Analysis of secondary oxide-scale failure at entry into the roll gap

Both numerical analysis based on finite-element (FE) modeling and experimental evidence concerning the secondary oxide-scale failure at entry into the roll gap are presented and reviewed for a better understanding of events at the roll-workpiece interface, in turn, leading to better definition of the boundary conditions for process models. Attention is paid to the two limit modes leading to oxide-scale failure, which were observed earlier during tensile testing under rolling conditions. These are considered in relation to the temperature, the oxide-scale thickness, and other hot-rolling parameters. The mathematical model used for the analysis is composed of macro and micro parts, which allow for simulation of metal/scale flow, heat transfer, cracking of the oxide scale, as well as sliding along the oxide/metal interface and spallation of the scale from the metal surface. The different modes of oxide-scale failure were predicted, taking into account stress-directed diffusion, fracture and adhesion of the oxide scale, strain, strain rate, and temperature. Stalled hot-rolling tests under controlled conditions have been used to verify the types of oxide-scale failure and have shown good predictive capabilities of the model. The stock temperature and the oxide-scale thickness are important parameters, which, depending on other rolling conditions, may cause either through-thickness cracking of the scale at the entry or lead to entry of a nonfractured scale when the scale/metal interface is not strong enough to transmit the metal deformation.     

板坯辊缝收缩优化对铸坯质量的影响

简述了板坯辊缝静态收缩的原理和作用,通过对压下区间的选择和各段压下量控制配比的研究,重新确定了新的板坯辊缝收缩方案并对其使用效果进行了比较.通过在实际生产中的应用使得铸坯的中心偏析级别明显降低,中心疏松消除,内部质量得到改善;铸坯轧后性能检验合格率得到提高,试样拉伸后产生的中心分层问题得到解决,取得了满意效果.     

新型电磁调控轧机弯辊辊型电磁补偿及初始辊缝

 为解决薄带轧制过程中的各类板形问题,以新型电磁调控轧机为研究对象,利用Marc建立三维热-力耦合有限元模型,分析了弯辊和电磁调控轧辊综合作用下弯辊力和轧制力对轧辊辊型状态、板形分布、板坯边部应力、辊间接触应力、承载辊缝形状的影响规律。结果表明,弯辊机制的施加将直接促进电磁调控轧辊的稳定胀形,使电磁调控轧辊胀形凸度得到整体性补偿,并以板形良好为依据,给出新型调控轧机合理的弯辊力施加范围。对比分析了不同弯辊力和轧制力下辊缝函数的变化情况,形成不同的二次、四次凸度,为板形控制及初始辊缝设定提供依据。     

CSP平整机辊缝自动标定原理及应用

CSP平整机辊缝标定技术,是武钢CSP最为复杂的HGC自动控制中精度要求最高的环节之一。由于其工艺要求不同,与轧机标定存在差别,投产时间短等原因,现场维护人员对平整机辊缝标定认识很模糊,在出现辊缝标定问题时无从下手。通过对平整线资料的消化吸收和现场的观察分析,从辊缝标定的基础理论和实际标定过程出发,阐述了轧制线标高和平整机标定如何实现,同时对标定过程中出现的一些典型故障进行分析总结,为处理同类故障积累了经验。     

考虑辊缝变化的板带热轧动态理论模型

精准的轧制模型是生产优质带材的关键,目前常用的热轧模型仅适用于研究静态轧制过程.当面对变厚度轧制及轧机振动等动态轧制过程时,由于常用的静态模型不包含辊缝变化速度参数,因此其模型结构缺乏完整性.为了对动态轧制进行全面深入的研究,需要建立一个包含辊缝变化速度参数的动态轧制模型.基于Orowan方程,同时考虑辊缝变化速度对带...     

冷连轧机辊缝自动标定原理及应用

冷连轧机辊缝自动标定是液压辊缝控制中精度要求最高的环节之一,2007年鞍钢股份有限公司新建1450 mm冷轧机采用德国Siemens公司TDC控制系统,实现了辊缝自动标定功能.作者从应用角度分析了轧机辊缝自动标定的分类与过程,阐述了轧机辊缝自动标定时,如何实现相对轧制力、辊缝位置、辊缝倾斜的零点标准,同时,对现场标定过程出现的典型故障进行分析并提出解决方法.实践证明通过辊缝自动标定,可以提高轧机HGC精度,保证成品带钢的厚度要求.     

