Self healing capacity of asphalt binders

To test self healing capability of asphalt binders,three asphalt specimens(pure asphalt,modified asphalt and aged asphalt) were prepared.Every specimen was tested by dynamic shear rheometer(DSR).The temperature sweeps result indicates that both aging and SBS modifying influence the self healing capability of asphalt binder.The fatigue-heal-fatigue test was introduced to study the self healing capability of asphalt in its serving periods.Furthermore,three different periods(0.5 h,1 h,3 h) were set up to study the influence of rest time on fatigue time.It is concluded that longer rest time,less load will delay the appearance of cracks and extend the service life of asphalt binders.     

可变模糊集理论研究进展及其在水科学中的应用

介绍了可变模糊集理论的哲学基础及工程背景,简要描述了其相关概念及其理论方面的突破与进展,重点阐述了唯物辩证法三大基本规律——对立统一、质量互变与否定之否定定理的数学表达的研究情况。以此理论为基础建立的可变模糊聚类、模式识别、优选、评价的理论与模型,是可变模糊集通向实际应用的桥梁,详细评述了其在水资源评价、水质评价、水库调度与防洪、灾情评价、径流预报、农业水利工程等领域的应用。     

基于互信息博弈的侧信道攻击风险评估模型

将互信息博弈理论引入密码芯片设计者(防御方)和攻击者的决策过程,建立一种互信息博弈的风险量化评估模型。考察攻防策略的选择对安全风险的影响,并结合互信息的量化方法,给出Nash均衡条件下攻防双方的优化策略选择方法及互信息收益。通过案例分析,验证了该策略的有效性。     

基于互信息的贝叶斯网络结构学习算法

结构学习是贝叶斯网络的重要分支之一,而由数据学习贝叶斯网络是NP-完全问题,提出了一个由数据学习贝叶斯网络的改进算法。该算法基于互信息知识构造初始无向图,并通过条件独立测试对无向边添加方向;同时提出了一个针对4节点环和5节点环的局部优化方法来构造初始框架,最后利用贪婪搜索算法得到最优网络结构。数值实验结果表明,改进的算法无论是在BIC评分值,还是在结构的误差上都有一定的改善,并且在迭代次数、运行时间上均有明显降低,能较快地确定出与数据匹配程度最高的网络结构。     

基于可行域的遗传约简算法

在已有的遗传属性约简算法的基础上，通过引入约简的可行域概念，提出了基于可行域的遗传约简算法．可行域保持系统的分类能力，缩小了原问题的搜索空间，进而减小了问题的复杂度．适应度函数中引入与互信息相关的惩罚因子保证了算法在可行域中搜索．实验结果表明谊算法既克服了启发性算法的缺陷，较之已有的基于遗传算法的约简算法也有效率改进．     

制氧机闲置的氪、氙回收设备的恢复利用

将三套全提取空气分离设备的氪氙系统进行组合,实现互联、互替,从而解决了其中一套氪氙系统设备因缺陷而不能生产的问题。     

论发展城市旅游对城市规划的要求

针对城市旅游在当前正蓬勃发展的现象,论述了城市旅游对城市规划的要求.首先指出它的发展虽有城市旅游相关规划作为指导,但这一相关规划有其局限性,城市旅游的发展需要城市规划的配合.接着分析了目前的城市规划在面向城市旅游方面存在着明显不足.最后提出为促进城市旅游的发展,城市规划应针对不足,做出相应的改进和调整.     

基于文本挖掘的搭配词典自动架构探讨

研究词语搭配的关系对于自然语言处理有很大的帮助。目前对计算机用的搭配词典是用人工方法实现的，它由人工进行维护，有更新慢、收藏的词少等缺点。为此，利用文本挖掘技术对大规模语料库进行分析，挖掘词语搭配的深层关系，在此基础上自动建立词语搭配词典，实验结果显示该方法是有效的。     

Classic NSAID and selective cyclooxygenase (COX)-1 and COX-2 inhibitors in healing of chronic gastric ulcers

Prostaglandins (PG) derived from COX-1 are essential for the maintenance of mucosal integrity but COX-2 isoform synthesizes PG at a site of inflammation. Recently, COX-2 mRNA expression was demonstrated at the ulcer edge during healing of chronic gastric ulcers but the role for expression of COX-2 and its products such as PGE(2) and cytokines including interleukin (IL-1beta) and tumor necrosis factor alpha (TNFalpha) in ulcer healing remains unknown. In this study, Wistar rats with gastric ulcers produced by serosal application of acetic acid (ulcer area 28 mm(2)) received daily treatment either with: (1) vehicle (saline); (2) NS-398 (10 mg/kg-d i.g.) and Vioxx (5 mg/kg-d i.g.), both, highly specific COX-2 inhibitors; (3) meloxicam (5 mg/kg-d i.g.), a preferential inhibitor of COX-2; (4) resveratrol (10 mg/kg-d i.g.), a specific COX-1 inhibitor; (5) indomethacin (5 mg/kg-d i.g); and (6) aspirin (ASA; 50 mg/kg-d i.g.), non-selective inhibitors of both COX-1 and COX-2. At day 3, 7, and 14 after ulcer induction, the animals were sacrificed and the area of gastric ulcers was determined by planimetry and histology, gastric blood flow (GBF) at ulcer base and margin was measured by H(2) clearance technique, and blood was withdrawn for measurement of plasma IL-1beta and TNFalpha levels. The mucosal biopsy samples were taken for the determination of PGE(2) generation by RIA and expression of COX-1, COX-2, IL-1beta, and TNFalpha mRNA by RT-PCR. In vehicle-treated rats, gastric ulcers healed progressively and at day 14 the healing was completed, accompanied by a significant rise in the GBF at ulcer margin. The IL-1beta, TNFalpha, and COX-1 mRNA were detected in intact and ulcerated gastric mucosa, whereas COX-2 mRNA were upregulated only in ulcerated mucosa with peak observed at day 3 after ulcer induction. The plasma IL-1beta level was significantly increased at day 3 and 7 but then declined at day 14 to that measured in vehicle-controls. Indomethacin and ASA, which suppressed PGE(2) generation both in the non-ulcerated and ulcerated gastric mucosa, significantly delayed the rate of ulcer healing and this was accompanied by the fall in GBF at ulcer margin and further elevation of plasma IL-1beta and TNFalpha levels, which was sustained up to the end of the study. Treatment with NS-398 and Vioxx, which caused only a moderate decrease in the PGE(2) generation in the non-ulcerated gastric mucosa, delayed ulcer healing and attenuated significantly the GBF at ulcer margin and PGE(2) generation in the ulcerated tissue, while raising the plasma IL-1beta and TNFalpha similarly to those observed in indomethacin- and ASA-treated rats. Resveratrol, which suppressed the PGE(2) generation in both non-ulcerated and ulcerated gastric mucosa, prolonged ulcer healing and this was accompanied by the fall in the GBF at the ulcer margin and a significant increase in plasma IL-1beta and TNFalpha levels. We conclude that (1) classic NSAID delay ulcer healing due to suppression of endogenous PG, impairment in GBF at ulcer area, and excessive cytokine expression and release, and (2) this deleterious effect of classic NSAID on the healing of pre-existing ulcers can be reproduced by selective COX-1 and COX-2 inhibitors, suggesting that both COX isoforms are important sources of PG that appear to contribute to ulcer healing.