性中心进行了量子化学计算，由其分子轨道能量，电荷分布和前线轨道的贡献可以预见，Ni-SOD具有较高的结构稳定性和催化超氧离子的活性。     

阴离子活性中心的自发终止

本文综述了文献中出现的阴离子活性中心的自发终止现象的研究结果。对聚苯乙烯,聚异戊二烯、聚丁二烯和聚甲基丙烯酸甲酯的阴离子活性中心进行了讨论和比较。通常,至少存在三种不同类型的自发终止过程:“转化”、“衰变”以及“转化”和“衰变”同时出现。这些自发终止反应可以用紫外光谱进行观察。     

还原型FeSOD活性中心量子化学计算

运用G94程序，采用HF方法LANL2DZ基组对于还原型FeSOD的晶体结构活性中心进行了量子化学从头计算，获得了分子轨道能量，电荷分布及原子轨道对前沿分子轨道贡献的信息。结果表明，其活性中心易于接受超氧自由基（O2^-.）的进攻并完成其生理功能。     

活化CO活性中心的abinitio研究

用ａｂｉｎｉｔｉｏ计算Ｃｕ＾ｍｎ－ＣＯ（ｎ＝１，２；ｍ＝０，＋１）考虑了ＣＯ与Ｃｕ＾ｍ２（ｍ＝０，＋１）结合的端位和桥位两种构型，根据计算的结果得到Ｃｕ＾ｍ２（ｍ＝０，＋１）桥位吸附有利于ＣＯ的活化，是活性中心。     

FT—IR研究RbNO3／LiX催化剂上乙醇缩合反应的活性中心

采用ＦＴ－ＩＲ技术研究了ＲｂＮＯ３／ＬｉＸ催化剂上的乙醇缩合反应的活性中心。当反应温度≥６３３Ｋ时，乙醇发生热解反应，导致表面负载ＲｂＮＯ３分解，并检测到表面存在ＮＯ２＾－、ＣＯ３＾２－、桥联结构的硝基配合物和酰基物种等。结果表明：亚硝酸盐不是硝酸盐分解的终产物，也不是催化反应的活性中心。反应活性物种可能主要是碱金属氧化物或直接形成的ＯＨ＾－即Ｂ碱。     

可及性与英汉指称词语的翻译

可及性是认识主体达到某一指称对象的难易程度。英汉指称形式存在共性，也有以下显著差异：英语中的代词和汉语中的零代词具有相同的可及性，而且汉语中处于主题位置上的代词和指示词语也具有高可及性；英语中的指示代词主要出现在中距离篇章语境中，是中可及性标示语，汉语中的中可及性标示语通常由宾语位置上的代词和指示词语充当；英汉语中，专有名词和有定描述语尽管同属于低可及性标示语，但仍存在差异。上述各方面差异，给英汉互译造成障碍，可通过分析其异质性表现来探索互译策略。     

指称词语可及性的认知研究

指称是名词性成分与其所指物之间的关系,除了语言学家以外,指称理论历来还受到哲学家的重视,以弗雷格、罗素、斯特劳森等为代表的分析哲学流派的指称理论具有很大的代表性,但体验哲学的视角也为指称理论研究提供了一个新的途径和契机.文章以认知语言学为切入点,从Ariel的可及性理论和Fauconnier的心理空间理论两个不同的视角入手,把指称置于更为广泛的话语交际框架中,分析指称词语与指称对象之间的可及性联系和有定指称如何进行认知建构.     

用NMR法研究色氨酸化学振荡反应的活性中心

利用核磁共振波谱仪研究了色氨酸的化学振荡反应。由ＮＭＲ波谱得知，振荡反应中存在着结合Ｂｒ２的活性基团，这些活性基团构成了振荡反应的活性中心，它们控制着振荡反 能否进行以及振荡寿命。     

酪氨酸酶活性中心模型化合物的合成与表征

合成了5种芳香酸类化合物:2,4-二羟基苯甲酸,3,5-二羟基苯甲酸,水杨酸,3,5-二硝基水杨酸,香草酸,利用它们来作为双氧桥分别与邻菲咯啉、铜盐合成三元混合配合物,来模拟酪氨酸酶的活性中心,并对所合成的配合物进行了红外光谱、紫外光谱的表征.     

