993 resultados para Fatigue Damage


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Structural Health Monitoring (SHM) is defined as the use of on-structure sensing system to monitor the performance of the structure and evaluate its health state. Recent bridge failures, such as the collapses of the 1-35W Highway Bridge in USA, the collapse of the Can Tho Bridge in Vietnam and the Xijiang River Bridge in the Mainland China, all of which happened in the year 2007, have alerted the importance of structural health monitoring. This book presents a background of SHM technologies together with its latest development and successful applications. It is a book launched to celebrate the establishment of the Australian Network of Structural Health Monitoring (ANSHM). The network comprising leading SHM experts in Australia promotes and advances SHM research, application, education and development in Australia.

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Structural health monitoring has been accepted as a justified effort for long-span bridges, which are critical to a region's economic vitality. As the most heavily instrumented bridge project in the world, WASHMS - Wind And Structural Health Monitoring System has been developed and installed on the cable-supported bridges in Hong Kong (Wong and Ni 2009a). This chapter aims to share some of the experience gained through the operations and studies on the application of WASHMS. It is concluded that Structural Health Monitoring should be composed of two main components: Structural Performance Monitoring (SPM) and Structural Safety Evaluation (SSE). As an example to illustrate how the WASHMS could be used for structural performance monitoring, the layout of the sensory system installed on the Tsing Ma Bridge is briefly described. To demonstrate the two broad approaches of structural safety evaluation - Structural Health Assessment and Damage Detection, three examples in the application of SHM information are presented. These three examples can be considered as pioneer works for the research and development of the structural diagnosis and prognosis tools required by the structural health monitoring for monitoring and evaluation applications.

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Bearing damage in modern inverter-fed AC drive systems is more common than in motors working with 50 or 60 Hz power supply. Fast switching transients and common mode voltage generated by a PWM inverter cause unwanted shaft voltage and resultant bearing currents. Parasitic capacitive coupling creates a path to discharge current in rotors and bearings. In order to analyze bearing current discharges and their effect on bearing damage under different conditions, calculation of the capacitive coupling between the outer and inner races is needed. During motor operation, the distances between the balls and races may change the capacitance values. Due to changing of the thickness and spatial distribution of the lubricating grease, this capacitance does not have a constant value and is known to change with speed and load. Thus, the resultant electric field between the races and balls varies with motor speed. The lubricating grease in the ball bearing cannot withstand high voltages and a short circuit through the lubricated grease can occur. At low speeds, because of gravity, balls and shaft voltage may shift down and the system (ball positions and shaft) will be asymmetric. In this study, two different asymmetric cases (asymmetric ball position, asymmetric shaft position) are analyzed and the results are compared with the symmetric case. The objective of this paper is to calculate the capacitive coupling and electric fields between the outer and inner races and the balls at different motor speeds in symmetrical and asymmetrical shaft and balls positions. The analysis is carried out using finite element simulations to determine the conditions which will increase the probability of high rates of bearing failure due to current discharges through the balls and races.

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Patients with idiopathic small fibre neuropathy (ISFN) have been shown to have significant intraepidermal nerve fibre loss and an increased prevalence of impaired glucose tolerance (IGT). It has been suggested that the dysglycemia of IGT and additional metabolic risk factors may contribute to small nerve fibre damage in these patients. Twenty-five patients with ISFN and 12 aged-matched control subjects underwent a detailed evaluation of neuropathic symptoms, neurological deficits (Neuropathy deficit score (NDS); Nerve Conduction Studies (NCS); Quantitative Sensory Testing (QST) and Corneal Confocal Microscopy (CCM)) to quantify small nerve fibre pathology. Eight (32%) patients had IGT. Whilst all patients with ISFN had significant neuropathic symptoms, NDS, NCS and QST except for warm thresholds were normal. Corneal sensitivity was reduced and CCM demonstrated a significant reduction in corneal nerve fibre density (NFD) (Pb0.0001), nerve branch density (NBD) (Pb0.0001), nerve fibre length (NFL) (Pb0.0001) and an increase in nerve fibre tortuosity (NFT) (Pb0.0001). However these parameters did not differ between ISFN patients with and without IGT, nor did they correlate with BMI, lipids and blood pressure. Corneal confocal microscopy provides a sensitive non-invasive means to detect small nerve fibre damage in patients with ISFN and metabolic abnormalities do not relate to nerve damage.

