243 resultados para Crack-growth resistance

em Queensland University of Technology - ePrints Archive


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Large deformation finite element analysis has been carried out to investigate the stress-strain fields ahead of a growing crack for compact tension .a=W D 0:5/ and three-point bend .a=W D 0:1 and 0:5/ specimens under plane stress condition. The crack growth is controlled by the experimental J -integral resistance curves measured by Sun et al. The results indicate that the distributions of opening stress, equivalent stress and equivalent strain ahead of a growing crack are not sensitive to specimen geometry. For both stationary and growing cracks, similar distributions of opening stress and triaxiality can be found along the ligament. During stable crack growth, the crack-tip opening displacement (CTOD) resistance curve and the cohesive fracture energy in the fracture process zone are independent of specimen geometry and may be suitable criteria for characterizing stable crack growth in plane stress.

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Ductile-brittle fracture transition was investigated using compact tension (CT) specimens from -70oC to 40oC for a carbon steel. Large deformation finite element analysis has been carried out to simulate the stable crack growth in the compact tension (CT, a/W=0.6), three point-point bend (SE(B), a/W=0.1) and centre-cracked tension (M(T), a/W=0.5) specimens. Experimental crack tip opening displacement (CTOD) resistance curve was employed as the crack growth criterion. Ductile tearing is sensitive to constraint and tearing modulus increases with reduced constraint level. The finite element analysis shows that path-dependence of J-integral occurs from the very beginning of crack growth and ductile crack growth elevates the opening stress on the remaining ligament. Cleavage may occur after some ductile crack growth due to the increase of opening stress. For both stationary and growing cracks, the magnitude of opening stress increases with increasing in-plane constraint. The ductile-brittle transition takes place when the opening stress ahead of the crack tip reaches the local cleavage stress as the in-plane constraint of the specimen increases.

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Initial crack widely exists in the welded members of steel bridge induced by the welding procedure or by the fatigue damage crack initiation. The behavior of crack growth with a view to fatigue damage accumulation on the tip of cracks is discussed. Fatigue life of welded components with initial crack in bridges under traffic loading is investigated. Based on existing fatigue experiment results of welded members with initial crack and the fatigue experiment results of welded bridge members under constant stress cycles, the crack would keep semi-elliptical shape with variable ratio of a/c during the crack propagation. Based on the concept of continuum damage accumulated on the tip of fatigue cracks,the fatigue damage law suitable for steel bridge members under traffic loading is modified to consider the crack growth.The virtual crack growth method and the semi-elliptical crack shape assumption are proposed in this paper to deduce a new model of fatigue crack growth rate for welded bridge members under traffic loading. And the calculated method of the stress intensity factor necessary for evaluation of the fatigue life of welded bridge members with cracks is discussed.The proposed fatigue crack growth model is then applied to calculate the crack growth and the fatigue life of existing welded members with fatigue experimental results. The fatigue crack propagation computation results show that the ratio of crack depth to the half crack surface length a/c is variable during crack propagation process and the stress cycle increases with the increase of a0/c0 with certain a0/t0 .The calculated and measured fatigue lives are generally in good agreement,at some initial conditions of cracking, for welded members widely used in steel bridges.

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Identification of vulnerable plaque pre-rupture is extremely important for patient risk stratification. The mechanism of plaque rupture is still not entirely clear, but it is thought to be a process involving multiple factors. From a biomechanical viewpoint, plaque rupture is usually seen as a structural failure when the plaque cannot resist the hemodynamic blood pressure and shear stress exerted on it. However, the cardiovascular system is naturally a cyclical hemodynamic environment, and myocardial infarction can be a symptomatically quiescent but potentially progressive process when plaque ruptures at stresses much lower than its strength. Therefore, fatigue accumulation is a possible mechanism for plaque rupture. In this study, a crack growth model was developed, and the previously-mentioned hypothesis was tested by conducting a comparative study between 18 symptomatic and 16 asymptomatic patients with carotid stenosis.

