土体加、卸载土工参数的区别

围绕卸荷问题研究了卸载土体抗剪强度、静止土压力系数及回弹模量等的变化规律,并就土体加、卸载状态的区别进行了分析,意在强调加、卸载土工参数的选取应有所不同.     

稀浆封层路面层间黏结性能试验研究

为了对稀浆封层层间黏结性能进行评价,自行设计了以改进的剪切仪为基础的试验方法,能较好地模拟路面真实受力情况.试验结果说明,随着温度的升高,稀浆封层与沥青碎石下面层之间黏结强度在减小;不同的路面层间处理措施对黏结强度均有明显的影响;采用较大公称粒径的沥青混合料,或者对路面做凿毛处理均可以有效提高层间黏结强度.     

大粒径碎石桩在饱和超软土地基中的应用

对广东省西江下游航道整治工程中不排水抗剪强度7~15 kPa的淤泥土地基进行了碎石桩现场试验,得出了采用大粒径碎石桩加固不排水抗剪强度小于20 kPa软土地基的合理施工控制参数:碎石填料主要粒径为5~15 cm;充盈系数为1.4~1.6;密实电流大于50A;留振时间为5~15 s.现场桩径检测、动力触探试验和复合地基大型直剪试验结果表明,采用大粒径碎石桩加固超软土地基是可行的,大粒径碎石桩对增强地基土的抗剪强度和提高软土地基承载力十分有效.     

排水板施工对软黏土扰动的现场试验研究

通过软黏土地基上塑料排水板施工过程的孔隙水压力观测及现场十字板强度试验,研究了排水板施工前后地基土体孔隙水压力增长和消散的规律,并且从软黏土地基的有效应力变化和结构扰动等方面分析了土体强度损失及恢复过程.结果表明:单根排水板施工引起的孔隙水压力增长较小,仅对表层孔隙水压力影响大;板群的施工对4 m范围内土体孔隙水压力的增长有叠加效应;排水板施工一方面使软土地基内的孔隙水压力增长,有效应力减小,导致软土强度的降低,另一方面使地基软土结构发生破坏而引起软土强度降低;孔隙水压力的增长引起的地基土强度损失恢复较快,而结构扰动引起的强度损失恢复较慢.     

剪切荷载对裂隙渗透性影响研究现状

综述了剪切荷载对裂隙岩体渗流特性影响的研究现状,认为:目前这方面的研究主要采用室内试验和数值模拟2种方法.室内试验方法可以准确地得到剪应力和裂隙渗透系数的关系,但对试验仪器精度的要求比较高,试样的制作比较复杂,试验的可重复性差;数值模拟方法能够定性地模拟出剪应力对裂隙渗透性的影响,但裂隙的宽度、走向、密度和长度等参数较难确定.总结了剪切过程中裂隙岩体渗透系数的变化规律,即:剪胀发生前,裂隙渗透系数随剪切位移的增加而减小;剪胀发生后,裂隙渗透系数随剪切位移的增加急剧增大,达到峰值位移后裂隙渗透系数趋于稳定甚至会减小.指出了需要进一步研究的问题:剪切荷载作用下裂隙变形和破坏规律;不同法向荷载作用下剪切荷载对裂隙渗透性的影响;裂隙岩体本构关系;等等.     

Diversity in enoyl-acyl carrier protein reductases

The enoyl-acyl carrier protein reductase (ENR) is the last enzyme in the fatty acid elongation cycle. Unlike most enzymes in this essential pathway, ENR displays an unusual diversity among organisms. The growing interest in ENRs is mainly due to the fact that a variety of both synthetic and natural antibacterial compounds are shown to specifically target their activity. The primary anti-tuberculosis drug, isoniazid, and the broadly used antibacterial compound, triclosan, both target this enzyme. In this review, we discuss the diversity of ENRs, and their inhibitors in the light of current research progress. Received 3 November 2008; received after revision 5 December 2008; accepted 8 December 2008     

Digoxin and ouabain increase the synthesis of cholesterol in human liver cells

Digoxin and ouabain are steroid drugs that inhibit the Na⁺/K⁺-ATPase, and are widely used in the treatment of heart diseases. They may also have additional effects, such as on metabolism of steroid hormones, although until now no evidence has been provided about the effects of these cardioactive glycosides on the synthesis of cholesterol. Here we report that digoxin and ouabain increased the synthesis of cholesterol in human liver HepG2 cells, enhancing the activity and the expression of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), the rate-limiting enzyme of the cholesterol synthesis. This effect was mediated by the binding of the sterol regulatory element binding protein-2 (SREBP-2) to the HMGCR promoter, and was lost in cells silenced for SREBP-2 or loaded with increasing amounts of cholesterol. Digoxin and ouabain competed with cholesterol for binding to the SREBP-cleavage-activating protein, and are critical regulators of cholesterol synthesis in human liver cells. Received 10 January 2009; received after revision 11 February 2009; accepted 6 March 2009     

Sugar-mimicking glycosidase inhibitors: bioactivity and application

A large number of compounds mimicking the structures of monosaccharides or oligosaccharides have been discovered from natural sources. Such sugar mimics inhibit carbohydrate-degrading enzymes because of a structural resemblance to the sugar moiety of the natural substrate. Carbohydrate-degrading enzymes are involved in a wide range of important biological processes, such as intestinal digestion, posttranslational processing of the sugar chain of glycoproteins, their quality control mechanisms, lysosomal catabolism of glycoconjugates, and some viral infections. It has now been realized that inhibitors of the enzymes have enormous therapeutic potential in diabetes and lysosomal storage disorders. In this review, the general bioactivity, current applications, and the prospects for new therapeutic applications are described. Received 27 August 2008; received after revision 08 November 2008; accepted 03 December 2008     

Direct inhibition of phospholipid scrambling activity in erythrocytes by potassium ions

The exposure of phosphatidylserine (PS) at the cell surface plays a critical role in blood coagulation and serves as a macrophage recognition moiety for the engulfment of apoptotic cells. Previous observations have shown that a high extracellular [K⁺] and selective K⁺ channel blockers inhibit PS exposure in platelets and erythrocytes. Here we show that the rate of PS exposure in erythrocytes decreases by ~50% when the intracellular [K⁺] increases from 0 to physiological concentrations. Using resealed erythrocyte membranes, we further show that lipid scrambling is inducible by raising the intracellular [Ca²⁺] and that K⁺ ions have a direct inhibitory effect on this process. Lipid scrambling in resealed ghosts occurs in the absence of cell shrinkage and microvesicle formation, processes that are generally attributed to Ca²⁺-induced lipid scrambling in intact erythrocytes. Thus, opening of Ca²⁺-sensitive K⁺ channels causes loss of intracellular K⁺ that results in reduced intrinsic inhibitory effect of these ions on scramblase activity. Received 11 September 2008; received after revision 17 October 2008; accepted 27 October 2008