125 resultados para Damage mechanism
Resumo:
Ultrasonic technique is used to detect the velocity change of stress wave propagated in the cement mortar immersed in the solution of sodium sulfate for 425 days. Also the density change of specimens at different erosion time is measured. By curve fitting, the effect of solutions' concentration and water/cement ratio on the damage evolution is analyzed. The SEM observation on the growth of delayed ettringite is also performed. It shows that the damage evolution of specimens attacked by sulphate solution is dominantly induced by the nucleation and growth of delayed ettringite, and the average size of microvoids in cement mortar affects the damage evolution significantly. (c) 2008 Elsevier Ltd. All rights reserved.
Resumo:
Finite element analysis is employed to investigate void growth embedded in elastic-plastic matrix material. Axisymmetric and plane stress conditions are considered. The simulation of void growth in a unit cell model is carried out over a wide range of triaxial tensile stressing or large plastic straining for various strain hardening materials to study the mechanism of void growth in ductile materials. Triaxial tension and large plastic strain encircling around the void are found to be of most importance for driving void growth. The straining mode of incremental loading which favors the necessary strain concentration around void for its growth can be characterized by the vanishing condition of a parameter called "the third invariant of generalized strain rate". Under this condition, it accentuates the internal strain concentration and the strain energy stored/dissipated within the material layer surrounding the void. Experimental results are cited to justify the effect of this loading parameter. (C) 2000 Elsevier Science Ltd. All rights reserved.
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The nucleation of microdamage under dynamic loading was investigated through planar impact experiments accomplished with a light gas gun. The microscopic observation of recovered and sectioned specimens showed that microcracks were nucleated only by cracking of brittle particles inside material. However, for comparison the in situ static tensile tests on the same material conducted with a scanning electron microscope showed that the microcracks were nucleated by many forms those were fracture of ductile matrix, debonding particles from matrix and cracking of brittle particles. The quantitative metallographic observations of the specimens subjected to impact loading showed that most of the cracked particles were situated on grain boundaries of the aluminium matrix. These facts suggested the concept of critical size and incubation time of submicroscopic cavities in the dynamic case and the mechanism of embryo-damage induced nucleation by fracture of brittle particles in the aluminium alloy under impact loading was proposed.
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In this paper, a damage function defined by the residual strength of spalled specimens of an aluminium alloy is given to characterize the spallation of the material. Based on this function a simple method for continuously describing the spallation may be developed. Stress wave profiles showing the signal of spallation were successfully obtained with carbon gauges. Microscopic observations of the spalled aluminium alloy specimens reveal that the nucleation of spallation initiates from cracking of the second phase particles. Spallation is a process of crack nucleation, growth and coalescence to final, complete disintegration.
Resumo:
The mechanism of ductile damage caused by secondary void damage in the matrix around primary voids is studied by large strain, finite element analysis. A cylinder embedding an initially spherical void, a plane stress cell with a circular void and plane strain cell with a cylindrical or a flat void are analysed under different loading conditions. Secondary voids of smaller scale size nucleate in the strain hardening matrix, according to the requirements of some stress/strain criteria. Their growth and coalescence, handled by the empty element technique, demonstrate distinct mechanisms of damage as circumstances change. The macroscopic stress-strain curves are decomposed and illustrated in the form of the deviatoric and the volumetric parts. Concerning the stress response and the void growth prediction, comparisons are made between the present numerical results and those of previous authors. It is shown that loading condition, void growth history and void shape effect incorporated with the interaction between two generations of voids should be accounted for besides the void volume fraction.
Resumo:
In order to understand the mechanism of the incipient spallation in rolled metals, a one dimensional statistical mode1 on evolution of microcracks in spallation was proposed. The crack length appears to be the fundamental variable in the statistical description. Two dynamic processes, crack nucleation and growth, were involved in the model of damage evolution. A simplified case was examined and preliminary correlation to experimental observations of spallation was made.