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The modal strain energy method, which depends on the vibration characteristics of the structure, has been reasonably successful in identifying and localising damage in the structure. However, existing strain energy methods require the first few modes to be measured to provide meaningful damage detection. Use of individual modes with existing strain energy methods may indicate false alarms or may not detect the damage at or near the nodal points. This paper proposes a new modal strain energy based damage index which can detect and localize the damage using any one of the modes measured and illustrates its application for beam structures. It becomes evident that the proposed strain energy based damage index also has potential for damage quantification.

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Safety interventions (e.g., median barriers, photo enforcement) and road features (e.g., median type and width) can influence crash severity, crash frequency, or both. Both dimensions—crash frequency and crash severity—are needed to obtain a full accounting of road safety. Extensive literature and common sense both dictate that crashes are not created equal, with fatalities costing society more than 1,000 times the cost of property damage crashes on average. Despite this glaring disparity, the profession has not unanimously embraced or successfully defended a nonarbitrary severity weighting approach for analyzing safety data and conducting safety analyses. It is argued here that the two dimensions (frequency and severity) are made available by intelligently and reliably weighting crash frequencies and converting all crashes to property-damage-only crash equivalents (PDOEs) by using comprehensive societal unit crash costs. This approach is analogous to calculating axle load equivalents in the prediction of pavement damage: for instance, a 40,000-lb truck causes 4,025 times more stress than does a 4,000-lb car and so simply counting axles is not sufficient. Calculating PDOEs using unit crash costs is the most defensible and nonarbitrary weighting scheme, allows for the simple incorporation of severity and frequency, and leads to crash models that are sensitive to factors that affect crash severity. Moreover, using PDOEs diminishes the errors introduced by underreporting of less severe crashes—an added benefit of the PDOE analysis approach. The method is illustrated with rural road segment data from South Korea (which in practice would develop PDOEs with Korean crash cost data).

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Dynamic computer simulation techniques are used to develop and apply a multi-criteria procedure, incorporating changes in natural frequencies, modal flexibility and the modal strain energy, for damage localisation in beams and plates. Numerically simulated modal data obtained through finite element analyses are used to develop algorithms based on changes of modal flexibility and modal strain energy before and after damage and used as the indices for assessment of the state of structural health. The proposed procedure is illustrated through its application to flexural members under different damage scenarios and the results confirm its feasibility for damage assessment.

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Fatigue has been recognised as the primary contributing factor in approximately 15% of all fatal road crashes in Australia. To develop effective countermeasures for managing fatigue, this study investigates why drivers continue to drive when sleepy, and driver perceptions and behaviours in regards to countermeasures. Based on responses from 305 Australian drivers, it was identified that the major reasons why these participants continued to drive when sleepy were: wanting to get to their destination; being close to home; and time factors. Participants’ perceptions and use of 18 fatigue countermeasures were investigated. It was found that participants perceived the safest strategies, including stopping and sleeping, swapping drivers and stopping for a quick nap, to be the most effective countermeasures. However, it appeared that their knowledge of safe countermeasures did not translate into their use of these strategies. For example, although the drivers perceived stopping for a quick nap to be an effective countermeasure, they reported more frequent use of less safe methods such as stopping to eat or drink and winding down the window. This finding suggests that, while practitioners should continue educating drivers, they may need a greater focus on motivating drivers to implement safe fatigue countermeasures.

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Cancer-related fatigue (CRF) is one of themost debilitating symptoms in patients with cancer. It is prevalent at the time of diagnosis and during and after antineoplastic treatment and in patients with advanced disease. The multifactorial and complex nature of CRF makes it challenging for health professionals to identify a clear underlying mechanism and manage this symptom effectively. Often, the management plan for CRF (whether pharmacological or nonpharmacological) can be further complicated by the coexistence of other symptoms. This systematic review1 is therefore important in informing health professionals on the effectiveness of pharmacological management for CRF.