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Rupture of atheromatous plaque is the major cause of stroke or heart attack. Considering that the cardiovascular system is a classic fatigue environment, plaque rupture was treated as a chronic fatigue crack growth process in this study. Fracture mechanics theory was introduced to describe the stress status at the crack tip and Paris' law was used to calculate the crack growth rate. The effect of anatomical variation of an idealized plaque cross-section model was investigated. The crack initiation was considered to be either at the maximum circumferential stress location or at any other possible locations around the lumen. Although the crack automatically initialized at the maximum circumferential stress location usually propagated faster than others, it was not necessarily the most critical location where the fatigue life reached its minimum. We found that the fatigue life was minimum for cracks initialized in the following three regions: the midcap zone, the shoulder zone, and the backside zone. The anatomical variation has a significant influence on the fatigue life. Either a decrease in cap thickness or an increase in lipid pool size resulted in a significant decrease in fatigue life. Comparing to the previously used stress analysis, this fatigue model provides some possible explanations of plaque rupture at a low stress level in a pulsatile cardiovascular environment, and the method proposed here may be useful for further investigation of the mechanism of plaque rupture based on in vivo patient data.

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In most materials, short stress waves are generated during the process of plastic deformation, phase transformation, crack formation and crack growth. These phenomena are applied in acoustic emission (AE) for the detection of material defects in a wide spectrum of areas, ranging from nondestructive testing for the detection of materials defects to monitoring of microseismical activity. AE technique is also used for defect source identification and for failure detection. AE waves consist of P waves (primary longitudinal waves), S waves (shear/transverse waves) and Rayleigh (surface) waves as well as reflected and diffracted waves. The propagation of AE waves in various modes has made the determination of source location difficult. In order to use acoustic emission technique for accurate identification of source, an understanding of wave propagation of the AE signals at various locations in a plate structure is essential. Furthermore, an understanding of wave propagation can also assist in sensor location for optimum detection of AE signals along with the characteristics of the source. In real life, as the AE signals radiate from the source it will result in stress waves. Unless the type of stress wave is known, it is very difficult to locate the source when using the classical propagation velocity equations. This paper describes the simulation of AE waves to identify the source location and its characteristics in steel plate as well as the wave modes. The finite element analysis (FEA) is used for the numerical simulation of wave propagation in thin plate. By knowing the type of wave generated, it is possible to apply the appropriate wave equations to determine the location of the source. For a single plate structure, the results show that the simulation algorithm is effective to simulate different stress waves.

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In most materials, short stress waves are generated during the process of plastic deformation, phase transformation, crack formation and crack growth. These phenomena are applied in acoustic emission (AE) for the detection of material defects in wide spectrum areas, ranging from non-destructive testing for the detection of materials defects to monitoring of microeismical activity. AE technique is also used for defect source identification and for failure detection. AE waves consist of P waves (primary/longitudinal waves), S waves (shear/transverse waves) and Rayleight (surface) waves as well as reflected and diffracted waves. The propagation of AE waves in various modes has made the determination of source location difficult. In order to use the acoustic emission technique for accurate identification of source location, an understanding of wave propagation of the AE signals at various locations in a plate structure is essential. Furthermore, an understanding of wave propagation can also assist in sensor location for optimum detection of AE signals. In real life, as the AE signals radiate from the source it will result in stress waves. Unless the type of stress wave is known, it is very difficult to locate the source when using the classical propagation velocity equations. This paper describes the simulation of AE waves to identify the source location in steel plate as well as the wave modes. The finite element analysis (FEA) is used for the numerical simulation of wave propagation in thin plate. By knowing the type of wave generated, it is possible to apply the appropriate wave equations to determine the location of the source. For a single plate structure, the results show that the simulation algorithm is effective to simulate different stress waves.