DNA sequence and expression of the B95-8 Epstein-Barr virus genome

The complete (172,282 base pairs) nucleotide sequence of the B95-8 strain of Epstein-Barr virus has been established using the dideoxynucleotide/M13 sequencing procedure. Many RNA polymerase II promoters have been mapped and the mRNAs from these promoters have been assigned to the latent or early/late productive virus cycles. Likely protein-coding regions have been identified and three of these have been shown to encode a ribonucleotide reductase, a DNA polymerase and two surface glycoproteins.     

基于编码电缆的自动化立体仓库的地址检测

采用编码电缆位移传感器作为立体仓库位置检测元件,直接将一条传感器安装在轨道旁检测堆垛机大车水平方向的地址,另一条传感器安装在堆垛机立柱上检测堆垛机小车垂直方向的地址,能够方便地导引堆垛机驶入狭长的仓储巷道.由编码电缆位移传感器导引堆垛机组成的自动化立体仓库系统可以有效解决红外线导引堆垛机导致前后运行精度较低、反射板的布置困难以及反射光线之间相互干涉等技术难题,提高立体仓库堆垛机的水平方向和垂直方向定位精度和稳定性,减少一些外在因素引起的系统误差,实现物料输送的智能自动化.     

Binding of labelled influenza matrix peptide to HLA DR in living B lymphoid cells

T cells recognize protein antigens as fragments (peptides) held in a defined binding site of class I or class II major histocompatibility (MHC) molecules. The formation of complexes between various immunologically active peptides and different MHC molecules has been demonstrated directly in binding studies between the peptides and solubilized, purified molecules of class II MHC. Studies with intact cells, living or fixed, have not directly demonstrated the binding of the peptides to MHC molecules on antigen-presenting cells, but the formation of such complexes has been shown indirectly through the capacity of antigen-presenting cells to stimulate specific T cells. Here we report evidence that supports directly the binding of radiolabelled influenza matrix peptide 17-29 to products of the human class II MHC locus HLA-DR, on living homozygous B-cell lines, and we show that the kinetics of such binding is much faster with living cells than with fixed cells. Furthermore, whereas the peptide reacts with HLA-DR molecules of all alleles, it binds preferentially to DR1, the restricting element in antigen presentation.     

Presence of integrated hepatitis B virus DNA sequences in cellular DNA of human hepatocellular carcinoma

Hepatitis B virus (HBV) may be one of the agents involved in the aetiology of human primary liver cancer. This hypothesis is supported by (1) the similarity between the geographical distribution of chronic carriers of the viral surface antigen (HBsAg) and that of hepatocellular carcinoma (HCC); (2) the increase in the prevalence of HBV markers in serum of patients with primary liver cancer when compared with the general population; (3) the observation that HBV infection precedes the development of the tumour. Moreover, these epidemiological indications of an association between HBV infecton and hepatocellular carcinoma are supported by the detection of HBV markers such as HBsAg or viral DNA sequences, although in a non-integrated form in tumour tissue. To study the relationship between HBV and primary liver cancer further, we looked for the presence of free or integrated viral DNA in tumour tissue of human hepatocellular carcinomas and in a HBsAg-producing human hepatoma cell line. Using the blot-transfer hybridization technique and cloned HBV DNA as a probe, we have now demonstrated that the viral DNA is integrated in the cellular genome both in tumour tissue and in a hepatoma cell line.     

关于李超代数B(m,n)的包络代数的中心

设G=B(m,n),π是S(G)到S(H)上的投影算子,我们得到π(S(G)~G)属于S(H)~W的一个由P个元素生成的理想,p=max(m,n)。     

DNA damage defines sites of recurrent chromosomal translocations in B lymphocytes

Recurrent chromosomal translocations underlie both haematopoietic and solid tumours. Their origin has been ascribed to selection of random rearrangements, targeted DNA damage, or frequent nuclear interactions between translocation partners; however, the relative contribution of each of these elements has not been measured directly or on a large scale. Here we examine the role of nuclear architecture and frequency of DNA damage in the genesis of chromosomal translocations by measuring these parameters simultaneously in cultured mouse B lymphocytes. In the absence of recurrent DNA damage, translocations between Igh or Myc and all other genes are directly related to their contact frequency. Conversely, translocations associated with recurrent site-directed DNA damage are proportional to the rate of DNA break formation, as measured by replication protein A accumulation at the site of damage. Thus, non-targeted rearrangements reflect nuclear organization whereas DNA break formation governs the location and frequency of recurrent translocations, including those driving B-cell malignancies.