混凝土材料非线性多轴动态强度准则

将广义非线性强度理论的4个材料参数转化为混凝土材料的基本强度参数,通过混凝土材料的基本强度特性,分析了4个材料参数的变化规律与取值范围.基于S准则建立了混凝土材料4个基本强度参数的率效应表达式,建立了混凝土材料的非线性多轴动态强度准则,分析了动态强度参数的率效应规律,结果表明,混凝土材料的强度特性随着应变率的提高,逐渐向金属材料的强度特性过渡,在应变率从-3~3,应变率对混凝土动态强度的影响较大,并且动强度不是随着应变率的提高无限增大的,而是存在动强度峰值.通过与3组双轴压-压和2组双轴拉-压动态加载时混凝土材料试验结果的比较,表明非线性多轴动态强度准则可较好地描述混凝土材料双轴动强度规律.在同一应变率下,可较好地描述强度的非线性特性;不同应变率下,动强度面互不相交,即应变率效应与多轴应力状态对强度规律不存在耦合影响.     

三维应力作用下岩石裂缝水渗流物性规律的实验研究

详细介绍了三维应力作用下岩石裂缝渗流物性规律的实验方法及其结果,结合理论与实验结果分析,给出了反映裂缝连通系数、法向刚度、三维应力、初始张开度和Ｐｏｉｓｓｏｎ比的渗透系数公式。     

时变有向网络下仿射多个体系统的状态一致性

本文探讨时变网络下多个体系统的状态一致性,研究了平稳离散时变有向网络下仿射多个体协同系统趋于状态一致的充分必要条件.由于线性多个体系统是仿射多个体系统的特例、非时变网络是平稳离散时变网络的特例、无向网络(对称网络)是有向网络的特例,因此本文的结论涵盖了此前有关一阶多个体协同系统状态一致性的主要理论结果.     

应力波作用下岩石类孔隙介质变形破坏与能量耗散机制的数值模拟研究

通过CT扫描、X射线衍射和物理实验等方法获取了天然砂岩的孔隙结构参数、矿物组成和物理力学性质,研制了具有与天然砂岩相同的孔隙结构特征和基体性质、但孔隙率不同的岩石类孔隙介质的物理模型．利用孔隙介质物理模型的CT扫描图像和MIMICS构建了具有不同孔隙率的孔隙结构三维有限元模型．通过设定应力波动理论假设的条件模拟了孔隙介质SHPB冲击破坏过程,分析了波动应力作用下岩石类孔隙介质的动力学响应、应力传递模式和变形破坏机制．研究表明：利用孔隙介质三维有限元模型可以直观定量地分析应力波传播过程中岩石类介质内部孔隙和基体的应力、应变状态及变形破坏机制．一定压强和波速的应力波传播过程中,孔隙率低于15％的岩石介质内部的孔隙未发生明显变形,变形主要体现为孔隙周边基体的微塑性（剪切变形）和开裂（横向拉应变）,以及孔隙周边开裂区域的相互连通．剪应力使基体单元产生微塑性,拉应力使基体单元开裂．孔隙周边基体单元的破坏及相互贯通主要是由于基体单元的横向拉应力或拉应变超过材料的极限值．模拟得到的孔隙介质的应力波传播规律、变形与破坏模式以及能量耗散性质与物理模型的实验结果相吻合．本文研究为解析岩石类孔隙介质的复杂多变动力学响应的内在机制、应力传递模式、变形破坏与致灾机理提供了参考．     

高应变率下RPC动态力学性能的试验研究

利用5种钢纤维掺量活性粉末混凝土(RPC)圆柱形试件的SHPB冲击压缩实验研究了10×100~1.1×102s?1应变率范围内RPC的动态力学性能,分析了不同应变率和钢纤维掺量下RPC的应力波动特征、破坏模式、强度及耗能能力的变化规律以及应变率和钢纤维掺量的影响.提出了不同应变率和钢纤维掺量条件下RPC动态应力-应变响应的基本模式与本构模型.研究表明:应力波作用下素RPC的应力响应高于应变响应,脆性特征显著.掺入适量钢纤维后,RPC碎裂时的应变率和变形能力较素RPC有明显提高.相同钢纤维掺量下,应变率增加时,RPC的峰值抗压强度、峰值应变和残余应变均有不同程度的提高,其中残余应变提高的幅度最大.相同应变率条件下,提高钢纤维掺量对于改善RPC碎裂后的残余变形能力作用不大.钢纤维对RPC峰值抗压强度和峰值变形能力的影响不同,相同应变率下,钢纤维率不超过1.75%时,峰值抗压强度随纤维率增加而增加;纤维率超过1.75%后,峰值抗压强度开始逐步下降;峰值应变随钢纤维掺量增加而持续增大.相同应变率下,从冲击开始至残余变形阶段RPC的总耗能Edisp随钢纤维掺量增加而逐步提高,但纤维率超过2%后总耗能Edisp则开始逐步下降.不同变形阶段钢纤维对RPC耗能所起的作用不同.钢纤维率不超过2%时,钢纤维对提高峰值变形前耗能的作用大于对提高峰值变形后耗能的作用.应变率对总耗能和各阶段耗能均有显著影响,应变率越高,各阶段的耗能越大,动态冲击时的韧性越好.给出了RPC峰值抗压强度、峰值变形、残余变形,以及各阶段耗能随应变率和钢纤维率变化的经验模型.采用标准化的应力和应变作为广义应力与广义应变,以应变率和钢纤维率为界,将RPC的动态应力-应变响应模式简化为4类基本模型,并给出了每类模型的数学表达式.     