Taurine entry into perilymph of the guinea pig

Taurine is a beta-aminosulfonic acid and is a ubiquitous amino acid whose role in the cochlea is not well established. In this study, its entry from blood into perilymph was investigated in the guinea pig as animal model. The penetration rate of [3H]taurine (molecular weight 125) into the perilymph of the scala vestibuli was measured 1 and 2 h after the intravenous infusion of [3H]taurine in nephrectomized animals. Results showed a rate of penetration in perilymph related to plasma at 36 +/- 4.7% (n = 5) after 1 h and 43 +/- 5.6% (n = 5) after 2 h. Compared to the penetration rate of urea (molecular weight 60) and mannitol (molecular weight 186) reported previously in rats, a passive entry of taurine into perilymph through the blood-perilymph barrier is suggested.     

Synaptic laminin prevents glial entry into the synaptic cleft

Presynaptic and postsynaptic membranes directly oppose each other at chemical synapses, minimizing the delay in transmitting information across the synaptic cleft. Extrasynaptic neuronal surfaces, in contrast, are almost entirely covered by processes from glial cells. The exclusion of glial cells from the synaptic cleft, and the long-term stability of synapses, presumably result in large part from the tight adhesion between presynaptic and postsynaptic elements. Here we show that there is another requirement for synaptic maintenance: glial cells of the skeletal neuromuscular synapse, Schwann cells, are actively inhibited from entering the synaptic cleft between the motor nerve terminal and the muscle fibre. One inhibitory component is laminin 11, a heterotrimeric glycoprotein that is concentrated in the synaptic cleft. Regulation of an inhibitory interaction between glial cells and synaptic cleft components may contribute to synaptic rearrangements, and loss of this inhibition may underlie the loss of synapses that results from injury to the postsynaptic cell.     

Bacterial entry into epithelial cells: the paradigm of Shigella

Shigella flexneri is a model for the entry of bacterial pathogens into nonphagocytic epithelial cells. On contact with the epithelial cell surface, the Ipa proteins are secreted from the bacterium. The Ipa complex then triggers a reorganization of the host-cell cytoskeleton leading to the formation of membrane ruffles, which engulf the bacterium.     

HCW轧机内辊缝闭环厚控系统的弯辊力补偿方法

分析了HCW轧机内辊缝闭环时弯辊力变化对带材厚度的影响 ;针对西南精密带钢厂HCW 6 5 0mm轧机的实际影响情况 ,回归了在线补偿数学模型。运行结果表明 ,提出的处理方法很好地解决了工作辊轴移和弯辊力变化对带材厚度的影响。     

基于辊缝动态摩擦方程的铝板冷轧机垂振机理分析

针对高速铝板轧制过程中频繁出现的冷轧机垂直振动现象,结合轧制工艺润滑原理和机械振动理论,建立基于辊缝动态摩擦方程的轧机垂直振动模型.该模型由辊缝几何形状模型,轧辊-轧件工作界面的动态摩擦模型,变形区内的正向轧制应力、摩擦应力分布模型,以及单机架铝板冷轧机二自由度垂向系统结构模型组成.同时,为研究轧辊-轧件工作界面动态摩擦机制影响下的冷轧机垂振机理及系统稳定性,采用某厂单机架铝轧机设备及工艺参数,搭建Matlab/Simulink平台,分别模拟仿真轧制压力和正向轧制应力曲线,验证该模型的有效性;并讨论分析了变形区混合摩擦状态,轧辊-轧件表面粗糙度、轧件入口厚度与系统稳定性的关系.     

Genetic regulation of entry into meiosis in Caenorhabditis elegans

The Caenorhabditis elegans germline is composed of mitotically dividing cells at the distal end that give rise to meiotic cells more proximally. Specification of the distal region as mitotic relies on induction by the somatic distal tip cell and the glp-1 signal transduction pathway. However, the genetic control over the transition from mitosis to meiosis is not understood. In this paper, we report the identification of a gene, gld-2, that has at least two functions in germline development. First, gld-2 is required for normal progression through meiotic prophase. Second, gld-2 promotes entry into meiosis from the mitotic cell cycle. With respect to this second function, gld-2 appears to be functionally redundant with a previously described gene, gld-1 (Francis, R., Barton, M. K., Kimble, J. and Schedl, T. (1995) Genetics 139, 579-606). Germ cells in gld-1(o) and gld-2 single mutants enter meiosis at the normal time, but germ cells in gld-2 gld-1(o) double mutants do not enter meiosis. Instead, the double mutant germline is mitotic throughout and forms a large tumor. We suggest that gld-1 and gld-2 define two independent regulatory pathways, each of which can be sufficient for entry into meiosis. Epistasis analyses show that gld-1 and gld-2 work downstream of the glp-1 signal transduction pathway. Therefore, we hypothesize that glp-1 promotes proliferation by inhibiting the meiosis-promoting functions of gld-1 and gld-2.     

