32 resultados para Defect induced damage model

em Deakin Research Online - Australia


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 In some advanced sheet metal forming processes such as the incremental forming process, a local fracture strain after necking is very important. In order to accurately predict necking and fracture phenomena, a crystal plasticity model is introduced in the finite element analysis of tensile tests. A tensile specimen is modeled by many grains that have their own crystalline orientation. And each of the grains is discretized by many elements. Using this analysis, necking behavior of a tensile specimen can be predicted without any initial imperfections. A damage model is also implemented to predict sudden drops of load carrying capacity after necking and to reflect the void nucleation and growth of the severely deformed region. From an analysis of the tensile test, the necking behavior is well predicted. Finally, analyses are carried out for various strain paths, and FLDs up to necking and fracture are predicted.

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Ply-scale finite element (FE) models are widely used to predict the performance of a composite structure based on material properties of individual plies. When simulating damage, these models neglect microscopic fracture processes which may have a significant effect on how a crack progresses within and between plies of a multidirectional laminate. To overcome this resolution limitation a multi-scale modelling technique is employed to simulate the effect micro-scale damage events have on the macro-scale response of a structure. The current paper discusses the development and validation of a hybrid mass-spring system and finite element modelling technique for multi-scale analysis. The model developed here is limited to elastic deformations; however, it is the first key step towards an efficient multi-scale damage model well suited to simulation of fracture in fibre reinforced composite materials. Various load cases have been simulated using the model developed here which show excellent accuracy compared to analytical and FE results. Future work is discussed, including extension of the model to incorporate damage modelling.

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The ‘wear mode diagram’ has been commonly used to classify the deformation regime of the soft work-piece during scratching, into three modes: ploughing, wedge formation and cutting. The scratch test is usedto evaluate wear modes and material removal associated with wear. There are different damage models in the literature used for the description of material behaviour after damage initiation under different loadingconditions. However, there has been little analysis to compare damage models during scratch test conditions. The first aim of this work is first to use a finite element modelling package (Abaqus/Explicit) to build a 3Dmodel to capture deformation modes during scratching with indenters with different attack angles. Three different damage models are incorporated into the model and patterns of damage initiation and propagation arecompared with experimental results from the literature. This work highlights the role of the damage model in accurately capturing wear modes and material removal during two body sliding interactions.

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Aims/hypothesis Islet transplantation is a potential cure for diabetes; however, rates of graft failure remain high. The aim of the present study was to determine whether amyloid deposition is associated with reduced beta cell volume in islet grafts and the recurrence of hyperglycaemia following islet transplantation.

Methods We transplanted a streptozotocin-induced mouse model of diabetes with 100 islets from human IAPP (which encodes islet amyloid polypeptide) transgenic mice that have the propensity to form islet amyloid (n = 8–12) or from non-transgenic mice that do not develop amyloid (n = 6–10) in sets of studies that lasted 1 or 6 weeks.

Results Plasma glucose levels before and for 1 week after transplantation were similar in mice that received transgenic or non-transgenic islets, and at that time amyloid was detected in all transgenic grafts and, as expected, in none of the non-transgenic grafts. However, over the 6 weeks following transplantation, plasma glucose levels increased in transgenic but remained stable in non-transgenic islet graft recipients (p < 0.05). At 6 weeks, amyloid was present in 92% of the transgenic grafts and in none of the non-transgenic grafts. Beta cell volume was reduced by 30% (p < 0.05), beta cell apoptosis was twofold higher (p < 0.05), and beta cell replication was reduced by 50% (p < 0.001) in transgenic vs non-transgenic grafts. In summary, amyloid deposition in islet grafts occurs prior to the recurrence of hyperglycaemia and its accumulation over time is associated with beta cell loss.

Conclusions/interpretation Islet amyloid formation may explain, in part, the non-immune loss of beta cells and recurrence of hyperglycaemia following clinical islet transplantation.

