氧化物半导瓷中晶界势垒的起源

提出了一个关于氧化物半导瓷晶界势垒起源的新观点，认为晶界势垒起源于烧结过程中外界氧在晶界中的扩散，与材料的结构、化学缺陷、掺杂、外界气氛、烧结工艺、组成状态等有密切关系，并用此理论解释了许多实验现象。     

交织扩展Golay码编译码器实现方案的研究

论述了交织编码的工作原理，给出了一种交织扩展Ｇｏｌａｙ码的改进型软件设计方案，用ＴＭＳ３２０Ｃ２５实现了其编译码器并给出了模拟实验结果。实验结果表明，它能准确地纠正不大于７２比特位的差错；处理１２８×１２８×８比特位的一幅图像数据的运行时间为０．４１２ｓ．     

激光开槽、埋槽电极硅太阳电池

报道一种新颖的激光开槽、埋槽电极硅太阳电池的结构、工艺流程及其研制结果。在ＡＭ１．５，２５℃，１００ｍＷ／ｃｍ２的条件下，以面积为４５ｃｍ３的３６片硅片研制的硅太阳电池的输出参数的平均值为ＪＳＣ＝３６．１ｍＡ／ｃｍ２，Ｖ∞＝６３３ｍＶ，Ｆ．Ｆ．＝０．７９８，η＝１８．２３％，最后分析了种高性能硅太阳电池的设计特点。     

Development and function of T cells in mice rendered interleukin-2 deficient by gene targeting.

Interleukin-2 (IL-2) is a lymphocytotropic hormone which is thought to have a key role in the immune response of mammalian cells. It is produced by a subpopulation of activated T-lymphocytes and acts in vitro as the principal auto- and paracrine T-cell growth factor (for reviews see refs 1-3). IL-2 is, however, not the sole T-cell growth factor, nor does it act exclusively on T cells, also promoting growth of NK cells and differentiation of B cells. A role for IL-2 in T-cell development has been postulated but remains controversial. Here we test the requirement for IL-2 in vivo using IL-2-deficient mice generated by targeted recombination. We find that mice homozygous for the IL-2 gene mutation are normal with regard to thymocyte and peripheral T-cell subset composition, but that a dysregulation of the immune system is manifested by reduced polyclonal in vitro T-cell responses and by dramatic changes in the isotype levels of serum immunoglobulins.     

Aeromonas caviae: ecologic adaptation in the intestinal tract of infants coupled to adherence and enterotoxin production as factors in enteropathogenicity

Aeromonas caviae isolated from stools of diarrheic formula-fed infants and environmental sources produce acetic acid when grown in glucose broth, which is bactericidal (suicide phenomenon). A. caviae grows anaerobically in a minimal medium or under permissive conditions such as the intestinal tract of formula-fed infants. These isolates adhered to HEp-2 cells and produced a cytotoxic and a cytotonic enterotoxin which underscore their enteropathogenicity.     

A small GTP-binding protein dissociates from synaptic vesicles during exocytosis.

Low-molecular-weight GTP-binding proteins are strong candidates for regulators of membrane traffic. In yeast, mutations in the sec4 or ypt1 genes encoding small GTP-binding proteins inhibit constitutive membrane flow at the plasma membrane or Golgi complex, respectively. It has been suggested that membrane fusion-fission events are regulated by cycling of small GTP-binding proteins between a membrane-bound and free state, but although most of these small proteins are found in both soluble and tightly membrane-bound forms, there is no direct evidence to support such cycling. In rat brain a small GTP-binding protein, rab3A, is exclusively associated with synaptic vesicles, the secretory organelles of nerve terminals. Here we use isolated nerve terminals to study the fate of rab3A during synaptic vesicle exocytosis. We find that rab3A dissociates quantitatively from the vesicle membrane after Ca2(+)-dependent exocytosis and that this dissociation is partially reversible during recovery after stimulation. These results are direct evidence for an association-dissociation cycle of a small GTP-binding protein during traffic of its host membrane.     

在UBBE框架下考虑不肯定的上界的估计方法

对目前的ＵＢＢＥ模型进行了适当的推广，使在解决估计问题时可以考虑那些可能是误差上界的数值，并在此基础上提出了一种方法，能够通过对估计精度和可靠性进行合理的权衡确定所需估计值，实际案例研究结果表明所提方法能够较好地解决估计精度和可靠性之间的矛盾。     

从著作权角度剖析逢甲大学校园数位内容经营服务管理计画

在数位化与网路化的学术典藏传播大趋势下 ,建构一个完整、方便、迅速与合理使用的校园数位内容经营服务体系 ,是兼具教育与研究两大使命的大学机构必须进行的工作 ,特别是对身负知识典藏与传播责任的图书馆来说 ,更是刻不容缓的任务 .本文介绍逢甲大学图书馆所规划推动的校园数位内容经营服务管理计画 ,探讨其征集服务范围以及提交、互评、加值典藏、传播与版权管理等作业流程 ,并说明所需要的支援团队和人力配置、所产出的产品形式和应用方式 .最后从著作权的角度分析校园数位内容经营服务所涉及的合理使用、著作财产权和著作授权使用问题     

The Huntington's disease candidate region exhibits many different haplotypes.

Analysis of 78 Huntington's disease (HD) chromosomes with multi-allele markers revealed 26 different haplotypes, suggesting a variety of independent HD mutations. The most frequent haplotype, accounting for about one third of disease chromosomes, suggests that the disease gene is between D4S182 and D4S180. However, the paucity of an expected class of chromosomes that can be related to this major haplotype by assuming single crossovers may reflect the operation of other mechanisms in creating haplotype diversity. Some of these mechanisms sustain alternative scenarios that do not require a multiple mutational origin for HD and/or its positioning between D4S182 and D4S180.