不同真空度下多层隔热组件传热性能的实验研究

针对月地高速再入返回飞行器在轨面临长期中真空环境的特殊挑战,热控设计需要评估不同真空度下多层隔热组件的传热性能差异.采用一维绝热型边界测试方法,对5单元、10单元、15单元与20单元多层隔热组件,在0.001~10000 Pa开展了传热性能的实验研究.根据测试数据,计算了不同真空度下的当量导热系数,在整器热分析模型中优选当量导热系数来计算整器温度水平,并利用正样热平衡试验和在轨温度遥测值验证了该方法的正确性.本文的测试结果不仅可为返回器提供基础数据,还可成为多层隔热组件不同真空条件下航天器热设计、热分析的重要依据.     

基于实测资料的外掺MgO微膨胀混凝土变形性态研究

外掺MgO混凝土产生的延迟性微膨胀能够补偿混凝土在温降过程中产生的收缩变形,从而防止或减少混凝土产生裂缝.本文通过对向家坝水电站导流底孔外掺氧化镁混凝土的室内试验和现场监测成果进行对比分析,探讨了外掺MgO与未掺MgO,同类混凝土中掺量不同对混凝土变形特性的影响.     

The effect of melatonin on the formation of gastric stress lesions in rats

Summary Prior melatonin administration (1,5 and 10 mg/kg b. wt) causes a significant reduction in gastric ulceration induced in male rats by restraint immobilization in the presence of low temperatures.     

The effect of chronic heat stress on cortisol levels in the antarctic fishPagothenia borchgrevinki

Radioimmunoassay was used to determine levels of the stress-inducible glucocorticoid, cortisol, circulating in the plasma of the extremely stenothermal Antarctic fishPagothenia borchgrevinki at rest and after heat stress. Fish sampled immediately after capture (–1.9°C) had low cortisol levels (10.4±1.4 ng ml^–1, mean±SEM) as did fish which were laboratory rested for 3 days. Sudden exposure to 5°C (48h) resulted in a peak cortisol value after 3 h (69.9±6.8 ng ml^–1) whereas exposure to 8°C (6h) resulted in a peak value after 1 h (73.5±8.0 ng ml^–1). At both temperatures levels remained significantly elevated (p<0.05) for the entire period of exposure. Increased temperature also resulted in a significant change in haemoglobin, haematocrit and mean cell haemoglobin concentration (MCHC) (p<0.05). Plasma lactate was significantly elevated only after exposure to 8°C (p<0.05). Plasma cortisol levels fromP. borchgrevinki are reported here for the first time and show this cryopelagic Antarctic species to have an unusual hormonal stress profile.     

The influence of cold or isolation stress on resistance of mice to West Nile virus encephalitis

Summary The effect of cold or isolation stress on mortality rate and brain virus level were investigated in mice infected with West Nile virus (WNV). Exposure of mice for 5 min/day to cold water (1±0.5°C) for 8–10 days resulted in 92% mortality as compared to 47% in control mice (p<0.001). Mice housed in individual cages (isolation stress) were also more susceptible to WN viral infection, as shown by increased mortality rate reaching 85% as compared to 50% in mice housed 6 per cage (p<0.01). Cold or isolation stress increased blood brain and spleen virus levels as early as 2 days after inoculation. After 8 days of isolation or cold stress, mice inoculated with WNV had 8.9 and 9.0 log₁₀ plaque forming units in the brain, respectively, as compared to 6.9 in the control (p<0.01–0.001). Furthermore, lymphoid organs such as spleen and thymus showed severe mass loss. These data suggest that physical or non-physical stress situations enhance WNV encephalitis by accelerating virus proliferation and increase mortality in mice.     