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In this study a modelling technique, namely, the embedded element method is assessed to evaluate its ability to predict Mode I interlaminar failure. The embedded element technique takes advantage of the embedded constraint in ABAQUS and allows the two constituents, fibre and matrix, to be meshed independently. Since the two constituents can be meshed independently a contiguous mesh is not required and the time taken to create an acceptable mesh is significantly reduced. The embedded element technique has been used to model fibre-reinforced composite structures, however, to date no studies have been conducted which combine the embedded element technique with an interlaminar damage model. The work described herein evaluates the ability of the embedded element technique to predict mode I interlaminar failure. DCB specimens were modelled using the embedded element method and a traditional 3D solid FE modelling approach with the predictions compared against experimental data. Both modelling approaches provided good agreement with experimental results. The good agreement demonstrates that the embedded element technique is capable of providing a response that is equivalent to a traditional 3D solid FE models and is particularly suited to modelling thick composite structures with complex geometry.

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Finding practical ways to robustly estimate abundance or density trends in threatened species is a key facet for effective conservation management. Further identifying less expensive monitoring methods that provide adequate data for robust population density estimates can facilitate increased investment into other conservation initiatives needed for species recovery. Here we evaluated and compared inference-and cost-effectiveness criteria for three field monitoring-density estimation protocols to improve conservation activities for the threatened Komodo dragon (Varanus komodoensis). We undertook line-transect counts, cage trapping and camera monitoring surveys for Komodo dragons at 11 sites within protected areas in Eastern Indonesia to collect data to estimate density using distance sampling methods or the Royle-Nichols abundance induced heterogeneity model. Distance sampling estimates were considered poor due to large confidence intervals, a high coefficient of variation and that false absences were obtained in 45 % of sites where other monitoring methods detected lizards present. The Royle-Nichols model using presence/absence data obtained from cage trapping and camera monitoring produced highly correlated density estimates, obtained similar measures of precision and recorded no false absences in data collation. However because costs associated with camera monitoring were considerably less than cage trapping methods, albeit marginally more expensive than distance sampling, better inference from this method is advocated for ongoing population monitoring of Komodo dragons. Further the cost-savings achieved by adopting this field monitoring method could facilitate increased expenditure on alternative management strategies that could help address current declines in two Komodo dragon populations.

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Application of damage model in combination with finite element analysis to design and optimization of equal channel angular pressing - conform of commercially pure titanium against ductile failure is demonstrated. The properties required for precise simulation of the process and prediction of damage accumulation (equivalent stress as function of equivalent strain and temperature and low bound ductility function) are obtained in the temperature interval 20-400 °C and described in details.

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BACKGROUND: Maternal antenatal creatine supplementation protects the brain, kidney, and diaphragm against the effects of birth asphyxia in the spiny mouse. In this study, we examined creatine's potential to prevent damage to axial skeletal muscles.

METHODS: Pregnant spiny mice were fed a control or creatine-supplemented diet from mid-pregnancy, and 1 d before term (39 d), fetuses were delivered by c-section with or without 7.5 min of birth asphyxia. At 24 h or 33 ± 2 d after birth, gastrocnemius muscles were obtained for ex-vivo study of twitch-tension, muscle fatigue, and structural and histochemical analysis.

RESULTS: Birth asphyxia significantly reduced cross-sectional area of all muscle fiber types (P < 0.05), and increased fatigue caused by repeated tetanic contractions at 24 h of age (P < 0.05). There were fewer (P < 0.05) Type I and IIa fibers and more (P < 0.05) Type IIb fibers in male gastrocnemius at 33 d of age. Muscle oxidative capacity was reduced (P < 0.05) in males at 24 h and 33 d and in females at 24 h only. Maternal creatine treatment prevented all asphyxia-induced changes in the gastrocnemius, improved motor performance.

CONCLUSION: This study demonstrates that creatine loading before birth protects the muscle from asphyxia-induced damage at birth.

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The characterisation of strain path with respect to the directionality of defect formation is discussed. The criterion of non-monotonic strain path is used in the scalar and tensor models for damage accumulation and recovery. Comparable analysis of models and their verification has been obtained by simulation of crack initiation in a two-stage metal forming operation consisting of wire drawing followed by constrained upsetting.