“Deborah Numbers”, Coupling Multiple Space and Time Scales and Governing Damage Evolution to Failure
Resumo:
Two different spatial levels are involved concerning damage accumulation to eventual failure. nucleation and growth rates of microdamage nN* and V*. It is found that the trans-scale length ratio c*/L does not directly affect the process. Instead, two independent dimensionless numbers: the trans-scale one * * ( V*)including the * **5 * N c V including mesoscopic parameters only, play the key role in the process of damage accumulation to failure. The above implies that there are three time scales involved in the process: the macroscopic imposed time scale tim = /a and two meso-scopic time scales, nucleation and growth of damage, (* *4) N N t =1 n c and tV=c*/V*. Clearly, the dimensionless number De*=tV/tim refers to the ratio of microdamage growth time scale over the macroscopically imposed time scale. So, analogous to the definition of Deborah number as the ratio of relaxation time over external one in rheology. Let De be the imposed Deborah number while De represents the competition and coupling between the microdamage growth and the macroscopically imposed wave loading. In stress-wave induced tensile failure (spallation) De* < 1, this means that microdamage has enough time to grow during the macroscopic wave loading. Thus, the microdamage growth appears to be the predominate mechanism governing the failure. Moreover, the dimensionless number D* = tV/tN characterizes the ratio of two intrinsic mesoscopic time scales: growth over nucleation. Similarly let D be the “intrinsic Deborah number”. Both time scales are relevant to intrinsic relaxation rather than imposed one. Furthermore, the intrinsic Deborah number D* implies a certain characteristic damage. In particular, it is derived that D* is a proper indicator of macroscopic critical damage to damage localization, like D* ∼ (10–3~10–2) in spallation. More importantly, we found that this small intrinsic Deborah number D* indicates the energy partition of microdamage dissipation over bulk plastic work. This explains why spallation can not be formulated by macroscopic energy criterion and must be treated by multi-scale analysis.
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In this paper, an elastic and statistically brittle (ESB) model is applied to the process of damage evolution induced catastrophic rupture and the influence of localization and softening on catastrophic rupture is discussed. According to the analysis, the uncertainty of catastrophic rupture should be attributed to the unknown scale of localized zone. Based on the elastic and statistically brittle model but local mean field approximation, the relation between the scale of localized zone and catastrophic rupture is obtained and then justified with experiments. These results can not only give a deeper understanding of the mechanism governing catastrophic rupture, but also provide a possible tool to foresee the occurrence of catastrophic rupture.
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The single- and multi-shot damage behaviors of HfO2/SiO2 high-reflecting (HR) coatings under Nd:YAG laser exposure were investigated. Fundamental aspects of multi-shot laser damage, such as the instability due to pulse-to-pulse accumulation of absorption defect and structural defect effect, and the mechanism of laser induced defect generation, are considered. It was found in multi-shot damage, the main factors influencing laser-induced damage threshold (LIDT) are accumulation of irreversible changes of structural defects and thermal stress that induced by thermal density fluctuations.
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The mechanism of improving 1064 nm, 12 ns laser-induced damage threshold (LIDT) of TiO2/SiO2 high reflectors (HR) prepared by electronic beam evaporation from 5.1 to 13.1 J/cm(2) by thermal annealing is discussed. Through optical properties, structure and chemical composition analysis, it is found that the reduced atomic non-stoichiometric defects are the main reason of absorption decrease and LIDT rise after annealing. A remarkable increase of LIDT is found at 300 degrees C annealing. The refractive index and film inhomogeneity rise, physical thickness decrease, and film stress changes from compress stress to tensile stress due to the structure change during annealing. (c) 2007 Elsevier B.V. All rights reserved.
Resumo:
Pyrogallol is a potent allelochemical on Microcystis aeruginosa, but its allelopathic mechanism is not fully known. In order to explore this mechanism, gene expressions for prx, mcyB, psbA, recA, grpE, fabZ under pyrogallol stress were studied, and activities of the main antioxidant enzymes were also measured. The results showed that expression of grpE and recA showed no significant change under pyrogallol stress, while psbA and mcyB were up-regulated at 4 mg L-1. Both prx and fabZ were up-regulated even under exposure to 1 mg L-1 pyrogallol concentration. The activities of superoxide dismutase (SOD) and catalase (CAT) were enhanced under pyrogallol stress. Levels of malodialdehyde (MDA) at 2 and 4 mg L-1 pyrogallol were significantly higher than those of the controls. It was concluded that oxidant damage is an important mechanism for the allelopathic effect of pyrogallol on M. aeruginosa. (c) 2009 Elsevier Ltd. All rights reserved.