Identification of a pre-hibernating state in myocardium from nonhibernating chipmunks

Summary During the hibermating season, the amplitude of the cardiac action potential plateau of nonhibernating chipmunks was reduced. Replacing external Ca by Sr inhibited the electromechanical responses of these preparations. Similar properties were observed in hibernating animal preparations, suggesting that changes in cardiac function are already triggered before hibernation begins.15 December 1986     

基于累积变形演化状态控制的高速铁路基床结构设计计算方法

实现长期循环荷载作用下基床结构累积变形有效控制是建造高速铁路的技术难点之一.基于高速铁路无砟与有砟轨道路基承受列车动荷载特征,提出和完善了用于基床结构设计的荷载作用模式;根据循环荷载作用下土工填料累积变形演化状态的分类及阈值判别准则,结合室内单元结构填土模型试验,获得了级配碎石基床填料变形状态演化的阈值参数.以设计荷载条件和填料设计参数为基础,针对无砟与有砟轨道对基床变形状态控制的不同要求,采用结构分析原理,构建了基于累积变形演化状态控制的高速铁路基床结构设计计算方法,确定了无砟与有砟轨道基床结构累积变形分别满足快速稳定和缓慢稳定的状态控制要求,以地基系数K30值表征的关键参数指标.研究成果为实现高速铁路基床结构由构造设计向状态控制定值分析转变奠定了基础.     

Causes of oxidative stress in Alzheimer disease

Oxidative stress is one of the earliest events of Alzheimer disease (AD), with implications as an important mediator in the onset, progression and pathogenesis of the disease. The generation of reactive oxygen species (ROS) and its consequent cellular damage/response contributes to much of the hallmark AD pathology seen in susceptible neurons. The sources of ROS-mediated damage appear to be multi-faceted in AD, with interactions between abnormal mitochondria, redox transition metals, and other factors. In this review, we provide an overview of these potential causes of oxidative stress in AD.     

基于UDEC巷道掘进矿压显现的数值模拟

通过采用UDEC软件,依据钻孔柱状图和采掘应力影响范围建立了相应的几何模型,根据煤岩体物理力学性质建立相应的材料模型,在此基础上结合地应力数据,从而完成数值模型.通过模拟实际巷道开挖尺寸及方位,得出巷道前方的应力分布和巷道两帮位移分布,为巷道冲击地压显现防治提供了理论支持.     

Role of bombesin-related peptides in the mediation or integration of the stress response

In addition to the relatively well established role of corticotropin-releasing hormone (CRH) and arginine-vasopressin (AVP) in the mediation of the stress response, there is reason to believe that bombesin-like peptides (BN-LPs) may also contribute to the mediation or integration of these responses and thus might be considered as putative 'stress peptides'. This review provides evidence supporting this contention by showing that (i) BN-LPs are present at brain sites known to be activated by stressors, (ii) stressor exposure alters utilization of BN-related peptides, (iii) exogenous BN administration mimics the endocrine, autonomic and/or behavioral effects elicited by stressors, and (iv) antagonism of BN action attenuates the behavioral and/or neurochemical effects of stressors or of exogenously administered peptide. The evidence presented also suggests that BN-LPs mediate their stress-relevant effects through activation of CRH and/or AVP neurons. Several hypothetical mechanisms for such peptidergic interactions are discussed as to the implications of considering BN-LPs as 'stress peptides'. Received 16 July 2001; received after revision 27 August 2001; accepted 28 August 2001     

Effects of myocardial ischemia and reperfusion on mitochondrial function and susceptibility to oxidative stress

We investigated the effects of ischemia duration on the functional response of mitochondria to reperfusion and its relationship with changes in mitochondrial susceptibility to oxidative stress. Mitochondria were isolated from hearts perfused by the Langendorff technique immediately after different periods of global ischemia or reperfusion following such ischemia periods. Rates of O₂ consumption and H₂O₂ release with complex I- and complex II-linked substrates, lipid peroxidation, overall antioxidant capacity, capacity to remove H₂O₂, and susceptibility to oxidative stress were determined. The effects of ischemia on some parameters were time dependent so that the changes were greater after 45 than after 20 min of ischemia, or were significantly different to the nonischemic control only after 45 min of ischemia. Thus, succinate-supported state 3 respiration exhibited a significant decrease after 20 min of ischemia and a greater decrease after 45 min, while pyruvate malate-supported respiration showed a significant decrease only after 45 min of ischemia, indicating an ischemia-induced early inhibition of complex II and a late inhibition of complex I. Furthermore, both succinate and pyruvate malate-supported H₂O₂ release showed significant increases only after 45 min of ischemia. Similarly, whole antioxidant capacity significantly increased and susceptibility to oxidants significantly decreased after 45 min of ischemia. Such changes were likely due to the accumulation of reducing equivalents, which are able to remove peroxides and maintain thiols in a reduced state. This condition, which protects mitochondria against oxidants, increases mitochondrial production of oxyradicals and oxidative damage during reperfusion. This could explain the smaller functional recovery of the tissue and the further decline of the mitochondrial function after reperfusion following the longer period of oxygen deprivation. Received 18 May 2001; received after revision 17 July 2001; accepted 24 July 2001