图书馆编目数据外包问题的探讨——以西安图书馆为例

对图书馆编目数据外包工作中产生的数据错误的原因进行了分析,并提出了防范数据错误的措施,以完善和促进编目数据外包工作。     

基于化学荧光法的双黄连口服液神经氨酸酶抑制活性测定

建立流感病毒神经氨酸酶体外活性荧光检测法测定双黄连口服液的NA抑制生物活性.采用化学荧光法测定双黄连口服液对神经氨酸酶的抑制率.结果表明,反应后溶液荧光强度与产物4-MU浓度在0.1~1.2μg/m L内成良好的线性相关系(Y=39482X-254.05(r=0.9994)),该测定方法的精密度与重复性良好,反应后溶液在4℃条件下4 h内稳定,双黄连口服液对流感病毒神经氨酸酶的抑制率高达64.20%.该方法可用于测定双黄连口服液对神经氨酸酶抑制活性测定.     

论减灾系统的远程公平化

远程公平化是偏向于远程的公平，旨在寻求系统整体的优化。在一定的约束条件下，通过域的分隔、变形，中心的定位与相应的远程运作机制，可消减不利因素对系统的干扰，扩大结构瓶颈，调优技术性弱点、难点、远点、易忽视点的指标期望与实现值，抑小扬大，隐近就远，弥补系统缺陷，或于不完备的条件下构建 完备系统，保障全局利益与远效，推进减灾管理的科学化，改善各个方面的减灾工作。     

液压油缸加工方式之探

阐述了液压传动系统中的执行元件-液压油缸缸筒的加工方式，着重介绍了缸筒的加工工序、内孔加工的重要刀具以及注意事项。     

NiO nanosheet assembles for supercapacitor electrode materials

In this paper, large scale hierarchically assembled Ni O nanosheets have been favorably fabricated through a facile hydrothermal route. The as-prepared Ni O nanosheet assembles were characterized in detail by various analytical techniques. The results showed these nanosheets present the thickness of about 30 nm and the surface area is 116.9 m~2 g~(-1). These NiO nanosheet assembles were used as the working electrode materials in electrochemical tests, which demonstrated a specific capacitance value of 81.67 Fg ~(-1)at the current density of 0.5 Ag~(-1)and excellent long cycle-life stability with 78.5% of its discharge specific capacitance retention after 3000 cycles at the current density of 0.5 Ag~(-1), revealing the as-synthesized NiO nanosheet assembles might be a promising electrode material for supercapacitor applications.     

NaCl和KCl溶液康普顿散射的影响因素

自康普顿散射提出以来,其理论研究和应用研究一直是国内外的热点。基于NaCl和KCl溶液的康普顿散射,通过一定的近似处理,从理论上分析适合这两种溶液的康普顿散射光子数与溶液浓度之间的关系表达式;然后,通过康普顿散射实验验证康普顿散射的理论和实验研究。为了从更微观的角度来把握NaCl和KCl溶液康普顿散射的机理,笔者立足于密度泛函理论对NaCl与KCl溶液的电子结构作了深入分析,得出结论:除质量密度、散射衰减因子以及溶液的浓度外,电子数密度和电子受到的束缚也对康普顿散射光子数有影响,其中,电子数密度是影响NaCl与KCl溶液康普顿散射光子数的主要因素。     

HDAC6 rescues neurodegeneration and provides an essential link between autophagy and the UPS

A prominent feature of late-onset neurodegenerative diseases is accumulation of misfolded protein in vulnerable neurons. When levels of misfolded protein overwhelm degradative pathways, the result is cellular toxicity and neurodegeneration. Cellular mechanisms for degrading misfolded protein include the ubiquitin-proteasome system (UPS), the main non-lysosomal degradative pathway for ubiquitinated proteins, and autophagy, a lysosome-mediated degradative pathway. The UPS and autophagy have long been viewed as complementary degradation systems with no point of intersection. This view has been challenged by two observations suggesting an apparent interaction: impairment of the UPS induces autophagy in vitro, and conditional knockout of autophagy in the mouse brain leads to neurodegeneration with ubiquitin-positive pathology. It is not known whether autophagy is strictly a parallel degradation system, or whether it is a compensatory degradation system when the UPS is impaired; furthermore, if there is a compensatory interaction between these systems, the molecular link is not known. Here we show that autophagy acts as a compensatory degradation system when the UPS is impaired in Drosophila melanogaster, and that histone deacetylase 6 (HDAC6), a microtubule-associated deacetylase that interacts with polyubiquitinated proteins, is an essential mechanistic link in this compensatory interaction. We found that compensatory autophagy was induced in response to mutations affecting the proteasome and in response to UPS impairment in a fly model of the neurodegenerative disease spinobulbar muscular atrophy. Autophagy compensated for impaired UPS function in an HDAC6-dependent manner. Furthermore, expression of HDAC6 was sufficient to rescue degeneration associated with UPS dysfunction in vivo in an autophagy-dependent manner. This study suggests that impairment of autophagy (for example, associated with ageing or genetic variation) might predispose to neurodegeneration. Morover, these findings suggest that it may be possible to intervene in neurodegeneration by augmenting HDAC6 to enhance autophagy.