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The human knee acts as a sophisticated shock absorber during landing movements. The ability of the knee to perform this function in the real world is remarkable given that the context of the landing movement may vary widely between performances. For this reason, humans must be capable of rapidly adjusting the mechanical properties of the knee under impact load in order to satisfy many competing demands. However, the processes involved in regulating these properties in response to changing constraints remain poorly understood. In particular, the effects of muscle fatigue on knee function during step landing are yet to be fully explored. Fatigue of the knee muscles is significant for 2 reasons. First, it is thought to have detrimental effects on the ability of the knee to act as a shock absorber and is considered a risk factor for knee injury. Second, fatigue of knee muscles provides a unique opportunity to examine the mechanisms by which healthy individuals alter knee function. A review of the literature revealed that the effect of fatigue on knee function during landing has been assessed by comparing pre and postfatigue measurements, with fatigue induced by a voluntary exercise protocol. The information is limited by inconsistent results with key measures, such as knee stiffness, showing varying results following fatigue, including increased stiffness, decreased stiffness or failure to detect any change in some experiments. Further consideration of the literature questions the validity of the models used to induce and measure fatigue, as well as the pre-post study design, which may explain the lack of consensus in the results. These limitations cast doubt on the usefulness of the available information and identify a need to investigate alternative approaches. Based on the results of this review, the aims of this thesis were to: • evaluate the methodological procedures used in validation of a fatigue model • investigate the adaptation and regulation of post-impact knee mechanics during repeated step landings • use this new information to test the effects of fatigue on knee function during a step-landing task. To address the aims of the thesis, 3 related experiments were conducted that collected kinetic, kinematic and electromyographic data from 3 separate samples of healthy male participants. The methodologies involved optoelectronic motion capture (VICON), isokinetic dynamometry (System3 Pro, BIODEX) and wireless surface electromyography (Zerowire, Aurion, Italy). Fatigue indicators and knee function measures used in each experiment were derived from the data. Study 1 compared the validity and reliability of repetitive stepping and isokinetic contractions with respect to fatigue of the quadriceps and hamstrings. Fifteen participants performed 50 repetitions of each exercise twice in randomised order, over 4 sessions. Sessions were separated by a minimum of 1 week’s rest, to ensure full recovery. Validity and reliability depended on a complex interaction between the exercise protocol, the fatigue indicator, the individual and the muscle of interest. Nevertheless, differences between exercise protocols indicated that stepping was less effective in eliciting valid and reliable changes in peak power and spectral compression, compared with isokinetic exercise. A key finding was that fatigue progressed in a biphasic pattern during both exercises. The point separating the 2 phases, known as the transition point, demonstrated superior between-test reliability during the isokinetic protocol, compared with stepping. However, a correction factor should be used to accurately apply this technique to the study of fatigue during landing. Study 2 examined alterations in knee function during repeated landings, with a different sample (N =12) performing 60 consecutive step landing trials. Each landing trial was separated by 1-minute rest periods. The results provided new information in relation to the pre-post study design in the context of detecting adjustments in knee function during landing. First, participants significantly increased or decreased pre-impact muscle activity or post-impact mechanics despite environmental and task constraints remaining unchanged. This is the 1st study to demonstrate this effect in healthy individuals without external feedback on performance. Second, single-subject analysis was more effective in detecting alterations in knee function compared to group-level analysis. Finally, repeated landing trials did not reduce inter-trial variability of knee function in some participants, contrary to assumptions underpinning previous studies. The results of studies 1 and 2 were used to modify the design of Study 3 relative to previous research. These alterations included a modified isokinetic fatigue protocol, multiple pre-fatigue measurements and singlesubject analysis to detect fatigue-related changes in knee function. The study design incorporated new analytical approaches to investigate fatiguerelated alterations in knee function during landing. Participants (N = 16) were measured during multiple pre-fatigue baseline trial blocks prior to the fatigue model. A final block of landing trials was recorded once the participant met the operational fatigue definition that was identified in Study 1. The analysis revealed that the effects of fatigue in this context are heavily dependent on the compensatory response of the individual. A continuum of responses was observed within the sample for each knee function measure. Overall, preimpact preparation and post-impact mechanics of the knee were altered with highly individualised patterns. Moreover, participants used a range of active or passive pre-impact strategies to adapt post-impact mechanics in response to quadriceps fatigue. The unique patterns identified in the data represented an optimisation of knee function based on priorities of the individual. The findings of these studies explain the lack of consensus within the literature regarding the effects of fatigue on knee function during landing. First, functional fatigue protocols lack validity in inducing fatigue-related changes in mechanical output and spectral compression of surface electromyography (sEMG) signals, compared with isokinetic exercise. Second, fatigue-related changes in knee function during landing are confounded by inter-individual variation, which limits the sensitivity of group-level analysis. By addressing these limitations, the 3rd study demonstrated the efficacies of new experimental and analytical approaches to observe fatigue-related alterations in knee function during landing. Consequently, this thesis provides new perspectives into the effects of fatigue in knee function during landing. In conclusion: • The effects of fatigue on knee function during landing depend on the response of the individual, with considerable variation present between study participants, despite similar physical characteristics. • In healthy males, adaptation of pre-impact muscle activity and postimpact knee mechanics is unique to the individual and reflects their own optimisation of demands such as energy expenditure, joint stability, sensory information and loading of knee structures. • The results of these studies should guide future exploration of adaptations in knee function to fatigue. However, research in this area should continue with reduced emphasis on the directional response of the population and a greater focus on individual adaptations of knee function.

