企业研发团队知识共享影响因素的实证研究

基于知识共享理论和研发团队知识共享特征和影响因素,提出企业研发团队知识共享影响因素概念模型及理论假设,并运用调查问卷和结构方程模型对研发团队知识共享影响因素进行实证研究.结果表明,知识提供者、接受者、共享手段和共享双方关系4因素对研发团队知识共享水平有显著影响,而知识共享文化对知识共享水平影响作用不显著.提出了提高企业研发团队知识共享水平的对策与建议.     

数学分析在高等代数中的某些应用

高等代数中的某些问题,若用代数学的方法解决起来可能相当繁琐,但若结合数学分析的方法,则问题往往会迎刃而解．该文使用数学分析中的函数连续性和无穷区间的广义积分知识解决某些矩阵问题和二次型问题．     

基于Simulink的动态电路分析

介绍了Simulink应用于动态电路仿真分析的方法,以一个实例详述了图形输入式建模、参数设置、仿真配置、Matlab绘图分析等步骤．指出了联合运用To File、To Workspace和Scope模块,实现不同参数情况下仿真分析的优越性．     

Inversion in the H-2 complex of t-haplotypes in mice

Mouse t-haplotypes demonstrate strong linkage disequilibrium between t-lethal genes and specific H-2 types, presumably a result of recombination suppression between t and normal chromosomes. The observation of free recombination occurring between two complementary t-haplotypes suggested a chromosomal mismatch between t and normal chromosomes. Recent data showing the H-2 complex to be misplaced relative to two other markers, T and tf, in t-haplotypes suggested that chromosomal rearrangement in t-haplotypes might be the basis for their 'mismatch' with the normal chromosome. Here, to analyse the molecular nature of the rearrangement, we have cloned a polymorphic H-2 class I restriction fragment, which had previously been shown to map centromeric to the serologically defined H-2 complex in t-haplotypes. Genetic mapping studies show that this cloned t-DNA is homologous to the H-2 D region of wild-type chromosomes, and that the E alpha Ia gene maps telomeric to this DNA fragment in t-haplotypes, in contrast to its orientation in wild-type chromosomes. These results give molecular evidence for an inversion of H-2 in t-haplotypes, which may be at least partially responsible for recombination suppression and thus for linkage disequilibrium.     

Polyreactivity increases the apparent affinity of anti-HIV antibodies by heteroligation

During immune responses, antibodies are selected for their ability to bind to foreign antigens with high affinity, in part by their ability to undergo homotypic bivalent binding. However, this type of binding is not always possible. For example, the small number of gp140 glycoprotein spikes displayed on the surface of the human immunodeficiency virus (HIV) disfavours homotypic bivalent antibody binding. Here we show that during the human antibody response to HIV, somatic mutations that increase antibody affinity also increase breadth and neutralizing potency. Surprisingly, the responding naive and memory B cells produce polyreactive antibodies, which are capable of bivalent heteroligation between one high-affinity anti-HIV-gp140 combining site and a second low-affinity site on another molecular structure on HIV. Although cross-reactivity to self-antigens or polyreactivity is strongly selected against during B-cell development, it is a common serologic feature of certain infections in humans, including HIV, Epstein-Barr virus and hepatitis C virus. Seventy-five per cent of the 134 monoclonal anti-HIV-gp140 antibodies cloned from six patients with high titres of neutralizing antibodies are polyreactive. Despite the low affinity of the polyreactive combining site, heteroligation demonstrably increases the apparent affinity of polyreactive antibodies to HIV.     

MATLAB应用于离散时间系统分析的教学探讨

在离散时间系统分析的课堂教学中，借助科学计算软件MATLAB能在阐述概念的同时。避免过多的手动运算，即时给出相关结果和函数图形，使得在有限的时间内展现整个系统分析的流程，节省了时间，改善了授课效果．     

Intravenous gammaglobulin suppresses inflammation through a novel T(H)2 pathway

High-dose intravenous immunoglobulin is a widely used therapeutic preparation of highly purified immunoglobulin G (IgG) antibodies. It is administered at high doses (1-2 grams per kilogram) for the suppression of autoantibody-triggered inflammation in a variety of clinical settings. This anti-inflammatory activity of intravenous immunoglobulin is triggered by a minor population of IgG crystallizable fragments (Fcs), with glycans terminating in α2,6 sialic acids (sFc) that target myeloid regulatory cells expressing the lectin dendritic-cell-specific ICAM-3 grabbing non-integrin (DC-SIGN; also known as CD209). Here, to characterize this response in detail, we generated humanized DC-SIGN mice (hDC-SIGN), and demonstrate that the anti-inflammatory activity of intravenous immunoglobulin can be recapitulated by the transfer of bone-marrow-derived sFc-treated hDC-SIGN(+) macrophages or dendritic cells into naive recipients. Furthermore, sFc administration results in the production of IL-33, which, in turn, induces expansion of IL-4-producing basophils that promote increased expression of the inhibitory Fc receptor FcγRIIB on effector macrophages. Systemic administration of the T(H)2 cytokines IL-33 or IL-4 upregulates FcγRIIB on macrophages, and suppresses serum-induced arthritis. Consistent with these results, transfer of IL-33-treated basophils suppressed induced arthritic inflammation. This novel DC-SIGN-T(H)2 pathway initiated by an endogenous ligand, sFc, provides an intrinsic mechanism for maintaining immune homeostasis that could be manipulated to provide therapeutic benefit in autoimmune diseases.     

Primary structure and genomic organization of the histidine-rich protein of the malaria parasite Plasmodium lophurae

The nucleotide sequence of a complete genomic clone for the histidine-rich protein of Plasmodium lophurae has been determined. The deduced amino acid sequence of the mature protein shows numerous tandemly repeated units preceded by a signal and a pro peptide. The gene is interrupted by an intron with a separate exon coding for the signal peptide. The signal peptide-encoding exon detects multiple cross-hybridizing sequences in the parasite genome.     

A chromosomal rearrangement in a P. falciparum histidine-rich protein gene is associated with the knobless phenotype

The significant morbidity and mortality associated with Plasmodium falciparum malaria results, in part, from the sequestration of parasitized erythrocytes in postcapillary venules, which may protect the parasite from splenic clearance and contribute to the pathogenesis of cerebral malaria. This sequestration has been linked to the expression of parasite-induced knob structures on the surface of the infected erythrocyte which mediate the cytoadherence phenomenon. While knobs are necessary for cytoadherence, they are not sufficient, requiring both parasite- and host-encoded proteins. Spontaneous mutants of P. falciparum have been isolated from in vitro cultures which lack the ability to express knobs and fail to cytoadhere. A histidine-rich protein has been described which is associated with the knobby phenotype and may be a constituent of the knob. We now report the isolation of complementary DNA clones for a knob-associated histidine-rich protein (KAHRP) and demonstrate that in knobless mutants the gene for this protein has undergone a rearrangement, resulting in a deletion in the 3' coding sequence. Moreover, the chromosome to which the KAHRP gene maps is rearranged in these mutants, producing a telomeric location of the truncated gene. These observations explain the loss of expression of the messenger RNA and protein in such mutants and may explain the loss of the knob itself. The implications for the generation of spontaneous mutations in the parasite by this novel mechanism are discussed.