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Oxidative damage is an important mechanism in X-ray-induced cell death. Radiolysis of water molecules is a source of reactive oxygen species (ROS) that contribute to X-ray-induced cell death. In this study, we showed by ROS detection and a cell survival assay that NADPH oxidase has a very important role in X-ray-induced cell death. Under X-ray irradiation, the upregulation of the expression of NADPH oxidase membrane Subunit gp91(phox) was dose-dependent. Meanwhile, the cytoplasmic subunit p47(phox) was translocated to the cell membrane and localized with p22(phox) and gp91(phox) to form reactive NADPH oxidase. Our data Suggest, for the first time, that NADPH oxidase-mediated generation of ROS is an important contributor to X-ray-induced cell death. This suggests a new target for combined gene transfer and radiotherapy.
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in order to investigate a new method of mitigating the deleterious effect of harmful algal blooms (HABs), the inhibition of the glycolipid biosurfactant sophorolipid on three common harmful algae Alexandrium tamarense, Heterosigma akashiwo and Cochlodinium polykrikoides was studied. The optimum preparation condition for sophorolipid, the inhibition capability of sophorolipid and the interaction mechanism of sophorolipid on the three algal species were investigated. Results showed that sophorolipid prepared by extraction with ethyl acetate exhibited the most prominent inhibition effect and that storage time of one year had little influence on the inhibition effect of sophorolipid. The optimum concentration of 10-20 mg/l sophorolipid inhibited the motility of about 90% of the tested harmful algal cells without recovery. Investigation of the algicidal process revealed that sophorolipid induced ecdysis of A. tamarense, quick lysis of H. akashiwo and swelling of C. polykrikoides in a relatively short time. Investigation of the nucleotides showed that more than 15% of the nucleotides were released from the cytoplasm under the effect of 10-20 mg/l sophorolipid, indicating the irreversible damage on the cellular membrane, which resulted in the disintegration of the harmful algal cells. (C) 2004 Elsevier B.V. All rights reserved.
Resumo:
A closed, trans-scale formulation of damage evolution based on the statistical microdamage mechanics is summarized in this paper. The dynamic function of damage bridges the mesoscopic and macroscopic evolution of damage. The spallation in an aluminium plate is studied with this formulation. It is found that the damage evolution is governed by several dimensionless parameters, i.e., imposed Deborah numbers De* and De, Mach number M and damage number S. In particular, the most critical mode of the macroscopic damage evolution, i.e., the damage localization, is deter-mined by Deborah number De+. Deborah number De* reflects the coupling and competition between the macroscopic loading and the microdamage growth. Therefore, our results reveal the multi-scale nature of spallation. In fact, the damage localization results from the nonlinearity of the microdamage growth. In addition, the dependence of the damage rate on imposed Deborah numbers De* and De, Mach number M and damage number S is discussed.
Detection and Characterization of Long-Pulse Low-Velocity Impact Damage in Plastic Bonded Explosives
Resumo:
Damage not only degrades the mechanical properties of explosives, but also influences the shock sensitivity, combustion and even detonation behavior of explosives. The study of impact damage is crucial in the vulnerability evaluation of explosives. A long-pulse low-velocity gas gun with a gas buffer was developed and used to induce impact damage in a hot pressed plastic bonded explosive. Various methods were used to detect and characterize the impact damage of the explosive. The microstructure was examined by use of polarized light microscopy. Fractal analysis of the micrographs was conducted by use of box counting method. The correlation between the fractal dimensions and microstructures was analyzed. Ultrasonic testing was conducted using a pulse through-transmission method to obtain the ultrasonic velocity and ultrasonic attenuation. Spectra analyses were carried out for recorded ultrasonic signals using fast Fourier transform. The correlations between the impact damage and ultrasonic parameters including ultrasonic velocities and attenuation coefficients were also analyzed. To quantitatively assess the impact induced explosive crystal fractures, particle size distribution analyses of explosive crystals were conducted by using a thorough etching technique, in which the explosives samples were soaked in a solution for enough time that the binder was totally removed. Impact induces a large extent of explosive crystal fractures and a large number of microcracks. The ultrasonic velocity decreases and attenuation coefficients increase with the presence of impact damage. Both ultrasonic parameters and fractal dimension can be used to quantitatively assess the impact damage of plastic bonded explosives.