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Aim/hypothesis Immune mechanisms have been proposed to play a role in the development of diabetic neuropathy. We employed in vivo corneal confocal microscopy (CCM) to quantify the presence and density of Langerhans cells (LCs) in relation to the extent of corneal nerve damage in Bowman's layer of the cornea in diabetic patients. Methods 128 diabetic patients aged 58±1 yrs with a differing severity of neuropathy based on Neuropathy Deficit Score (NDS—4.7±0.28) and 26 control subjects aged 53±3 yrs were examined. Subjects underwent a full neurological evaluation, evaluation of corneal sensation with non-contact corneal aesthesiometry (NCCA) and corneal nerve morphology using corneal confocal microscopy (CCM). Results The proportion of individuals with LCs was significantly increased in diabetic patients (73.8%) compared to control subjects (46.1%), P=0.001. Furthermore, LC density (no/mm2) was significantly increased in diabetic patients (17.73±1.45) compared to control subjects (6.94±1.58), P=0.001 and there was a significant correlation with age (r=0.162, P=0.047) and severity of neuropathy (r=−0.202, P=0.02). There was a progressive decrease in corneal sensation with increasing severity of neuropathy assessed using NDS in the diabetic patients (r=0.414, P=0.000). Corneal nerve fibre density (P<0.001), branch density (P<0.001) and length (P<0.001) were significantly decreased whilst tortuosity (P<0.01) was increased in diabetic patients with increasing severity of diabetic neuropathy. Conclusion Utilising in vivo corneal confocal microscopy we have demonstrated increased LCs in diabetic patients particularly in the earlier phases of corneal nerve damage suggestive of an immune mediated contribution to corneal nerve damage in diabetes.

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Aging is associated with loss of endurance; however, aging is also associated with decreased fatigue during maximal isometric contractions. The aims of this study were to examine the relationship between age and walking endurance (WE) and maximal isometric fatigue (MIF) and to determine which metabolic/fitness components explain the expected age effects on WE and MIF. Subjects were 96 pre-menopausal women. Oxygen uptake (walking economy) was assessed during a 3-mph walk; aerobic capacity and WE by progressive treadmill test; knee extension strength by isometric contractions, MIF during a 90-s isometric plantar flexion (muscle metabolism measured by 31P MRS). Age was related to increased walking economy (low VO2, r = −0.19, P < 0.03) and muscle metabolic economy (force/ATP, 0.34, P = 0.01), and reduced MIF (−0.26, P < 0.03). However, age was associated with reduced WE (−0.28, P < 0.01). Multiple regression showed that muscle metabolic economy explained the age-related decrease in MIF (partial r for MIF and age −0.13, P = 0.35) whereas walking economy did not explain the age-related decrease in WE (partial r for WE and age −0.25, P < 0.02). Inclusion of VO2max and knee endurance strength accounted for the age-related decreased WE (partial r for WE and age = 0.03, P > 0.80). In premenopausal women, age is related to WE and MIF. In addition, these results support the hypothesis that age-related increases in metabolic economy may decrease MIF. However, decreased muscle strength and oxidative capacity are related to WE.

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Cellular response to radiation damage is made by a complex network of pathways and feedback loops whose spatiotemporal organisation is still unclear despite its decisive role in determining the fate of the damaged cell. Revealing the dynamic sequence of the repair proteins is therefore critical in understanding how the DNA repair mechanisms work. There are also still open questions regarding the possible movement of damaged chromatin domains and its role as trigger for lesion recognition and signalling in the DNA repair context. The single-cell approach and the high spatial resolution offered by microbeams provide the perfect tool to study and quantify the dynamic processes associated with the induction and repair of DNA damage. We have followed the development of radiation-induced foci for three DNA damage markers (i.e. γ-H2AX, 53BP1 and hSSB1) using normal fibroblasts (AG01522), human breast adenocarcinoma cells (MCF7) and human fibrosarcoma cells (HT1080) stably transfected with yellow fluorescent protein fusion proteins following irradiation with the QUB X-ray microbeam (carbon X-rays <2 µm spot). The size and intensity of the foci has been analysed as a function of dose and time post-irradiation to investigate the dynamics of the above-mentioned DNA repair processes and monitor the remodelling of chromatin structure that the cell undergoes to deal with DNA damage.