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Acoustic emission (AE) analysis is one of the several diagnostic techniques available nowadays for structural health monitoring (SHM) of engineering structures. Some of its advantages over other techniques include high sensitivity to crack growth and capability of monitoring a structure in real time. The phenomenon of rapid release of energy within a material by crack initiation or growth in form of stress waves is known as acoustic emission (AE). In AE technique, these stress waves are recorded by means of suitable sensors placed on the surface of a structure. Recorded signals are subsequently analysed to gather information about the nature of the source. By enabling early detection of crack growth, AE technique helps in planning timely retrofitting or other maintenance jobs or even replacement of the structure if required. In spite of being a promising tool, some challenges do still exist behind the successful application of AE technique. Large amount of data is generated during AE testing, hence effective data analysis is necessary, especially for long term monitoring uses. Appropriate analysis of AE data for quantification of damage level is an area that has received considerable attention. Various approaches available for damage quantification for severity assessment are discussed in this paper, with special focus on civil infrastructure such as bridges. One method called improved b-value analysis is used to analyse data collected from laboratory testing.

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Structural health monitoring (SHM) refers to the procedure used to assess the condition of structures so that their performance can be monitored and any damage can be detected early. Early detection of damage and appropriate retrofitting will aid in preventing failure of the structure and save money spent on maintenance or replacement and ensure the structure operates safely and efficiently during its whole intended life. Though visual inspection and other techniques such as vibration based ones are available for SHM of structures such as bridges, the use of acoustic emission (AE) technique is an attractive option and is increasing in use. AE waves are high frequency stress waves generated by rapid release of energy from localised sources within a material, such as crack initiation and growth. AE technique involves recording these waves by means of sensors attached on the surface and then analysing the signals to extract information about the nature of the source. High sensitivity to crack growth, ability to locate source, passive nature (no need to supply energy from outside, but energy from damage source itself is utilised) and possibility to perform real time monitoring (detecting crack as it occurs or grows) are some of the attractive features of AE technique. In spite of these advantages, challenges still exist in using AE technique for monitoring applications, especially in the area of analysis of recorded AE data, as large volumes of data are usually generated during monitoring. The need for effective data analysis can be linked with three main aims of monitoring: (a) accurately locating the source of damage; (b) identifying and discriminating signals from different sources of acoustic emission and (c) quantifying the level of damage of AE source for severity assessment. In AE technique, the location of the emission source is usually calculated using the times of arrival and velocities of the AE signals recorded by a number of sensors. But complications arise as AE waves can travel in a structure in a number of different modes that have different velocities and frequencies. Hence, to accurately locate a source it is necessary to identify the modes recorded by the sensors. This study has proposed and tested the use of time-frequency analysis tools such as short time Fourier transform to identify the modes and the use of the velocities of these modes to achieve very accurate results. Further, this study has explored the possibility of reducing the number of sensors needed for data capture by using the velocities of modes captured by a single sensor for source localization. A major problem in practical use of AE technique is the presence of sources of AE other than crack related, such as rubbing and impacts between different components of a structure. These spurious AE signals often mask the signals from the crack activity; hence discrimination of signals to identify the sources is very important. This work developed a model that uses different signal processing tools such as cross-correlation, magnitude squared coherence and energy distribution in different frequency bands as well as modal analysis (comparing amplitudes of identified modes) for accurately differentiating signals from different simulated AE sources. Quantification tools to assess the severity of the damage sources are highly desirable in practical applications. Though different damage quantification methods have been proposed in AE technique, not all have achieved universal approval or have been approved as suitable for all situations. The b-value analysis, which involves the study of distribution of amplitudes of AE signals, and its modified form (known as improved b-value analysis), was investigated for suitability for damage quantification purposes in ductile materials such as steel. This was found to give encouraging results for analysis of data from laboratory, thereby extending the possibility of its use for real life structures. By addressing these primary issues, it is believed that this thesis has helped improve the effectiveness of AE technique for structural health monitoring of civil infrastructures such as bridges.

