关于大型科研仪器共享问题的一个产权理论解释

大型科研仪器的共享问题是我国科技资源配置和管理工作中面临的重要问题,现有研究和对策主要集中于促进共享理念的传播、加强共享效率的考核以及仪器中心等共享机制的建设方面,但对于为什么存在共享障碍等基本问题缺少关注。本文以经济学中的产权理论为基础,从大型科研仪器所有权与控制权分离的现实出发,探讨了当前我国仪器共享中存在的利益冲突和机制障碍。在此基础上,借鉴发达国家的一些做法,提出从仪器资助体制出发解决仪器共享问题的新思路。     

Far-infrared Absorption Spectra and Properties of SnO2 Nanorods

Nanostructured materials have drawn considerable attention because they are promising candidates for nextgeneration electronic and photonic devices with low power consumption[1-5]. A number of methods, such as laser ablation[6], template-induced growth[7], arc discharge [8], vapor transport [9], and molecular-beam epitaxy[10] have been developed to synthesize Si, Ge, MgO,SnO2, GaN, and Ga2O3 nanowires or nanorods[11-15].     

耐久性阻燃尼龙-6织物的研制

提出以羟甲基改性尼龙-6织物与反应型有机磷系,溴系阻燃剂进行,耐久性阻燃整理的新方法,讨论不同阻燃整理液对尼龙－6织物阻燃性能的影响,确定最佳阻燃整理液的配方,并通过正交化实验寻找合理的复合工艺参数,红外光谱和元素分析结果表明,羟甲基改性尼龙－6织物与阻燃剂通过化学键结合,所得织物手感良好,阻燃耐久性优良。     

Cloning of a representative genomic library of the human X chromosome after sorting by flow cytometry

A library of 50,000 recombinants representative of the human X chromosome has been constructed. Human X chromosomes were physically separated using a fluorescence-activated cell sorter. The DNA was purified from the chromosomes, digested to completion with the restriction enzyme EcoRI and cloned into the phage lambda gtWES.lambda B. The X-derived nature of the recombinants was confirmed by hybridization to rodent/human cell line DNA containing only the human X chromosome. Such libraries will be particularly useful for the investigation of genetic diseases such as Duchenne muscular dystrophy, where the basic defect has not been elucidated, and of neoplasia, where several specific chromosomal anomalies, particularly for the leukaemias, have been identified.     

高能p碰撞过程中的光生SM Higgs玻色子(英文)

计算了LHC条件下 ,p p以质心系能量为 s =1 4TeV以及 2 0 0TeV碰撞过程中的光生标准模型Higgs玻色子截面 .结果表明 ,在此条件下 ,可以在质量区 50～ 30 0GeV内测量到SMHiggs玻色子 .     

基于改进型BP算法的外债风险指标预测

利用人工神经网络进行时间序列预测是一种较新的方法,它具有不需建立复杂的数学模型以及非线性映射能力强等优点。采用动量法和学习率自适应调整的改进型BP算法对外债风险的各项指标进行了非线性时间序列的预测。仿真结果表明神经网络模型对外债风险的各项指标预测的结果是准确可靠的。     

Anthropogenic ocean acidification over the twenty-first century and its impact on calcifying organisms

Today's surface ocean is saturated with respect to calcium carbonate, but increasing atmospheric carbon dioxide concentrations are reducing ocean pH and carbonate ion concentrations, and thus the level of calcium carbonate saturation. Experimental evidence suggests that if these trends continue, key marine organisms--such as corals and some plankton--will have difficulty maintaining their external calcium carbonate skeletons. Here we use 13 models of the ocean-carbon cycle to assess calcium carbonate saturation under the IS92a 'business-as-usual' scenario for future emissions of anthropogenic carbon dioxide. In our projections, Southern Ocean surface waters will begin to become undersaturated with respect to aragonite, a metastable form of calcium carbonate, by the year 2050. By 2100, this undersaturation could extend throughout the entire Southern Ocean and into the subarctic Pacific Ocean. When live pteropods were exposed to our predicted level of undersaturation during a two-day shipboard experiment, their aragonite shells showed notable dissolution. Our findings indicate that conditions detrimental to high-latitude ecosystems could develop within decades, not centuries as suggested previously.     

Prion-like behaviour and tau-dependent cytotoxicity of pyroglutamylated amyloid-β

Extracellular plaques of amyloid-β and intraneuronal neurofibrillary tangles made from tau are the histopathological signatures of Alzheimer's disease. Plaques comprise amyloid-β fibrils that assemble from monomeric and oligomeric intermediates, and are prognostic indicators of Alzheimer's disease. Despite the importance of plaques to Alzheimer's disease, oligomers are considered to be the principal toxic forms of amyloid-β. Interestingly, many adverse responses to amyloid-β, such as cytotoxicity, microtubule loss, impaired memory and learning, and neuritic degeneration, are greatly amplified by tau expression. Amino-terminally truncated, pyroglutamylated (pE) forms of amyloid-β are strongly associated with Alzheimer's disease, are more toxic than amyloid-β, residues 1-42 (Aβ(1-42)) and Aβ(1-40), and have been proposed as initiators of Alzheimer's disease pathogenesis. Here we report a mechanism by which pE-Aβ may trigger Alzheimer's disease. Aβ(3(pE)-42) co-oligomerizes with excess Aβ(1-42) to form metastable low-n oligomers (LNOs) that are structurally distinct and far more cytotoxic to cultured neurons than comparable LNOs made from Aβ(1-42) alone. Tau is required for cytotoxicity, and LNOs comprising 5% Aβ(3(pE)-42) plus 95% Aβ(1-42) (5% pE-Aβ) seed new cytotoxic LNOs through multiple serial dilutions into Aβ(1-42) monomers in the absence of additional Aβ(3(pE)-42). LNOs isolated from human Alzheimer's disease brain contained Aβ(3(pE)-42), and enhanced Aβ(3(pE)-42) formation in mice triggered neuron loss and gliosis at 3 months, but not in a tau-null background. We conclude that Aβ(3(pE)-42) confers tau-dependent neuronal death and causes template-induced misfolding of Aβ(1-42) into structurally distinct LNOs that propagate by a prion-like mechanism. Our results raise the possibility that Aβ(3(pE)-42) acts similarly at a primary step in Alzheimer's disease pathogenesis.