冷连轧机辊缝位置与轧制力实际值的模拟及应用

介绍了冷连轧机组机械设备未全部安装、电气设备无法进行正常外部联合调试时辊缝位置和轧制力实际值模拟的实现方法和轧制力实际值的计算公式,并且使用模拟出的辊缝位置及轧制力实际值进行相应控制器的测试及辊缝自动标定。     

Cell proliferation enhances entry of Listeria monocytogenes into intestinal epithelial cells by two proliferation-dependent entry pathways

Bacterial entry into intestinal host cells is the result of a fairly sophisticated manipulation of host cell machinery by the pathogens. To study further the potential cell target of Listeria spp., the in-vitro entry of L. monocytogenes strains into intestinal cells was examined in relation to the metabolism, proliferation and differentiation of the cells by the alamarBlue assay, [3H] thymidine incorporation, and brush border-associated enzyme activities, respectively. The study showed that cell metabolism was not involved in the entry of L. monocytogenes in three cell models (two human and one porcine). On the other hand, entry was closely related to the proliferation process and poorly related to the differentiation state of the cells. The use of L. monocytogenes mutants lacking invasion proteins showed that InlA and InlB acted in synergy to mediate the entry of L. monocytogenes into proliferative cells, whereas InlA alone seemed to be involved in the entry into non-proliferative cells. These two entry pathways could correspond to the two cellular processes used by L. monocytogenes to enter proliferative and non-proliferative cells, as suggested by the use of cytochalasin D, nocodazole, chloroquine and monodansylcadaverine. Taken together, we propose a hypothesis in which the entry of L. monocytogenes is mediated by interaction between randomly distributed E-cadherin on the surface of proliferative cells. In contrast, the entry into non-proliferative cells may involve pp60c-src, a proto-oncogenic tyrosine kinase signal that modifies E-cadherin localisation. In conclusion, these results suggest that L. monocytogenes may preferentially enter crypt cells in vivo by a microfilament-dependent process, whereas the few bacteria that infect villus cells enter by an E-cadherin-internalin interaction that mediates microtubule-dependent endocytosis.     

Synaptic vesicle endocytosis mediates the entry of tetanus neurotoxin into hippocampal neurons

Tetanus neurotoxin causes the spastic paralysis of tetanus by blocking neurotransmitter release at inhibitory synapses of the spinal cord. This is due to the penetration of the toxin inside the neuronal cytosol where it cleaves specifically VAMP/synaptobrevin, an essential component of the neuroexocytosis apparatus. Here we show that tetanus neurotoxin is internalized inside the lumen of small synaptic vesicles following the process of vesicle reuptake. Vesicle acidification is essential for the toxin translocation in the cytosol, which results in the proteolytic cleavage of VAMP/ synaptobrevin and block of exocytosis.     

The entry of antiviral and antiretroviral drugs into the central nervous system

The ability of antiviral and antiretroviral drugs to enter the brain is a critical issue in the treatment of many viral brain diseases, including HIV-related neurologic disease. Much of the literature concerning nucleoside analog entry into the nervous system focuses on drug levels in the cerebrospinal fluid (CSF), equating these with drug levels in the brain extracellular fluid (ECF) as though the two compartments intermix freely. We review the anatomic and physiologic aspects of drug entry into CSF and into brain ECF, as well as the exchange processes between these two compartments. In most instances drug concentrations in the CSF and ECF compartments bear little relationship to one another and using CSF concentrations to extrapolate brain ECF concentrations may significantly overestimate the latter. Accepted terminology and methodology for making measurements of blood-brain barrier function are discussed. Studies of brain uptake that express results as brain:plasma ratios, or that have used microdialysis, may overestimate the amount of drug reaching the brain. Using published data, we present an estimate of the time course of Zidovudine (AZT) concentrations in brain ECF and show that brain concentrations of AZT will likely be below that necessary to inhibit HIV-1 replication when AZT is administered systemically. Antiviral nucleosides and oligonucleotides appear to have limited entry into the brain when given systemically, which may hinder therapy of viral brain diseases, while some of the protease inhibitors may enter the brain more readily. Alternative methods for increasing antiviral and antiretroviral drug delivery to brain are discussed.