海洋药物研究新进展及其开发战略

概述了国内外海洋药物研究的新进展,以及加入WTO后对我国医药行业的冲击,并对我国,尤其是海南省在海洋药物领域的发展战略作一展望.     

强化对流传质的物理机制及其控制

根据对流传质强度与流体中存在的各种内场及其外场的关系，阐明了降低浓度边界层厚度、增加流体扰动和增加近壁面速度梯度的强化对流传质方法的物理机制，其本质是控制流体中内场及其外场之间的相互协同。进一步给出了强化传质场协同控制方法，以此可指导发展强化对流传质单元的新方法。     

关联规则算法及其优化

介绍了关联规则的典型算法，提出了关联规则算法的优化方向．     

汽车尾气三效催化转化器及其最新进展

汽车尾气控制已成为现今中国环保的热门话题。在机外净化系统中，由于三效催化转化器的成熟性和可靠性，无疑是中国汽车尾气控制的首选技术。目前，中国新生产的小型车全部安装进口的三效催化转化器。但是，仅靠进口不能支撑汽车工业的发展，中国必须研究和开发适合自己国情的三效催化转化器。文章全面论述了汽车排气污染物的危害、三效催化转化器的构造、催化原理、制作工艺、失活机理等方面的问题，特别讨论了三效催化转化器的工作技术要求和满足这些要求的途径。在此基础上，指出了中国研究发展自己的三效催化转化器的方向。     

邻单胞菌邻苯二酚1,2-双加氧酶基因(tfdC)在拟南芥中表达的初步研究

将从一株邻单胞菌中克隆到的一个新的邻苯二酚1，2－双加氧酶基因（tfd C)的起始密码子由GTG突变成ATG，并克隆到农杆菌双元载体pPZPY122中，利用农杆菌介导转化模式植物拟南芥，获得了转化植株，经过PCR，PCR－Southern和Southern dot blot方法检测证实，ftd C基因已经整合到拟南芥基因组中，邻苯二酚1，2－双加氧酶酶活性检测表明，转基因植株具有一定的酶活性，而未转化的植株则不具有酶活性。     

基于网络的水库群防洪调度系统应用研究

利用数据库前墙开发工具PowerdBuilder，采用SQL Server数据库，设计开发了结构合理、功能齐全、界面友好，具有很强实用性的基于网络的水库群防洪调度系统，可实现从卫星云图、气象预报信息、水雨情实测信息、实时洪水预报信息的收集处理到水库群防洪调度方案的制定，评价与选择、防汛会商决策全过程，简要介绍了系统的功能设计及其实现的基本思想。     

基于压力速度耦合算法的PEMFC电堆空气分布

利用燃料电池流道简化方法和压力速度耦合算法,研究了U形和Z形2种结构的电堆空气分布,以及歧管宽度和燃料电池单体数量对空气分布的影响.结果表明:由于U形和Z形结构的歧管出口压力分布不同,导致2种结构的空气分布不同,Z形结构的空气分布要比U形结构好;歧管尺寸增大时,空气分布的均匀性得到了明显改善,当空气分布差异不大时,再增...     

Evolutionary plasticity of genetic interaction networks

Non-additive genetic interactions contribute to many genetic disorders, but they are extremely difficult to predict. Here we show that genetic interactions identified in yeast, unlike gene functions or protein interactions, are not highly conserved in animals. Genetic interactions are therefore unlikely to represent simple redundancy between genes or pathways, and genetic interactions from yeast do not directly predict genetic interactions in higher eukaryotes, including humans.     

Systematic mapping of genetic interactions in Caenorhabditis elegans identifies common modifiers of diverse signaling pathways

Most heritable traits, including disease susceptibility, are affected by interactions between multiple genes. However, we understand little about how genes interact because very few possible genetic interactions have been explored experimentally. We have used RNA interference in Caenorhabditis elegans to systematically test approximately 65,000 pairs of genes for their ability to interact genetically. We identify approximately 350 genetic interactions between genes functioning in signaling pathways that are mutated in human diseases, including components of the EGF/Ras, Notch and Wnt pathways. Most notably, we identify a class of highly connected 'hub' genes: inactivation of these genes can enhance the phenotypic consequences of mutation of many different genes. These hub genes all encode chromatin regulators, and their activity as genetic hubs seems to be conserved across animals. We propose that these genes function as general buffers of genetic variation and that these hub genes may act as modifier genes in multiple, mechanistically unrelated genetic diseases in humans.     

ATP-sensitive potassium channels mediate survival during infection in mammals and insects

Specific homeostatic mechanisms confer stability in innate immune responses, preventing injury or death from infection. Here we identify, from a screen of N-ethyl-N-nitrosourea-mutagenized mice, a mutation causing both profound susceptibility to infection by mouse cytomegalovirus and approximately 20,000-fold sensitization to lipopolysaccharide (LPS), poly(I.C) and immunostimulatory (CpG) DNA. The LPS hypersensitivity phenotype is not suppressed by mutations in Myd88, Trif, Tnf, Tnfrsf1a, Ifnb, Ifng or Stat1, genes contributing to LPS responses, and results from an abnormality extrinsic to hematopoietic cells. The phenotype is due to a null allele of Kcnj8, encoding Kir6.1, a protein that combines with SUR2 to form an ATP-sensitive potassium channel (K(ATP)) expressed in coronary artery smooth muscle and endothelial cells. In Drosophila melanogaster, suppression of dSUR by RNA interference similarly causes hypersensitivity to infection by flock house virus. Thus, K(ATP) evolved to serve a homeostatic function during infection, and in mammals it prevents coronary artery vasoconstriction induced by cytokines dependent on TLR and/or MDA5 immunoreceptors.