988 resultados para Zeólita. Beta hierarquizada. Híbrido micro-mesoporoso. Craqueamento
Resumo:
Models describing wet adhesion between indenters and substrates joined by liquid bridges are investigated. The influences of indenter shapes and various parameters of structures on capillary force are focused. In the former, we consider several shapes, such as conical, spherical and truncated conical indenter with a spherical end. In the latter, the effects of the contact angle, the environmental humidity, the gap between the indenter and the substrate, etc. are included. Different dependences of the capillary force on the indenter shapes and the geometric parameters are observed. Most interesting finding is that applying the present results to micro- and nano-indentation experiments shows the size effect in indentation hardness not produced but underestimated by the effects of capillary force.(4 refs)
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Cohesive zone characterizations of the interface between metal film and ceramic substrate at micro- and nano-scales are performed in the present research. At the nano-scale, a special potential for special material interface (Ag/MgO) is adopted to investigate the interface separation mechanism by using MD simulation, and stress-separation relationship will be obtained. At the micro-scale, peeling experiment is performed for the Al film/Al2O3 substrate system with an adhesive layer at the interface. Adhesive is a mixture of epoxy and polyimide with mass ratio 1:1, by which a brittle cohesive property is obtained. The relationships between energy release rate, the film thickness and the adhesive layer thickness are measured during the steady-state peeling. The experimental result has a similar trend as modeling result for a weak adhesion interface case.
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Two stages have been observed in micro-indentation experiment of a soft film on a hard substrate. In the first stage, the hardness of the thin film decreases with increasing depth of indentation when indentation is shallow; and in the second stage, the hardness of the film increases with increasing depth of indentation when the indenter tip approaches the hard substrate. In this paper, the new strain gradient theory is used to analyze the micro-indentation behavior of a soft film on a hard substrate. Meanwhile, the classic plastic theory is also applied to investigating the problem. Comparing two theoretical results with the experiment data, one can find that the strain gradient theory can describe the experiment data at both the shallow and deep indentation depths quite well, while the classic theory can't explain the experiment results.
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This book elucidates the methods of molecular gas dynamics or rarefied gas dynamics which treat the problems of gas flows when the discrete molecular effects of the gas prevail under the circumstances of low density, the emphases being stressed on the basis of the methods, the direct simulation Monte Carlo method applied to the simulation of non-equilibrium effects and the frontier subjects related to low speed microscale rarefied gas flows. It provides a solid basis for the study of molecular gas dynamics for senior students and graduates in the aerospace and mechanical engineering departments of universities and colleges. It gives a general acquaintance of modern developments of rarefied gas dynamics in various regimes and leads to the frontier topics of non-equilibrium rarefied gas dynamics and low speed microscale gas dynamics. It will be also of benefit to the scientific and technical researchers engaged in aerospace high altitude aerodynamic force and heating design and in the research on gas flow in MEMS
[1] Molecular structure and energy states | (21) | ||
[2] Some basic concepts of kinetic theory | (51) | ||
[3] Interaction of molecules with solid surface | (131) | ||
[4] Free molecular flow | (159) | ||
[5] Continuum models | (191) | ||
[6] Transitional regime | (231) | ||
[7] Direct simulation Monte-Carlo (DSMC) method | (275) | ||
[8] Microscale slow gas flows, information preservation method | (317) | ||
[App. I] Gas properties | (367) | ||
[App. II] Some integrals | (369) | ||
[App. III] Sampling from a prescribed distribution | (375) | ||
[App. IV] Program of the couette flow | (383) | ||
Subject Index | (399) |
Resumo:
1-42 beta-Amyloid (A beta(1-42)) peptide is a key molecule involved in the development of Alzheimer's disease. Some of its effects are manifested at the neuronal morphological level. These morphological changes involve loss of neurites due to cytoskeleton alterations. However, the mechanism of A beta(1-42) peptide activation of the neurodegenerative program is still poorly understood. Here, A beta(1-42) peptide-induced transduction of cellular death signals through the phosphatidylinositol 3-kinase (PI3K)/phosphoinositol- dependent kinase (PDK)/novel protein kinase C (nPKC)/Rac 1 axis is described. Furthermore, pharmacological inhibition of PDK1 and nPKC activities blocks Rac 1 activation and neuronal cell death. Our results provide insights into an unsuspected connection between PDK1, nPKCs and Rac 1 in the same signal-transduction pathway and points out nPKCs and Rac 1 as potential therapeutic targets to block the toxic effects of A beta(1-42) peptide in neurons.
Resumo:
Background/Aims: In diabetic ventricular myocytes, transient outward potassium current (I-to) amplitude is severely reduced because of the impaired catecholamine release that characterizes diabetic autonomic neuropathy. Sympathetic nervous system exhibits a trophic effect on I-to since incubation of myocytes with noradrenaline restores current amplitude via beta-adrenoceptor (beta AR) stimulation. Here, we investigate the intracellular signalling pathway though which incubation of diabetic cardiomyocytes with the beta AR agonist isoproterenol recovers I-to amplitude to normal values. Methods: Experiments were performed in ventricular myocytes isolated from streptozotocin-diabetic rats. I-to current was recorded by using the patch-clamp technique. Kv4 channel expression was determined by immunofluorescence. Protein-protein interaction was determined by coimmunoprecipitation. Results: Stimulation of beta AR activates first a G alpha s protein, adenylyl cyclase and Protein Kinase A. PKA-phosphorylated receptor then switches to the G alpha i protein. This leads to the activation of the beta AR-Kinase-1 and further receptor phosphorylation and arrestin dependent internalization. The internalized receptor-arrestin complex recruits and activates cSrc and the MAPK cascade, where Ras, c-Raf1 and finally ERK1/2 mediate the increase in Kv4.2 and Kv4.3 protein abundance in the plasma membrane. Conclusion: beta(2)AR stimulation activates a G alpha s and G alpha i protein dependent pathway where the ERK1/2 modulates the Ito current amplitude and the density of the Kv4.2 and Kv4.2 channels in the plasma membrane upon sympathetic stimulation in diabetic heart.
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本书系统地介绍了材料微尺度力学行为的尺寸效应实验现象,重点介绍了几种代表性的微尺度应变梯度塑性理论及对微尺度实验现象的解释;以及对裂纹尖端微尺度范围内解理断裂的应用。融会贯通的介绍了国内外学者的原创性工作和创新性学术思想。 全书共8章。第1章介绍了应变梯度塑性理论的应用背景及经典微极理论;第2章介绍了金属材料典型的微尺度力学实验现象;第3~7章介绍了几种典型的应变梯度理论及其应用;第8章介绍了应变梯度理论在微观断裂力学中的应用。 本书适合从事固体微尺度力学、先进材料的微结构设计与力学性能优化、微机电和微电子元件力学行为研究的科技工作者及工程师使用和参考,也可供力学专业及材料专业的高年级本科生和研究生阅读参考。