一类新型非线性光学材料——二苯甲酮衍生物的合成及性能研究

为寻求新型、高效、优质倍频材料,我们合成了一类新型二苯甲酮类化合物,并对其红外、紫外、光声光谱及倍频性能进行了系列研究,发现二苯甲酮类化合物具有较强的倍频效率和较短的截止吸收波长,有着广泛的应用前景。     

快速暂态过电压测试技术的研究

本文对气体绝缘配电站(GIS)中出现的快速暂态过电压提出了一种新的测量系统——电容探头-阻抗变换器测量系统。文中对电容探头,阻抗变换器的特性进行了系统的试验表述,并对测量电缆的补偿进行了计算,给出了决定最佳补偿参数的方法。     

莘县凹陷盆地模拟结果的地质解释

利用盆地模拟方法对勘探程度较低的莘县凹陷进行了油气生成和排出的定量模拟研究.讨论了模拟所需主要参数的确定方法,对模拟结果进行了地质解释.着重分析了主力生油层系的埋藏受热史、成熟度史及生、排油量史,初步划分了供油单元.研究指出,本区主力生油层系为下第三系沙三中下段,其次为沙四段.与相邻地区比,它们埋藏较浅,经受的最高地温及目前有机质的成熟度均偏低,总体上尚处于主要生油阶段的早中期.因主要排油期发生较晚,致使油气近距离运移为主,禹城洼陷和梁水镇洼陷两个主要油源区控制着凹陷中最有远景区的分布.     

论智能分布式模拟屏实时监控系统(DIRMSS)设计

本文提出一种全新的DIRMSS系统结构,该系统既能独立自成系统又可联网,既能实时又能非实时运行,既能支持实时动态图形表格显示,又可离线利用ECAD生成图形画面,同时还具备通讯信道自诊断故障定位、显示设备故障定位和路径敏化等优点。     

新氯化-水解法的原理和应用

本文详细论述了新氯化-水解法的水解平衡,氯络合平衡及氧化-还原平衡的量化方式和数模控制;重点介绍了新氯化-水解法在处理各种硫化锑矿原料,特别是极复杂的含锑矿物原料和中间物料方面的广泛应用。     

求解含裂纹正交各向异性平面问题应力强度因子的耦合法——位移间断法与边界元法的耦合

本文在推导出正交各向异性平面位移间断基本解的基础上,建立了一组求解裂纹表面位移的方程,并较精确地求出应力强度因子K_I和K_Ⅱ。将这一方法与边界元法相耦合,解决了含孔洞及裂纹群复杂问题。随着边界单元数目的增大,数值结果迅速趋于某一极限(精确解)。通过与现有数值结果比较,本耦合法具有很高的精度和极强的收敛性。     

Clonal expansion of p53 mutant cells is associated with brain tumour progression.

Tumour progression is a fundamental feature of the biology of cancer. Cancers do not arise de novo in their final form, but begin as small, indolent growths, which gradually acquire characteristics associated with malignancy. In the brain, for example, low-grade tumours (astrocytomas) evolve into faster growing, more dysplastic and invasive high-grade tumours (glioblastomas). To define the genetic events underlying brain tumour progression, we analysed the p53 gene in ten primary brain tumour pairs. Seven pairs consisted of tumours that were high grade both at presentation and recurrence (group A) and three pairs consisted of low-grade tumours that had progressed to higher grade tumours (group B). In group A pairs, four of the recurrent tumours contained a p53 gene mutation; in three of them, the same mutation was found in the primary tumour. In group B pairs, progression to high grade was associated with a p53 gene mutation. A subpopulation of cells were present in the low-grade tumours that contained the same p53 gene mutation predominant in the cells of the recurrent tumours that had progressed to glioblastoma. Thus, the histological progression of brain tumours was associated with a clonal expansion of cells that had previously acquired a mutation in the p53 gene, endowing them with a selective growth advantage. These experimental observations strongly support Nowell's clonal evolution model of tumour progression.     

Dynamin is a GTPase stimulated to high levels of activity by microtubules.

Dynamin was initially identified in calf brain tissue as a protein of relative molecular mass 100,000 which induced nucleotide-sensitive bundling of microtubules. Purified dynamin showed only trace ATPase activity. But in combination with an activating factor removed during the purification, it exhibited microtubule-activated ATPase activity and dynamin-induced bundles showed evidence of ATP-dependent force production. Dynamin is the product of the Drosophila gene shibire, which has been implicated in synaptic vesicle recycling and, more generally, in the budding of endocytic vesicles from the plasma membrane. Dynamin also shows extensive homology with proteins that participate in vacuolar protein sorting and spindle pole-body separation in yeast, and in interferon-induced viral resistance in mammals. All members of this family contain consensus sequence elements consistent with GTP binding near their amino termini, although none has been shown to have GTPase activity. We report here that dynamin is a specific GTPase which can be stimulated to very high levels of activity by microtubules.     

Different beta-subunits determine G-protein interaction with transmembrane receptors.

Regulatory GTP-binding proteins (G proteins) are membrane-attached heterotrimers (alpha, beta, gamma) that mediate cellular responses to a wide variety of extracellular stimuli. They undergo a cycle of guanine-nucleotide exchange and GTP hydrolysis, during which they dissociate into alpha-subunit and beta gamma complex. The roles of G-protein alpha-subunits in these processes and for the specificity of signal transduction are largely established; the beta- and gamma-subunits are essential for receptor-induced G-protein activation and seem to be less diverse and less specific. Although the complementary DNAs for several beta-subunits have been cloned, isolated subunits have only been studied as beta gamma complexes. Functional differences have been ascribed to the gamma-subunit on the basis of extensive sequence similarity among beta-subunits and apparent heterogeneity in gamma-subunit sequences. Beta gamma complexes can interact directly or indirectly with different effectors. They seem to be interchangeable in their interaction with pertussis toxin-sensitive alpha-subunits, so we tested this by microinjecting antisense oligonucleotides into nuclei of a rat pituitary cell line to suppress the synthesis of individual beta-subunits selectively. Here we show that two out of four subtypes of beta-subunits tested (beta 1 and beta 3) are selectively involved in the signal transduction cascades from muscarinic M4 (ref. 4) and somatostatin receptors, respectively, to voltage-dependent Ca2+ channels.     

Human aminopeptidase N is a receptor for human coronavirus 229E.

Human coronaviruses (HCV) in two serogroups represented by HCV-229E and HCV-OC43 are an important cause of upper respiratory tract infections. Here we report that human aminopeptidase N, a cell-surface metalloprotease on intestinal, lung and kidney epithelial cells, is a receptor for human coronavirus strain HCV-229E, but not for HCV-OC43. A monoclonal antibody, RBS, blocked HCV-229E virus infection of human lung fibroblasts, immunoprecipitated aminopeptidase N and inhibited its enzymatic activity. HCV-229E-resistant murine fibroblasts became susceptible after transfection with complementary DNA encoding human aminopeptidase N. By contrast, infection of human cells with HCV-OC43 was not inhibited by antibody RBS and expression of aminopeptidase N did not enhance HCV-OC43 replication in mouse cells. A mutant aminopeptidase lacking the catalytic site of the enzyme did not bind HCV-229E or RBS and did not render murine cells susceptible to HCV-229E infection, suggesting that the virus-binding site may lie at or near the active site of the human aminopeptidase molecule.