大坝变形信息判据与分析

应用概率统计原理，对水库大坝变形观测中的变形值与随机因素干扰建立了变形数学模型。为排除干扰，提取真正变形信息，正确判据和分析大坝变形状态与规律提供理论依据。该数学模型在水库的实际应用中获得良好效果。     

求解k阶线性递归方程组的一种更有效的并行算法

将求解ｋ（ｋ≥２）阶线性递归方程组问题转化为求矩阵序列部分积问题，在ＳＩＭＤ共享存储模型上提出了求解ｋ阶线性递归方程组的一种新的有效并行算法．研究表明，本算法的加速和效率比现有算法均有较大的改善．     

使过半数规则具有传递性的偏好断面的规模

证明了当ｎ＞３时，使过半数投票表决的结果具有传递性的个人偏好序的最大数目大于２￣（ｎ－），从而否定了Ｃｒａｖｅｎ猜想。文中给出了最大偏好序的递推公式以及确定相应约束集的三条规则。     

应用扩展的Monod模型关联醋酸菌比生长速率

应用扩展的Ｍｏｎｏｄ模型关联了醋酸菌ＩＡＭ１８０２和Ｍ２３的比生长速率，ＩＡＭ１８０２的比生长速率关联式为μ＝０．４８７（１－ＣＰ／２３．８）＾０．２４８ＣＡ／ＣＭ＋ＣＡ；Ｍ２３的关联式为μ＝０．５６８（１－ＣＰ／６１．０）＾０．３０６ＣＡ／ＣＭ＋ＣＡ除临界生长抑制剂浓度附近外，模型良好地表达了两种醋力的比生长速率。     

水轮发电机组变结构变参数控制

本文阐述了水轮机变结构变参数调速控制的基本问题,提出了相应的控制策略,并论证该控制策略的稳定性、最优性。仿真结果表明本文提出的策略控制效果优良。     

水轮机调速器智能化自完善控制策略

本文提出了智能化自完善控制策略,通过采用“知识库”存贮最佳的知识与经验,根据受控对象当前运行条件及状态,运用相应的分析逻辑及推理功能,实时地调整控制器结构及参数,以实现逐步改善控制系统性能的目的.文中将所论述的控制策略用于水轮机调速器开发研究.     

GM-CSF induces human neutrophil IgA-mediated phagocytosis by an IgA Fc receptor activation mechanism

Immunoglobulin A is the primary immunoglobulin isotype in tears, saliva, breast milk and other mucosal secretions, constituting between 6% and 15% of the total serum immunoglobulins. Human peripheral blood neutrophils have IgA receptors, but these cells do not normally participate in IgA-mediated phagocytosis. The haematopoietic factors granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) prime neutrophils to be more responsive to a variety of stimuli. We therefore studied their effect on IgA-mediated phagocytosis. GM-CSF and G-CSF both induce a change from low to high-affinity neutrophil IgA Fc crystallizable fragment receptors within 30 min; a change which is associated with the development of IgA-mediated phagocytosis. Human IL-3, which does not affect neutrophil function, is inactive in this system. These results define a new mechanism for CSF-augmented host defence whereby neutrophil function can be modulated by CSF-mediated IgA Fc receptor activation.     

Protease inhibitor domain encoded by an amyloid protein precursor mRNA associated with Alzheimer's disease

Amyloid B-protein/amyloid A4 is a peptide present in the neuritic plaques, neurofibrillary tangles and cerebrovascular deposits in patients with Alzheimer's disease and Down's syndrome (trisomy 21) and may be involved in the pathogenesis of Alzheimer's disease. Recent molecular genetic studies have indicated that amyloid protein is encoded as part of a larger protein by a gene on human chromosome 21 (refs 6-9). The amyloid protein precursor (APP) gene is expressed in brain and in several peripheral tissues, but the specific biochemical events leading to deposition of amyloid are not known. We have now screened complementary DNA libraries constructed from peripheral tissues to determine whether the messenger RNA encoding APP in these tissues is identical to that expressed in brain, and we identify a second APP mRNA that encodes an additional internal domain with a sequence characteristic of a Kunitz-type serine protease inhibitor. The alternative APP mRNA is present in both brain and peripheral tissues of normal individuals and those with Alzheimer's disease, but its pattern of expression differs from that of the previously reported APP mRNA.     

Novel precursor of Alzheimer's disease amyloid protein shows protease inhibitory activity

Alzheimer's disease is characterized by cerebral deposits of amyloid beta-protein (AP) as senile plaque core and vascular amyloid, and a complementary DNA encoding a precursor of this protein (APP) has been cloned from human brain. From a cDNA library of a human glioblastoma cell line, we have isolated a cDNA identical to that previously reported, together with a new cDNA which contains a 225-nucleotide insert. The sequence of the 56 amino acids at the N-terminal of the protein deduced from this insert is highly homologous to the basic trypsin inhibitor family, and the lysate from COS-1 cells transfected with the longer APP cDNA showed an increased inhibition of trypsin activity. Partial sequencing of the genomic DNA encoding APP showed that the 225 nucleotides are located in two exons. At least three messenger RNA species, apparently transcribed from a single APP gene by alternative splicing, were found in human brain. We suggest that protease inhibition by the longer APP(s) could be related to aberrant APP catabolism.