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Actin is the most abundantly distributed protein in living cells which plays critical roles in the cell interior force generation and transmission. The fracture mechanism of microfilament networks, whose principle component is actin, would provide insights which can contribute to the understandings of self-protective characters of cytoskeleton. In this study, molecular simulations are conducted to investigate the molecular mechanisms of disruption of microfilament networks from the viewpoint of biophysics. By employing a coarse-grained (CG) model of actin filament networks, we focused on the ultimate strength and crack growth mode of microfilament networks that have dependency on the crack length. It can be found that, the fracture mechanism of microfilament network has dependency on the structural properties of microfilament networks. The structure flaws marginally change the strength of microfilament networks which would explain the self-protective characters of cytoskeleton.

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BACKGROUND: Rupture of atheromatous plaque in the carotid artery often leads to thrombosis and subsequent stroke. The mechanism of plaque rupture is not entirely clear but is thought to be a multi-factorial process involving thinning and weakening of the fibrous cap and biomechanical stress as the trigger leading to plaque rupture. As the cardiovascular system is a classic fatigue environment, the weakening of plaque leading to rupture may be a fatigue process, which is a symptomatically quiescent but potentially progressive failure process. In this study, we used a fatigue analysis based on in vivo magnetic resonance imaging (MRI) to investigate the rupture initiation location, crack propagation path and fatigue life within plaques of asymptomatic and symptomatic individuals. METHODS: Forty non-consecutive subjects (20 symptomatic and 20 asymptomatic) underwent high-resolution multi-sequence in vivo MRI of the carotid bifurcation. Fatigue analysis was performed based on the plaque geometry derived from in vivo MRI of the carotid artery at the point of maximum stenosis. Paris’ Law in fracture mechanics is adopted to determine the fatigue crack growth rate. Incremental crack propagation was dynamically simulated based on stress distributions. Plaque initiation location, crack propagation path and fatigue cycle of symptomatic and asymptomatic individuals were compared. RESULTS: Cracks were often found to begin at the lumen wall at areas of stress concentration. The preferred rupture direction was radial from the lumen center. The crack initially advanced slowly but accelerated as it developed, depending on plaque morphology. The fatigue cycles of symptomatic plaques were significantly less than those in the asymptomatic group (2.3 ± 0.9 vs 3.1 ± 0.7 (x106); p = 0.003). CONCLUSIONS: The number of cycles to rupture in symptomatic patients was higher than those predicted in asymptomatic patients by fatigue analysis, suggesting the possibility that plaques with a less fatigue life may be more prone to be symptomatic and rupture. If further validated by large-scale longitudinal studies, fatigue analysis based on high resolution in vivo MRI could potentially act as a useful tool for risk assessment of carotid atheroma.

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The growth of a single cylindrical hole ahead of a blunt crack tip was studied using large deformation finite element analysis in three-point bend specimens with different precrack depth. The effect of small second phase particles was taken into account by incorporating Gurson’s constitutive equation. The effects of strain hardening and the initial distance from the hole to the crack tip were also investigated. The results show that the variation of crack tip opening displacement with load is not sensitive to constraint level. The effects of constraint on the growth of hole and ductile initiation toughness are diminished with decreasing initial distance from the hole to the blunt crack tip.

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Among the processes contributing to the progressive acquisition of the highly malignant phenotype in breast cancer are ovarian-independent growth, antioestrogen resistance and increased metastatic potential. We have previously observed that increased invasiveness and development of ovarian-independent growth occur independently. In an attempt to define the inter-relationships between these processes further, we have compared the phenotypes of ovarian-independent, invasive and antioestrogen-resistant sublines of the ovarian-dependent human breast cancer cell line MCF-7. Cells acquiring ovarian-independent growth can retain sensitivity to anti-oestrogens. One clone of MCF-7 cells selected for stable antioestrogen resistance has become non-tumorigenic but its invasive potential remains unaltered. Thus, acquisitions of some characteristics of the progressed phenotype can occur independently. This phenomenon of independent parameters in phenotypic progression could partly explain the considerable intra- and intertumour heterogeneity characteristic of breast tumours.