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Plant innate immunity to pathogenic microorganisms is activated in response to recognition of extracellular or intracellular pathogen molecules by transmembrane receptors or resistance proteins, respectively. The defense signaling pathways share components with those involved in plant responses to UV radiation, which can induce expression of plant genes important for pathogen resistance. Such intriguing links suggest that UV treatment might activate resistance to pathogens in normally susceptible host plants. Here, we demonstrate that pre-inoculative UV (254 nm) irradiation of Arabidopsis (Arabidopsis thaliana) susceptible to infection by the biotrophic oomycete Hyaloperonospora parasitica, the causative agent of downy mildew, induces dose- and time-dependent resistance to the pathogen detectable up to 7 d after UV exposure. Limiting repair of UV photoproducts by postirradiation incubation in the dark, or mutational inactivation of cyclobutane pyrimidine dimer photolyase, (6-4) photoproduct photolyase, or nucleotide excision repair increased the magnitude of UV-induced pathogen resistance. In the absence of treatment with 254-nm UV, plant nucleotide excision repair mutants also defective for cyclobutane pyrimidine dimer or (6-4) photoproduct photolyase displayed resistance to H. parasitica, partially attributable to short wavelength UV-B (280–320 nm) radiation emitted by incubator lights. These results indicate UV irradiation can initiate the development of resistance to H. parasitica in plants normally susceptible to the pathogen and point to a key role for UV-induced DNA damage. They also suggest UV treatment can circumvent the requirement for recognition of H. parasitica molecules by Arabidopsis proteins to activate an immune response.

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In the current study, the role of dynamic strain induced transformation on ferrite grain refinement was investigated using different thermomechanical processing routes. A Ni-30Fe austenitic model alloy was also employed to study the evolution of the deformation structure under different deformation conditions. It was shown that the extreme refinement of ferrite is more likely due to the formation of extensive high angle intragranular defects in the austenite through deformation. Among the different thermomechanical parameters, the deformation temperature had a significant effect on the intragranular defect characteristics. There was a transition where the cell dislocation structure changed to laminar microband structures with a decrease in the deformation temperature. Moreover, the ultrafine grained structure was also successfully produced through static transformation using warm deformation process; in other words, concurrent deformation and transformation are not necessary for ultrafine ferrite formation.

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Eccentrically biased exercise results in skeletal muscle damage and stimulates adaptations in muscle, whereby indexes of damage are attenuated when the exercise is repeated. We hypothesized that changes in ultrastructural damage, inflammatory cell infiltration, and markers of proteolysis in skeletal muscle would come about as a result of repeated eccentric exercise and that gender may affect this adaptive response. Untrained male (n = 8) and female (n = 8) subjects performed two bouts (bout 1 and bout 2), separated by 5.5 wk, of 36 repetitions of unilateral, eccentric leg press and 100 repetitions of unilateral, eccentric knee extension exercises (at 120% of their concentric single repetition maximum), the subjects' contralateral nonexercised leg served as a control (rest). Biopsies were taken from the vastus lateralis from each leg 24 h postexercise. After bout 2, the postexercise force deficit and the rise in serum creatine kinase (CK) activity were attenuated. Women had lower serum CK activity compared with men at all times (P < 0.05), but there were no gender differences in the relative magnitude of the force deficit. Muscle Z-disk streaming, quantified by using light microscopy, was elevated vs. rest only after bout 1 (P < 0.05), with no gender difference. Muscle neutrophil counts were significantly greater in women 24 h after bout 2 vs. rest and bout 1 (P < 0.05) but were unchanged in men. Muscle macrophages were elevated in men and women after bout 1 andbout 2 (P < 0.05). Muscle protein content of the regulatory calpain subunit remained unchanged whereas ubiquitin-conjugated protein content was increased after both bouts (P < 0.05), with a greater increase after bout 2. We conclude that adaptations to eccentric exercise are associated with attenuated serum CK activity and, potentially, an increase in the activity of the ubiquitin proteosome proteolytic pathway.

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Overuse tendinopathy is problematic to manage clinically. People of different ages with tendons under diverse loads present with varying degrees of pain, irritability, and capacity to function. Recovery is similarly variable; some tendons recover with simple interventions, some remain resistant to all treatments.

The pathology of tendinopathy has been described as degenerative or failed healing. Neither of these descriptions fully explains the heterogeneity of presentation. This review proposes, and provides evidence for, a continuum of pathology. This model of pathology allows rational placement of treatments along the continuum.

A new model of tendinopathy and thoughtful treatment implementation may improve outcomes for those with tendinopathy. This model is presented for evaluation by clinicians and researchers.