997 resultados para damage depth
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We investigated the effects of an Ironman triathlon race on markers of muscle damage, inflammation and heat shock protein 70 (HSP70). Nine well-trained male triathletes (mean +/- SD age 34 +/- 5 years; VO(2peak) 66.4 ml kg(-1) min(-1)) participated in the 2004 Western Australia Ironman triathlon race (3.8 km swim, 180 km cycle, 42.2 km run). We assessed jump height, muscle strength and soreness, and collected venous blood samples 2 days before the race, within 30 min and 14-20 h after the race. Plasma samples were analysed for muscle proteins, acute phase proteins, cytokines, heat shock protein 70 (HSP70), and clinical biochemical variables related to dehydration, haemolysis, liver and renal functions. Muscular strength and jump height decreased significantly (P < 0.05) after the race, whereas muscle soreness and the plasma concentrations of muscle proteins increased. The cytokines interleukin (IL)-1 receptor antagonist, IL-6 and IL-10, and HSP70 increased markedly after the race, while IL-12p40 and granulocyte colony-stimulating factor (G-CSF) were also elevated. IL-4, IL-1beta and tumour necrosis factor-alpha did not change significantly, despite elevated C-reactive protein and serum amyloid protein A on the day after the race. Plasma creatinine, uric acid and total bilirubin concentrations and gamma-glutamyl transferase activity also changed after the race. In conclusion, despite evidence of muscle damage and an acute phase response after the race, the pro-inflammatory cytokine response was minimal and anti-inflammatory cytokines were induced. HSP70 is released into the circulation as a function of exercise duration.
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The purpose of this study was to compare the effects of exercise intensity and exercise-induced muscle damage on changes in anti-inflammatory cytokines and other inflammatory mediators. Nine well-trained male runners completed three different exercise trials on separate occasions: (1) level treadmill running at 60% VO2max (moderate-intensity trial) for 60 min; (2) level treadmill running at 85% VO2max (high-intensity trial) for 60 min; (3) downhill treadmill running (-10% gradient) at 60% VO2max (downhill running trial) for 45 min. Blood was sampled before, immediately after and 1 h after exercise. Plasma was analyzed for interleukin-1 receptor antagonist (IL-1ra), IL-4, IL-5, IL-10, IL-12p40, IL-13, monocyte chemotactic protein-1 (MCP-1), prostaglandin E(2), leukotriene B(4) and heat shock protein 70 (HSP70). The plasma concentrations of IL-1ra, IL-12p40, MCP-1 and HSP70 increased significantly (P<0.05) after all three trials. Plasma prostaglandin E(2) concentration increased significantly after the downhill running and high-intensity trials, while plasma IL-10 concentration increased significantly only after the high-intensity trial. IL-4 and leukotriene B(4) did not increase significantly after exercise. Plasma IL-1ra and IL-10 concentrations were significantly higher (P<0.05) after the high-intensity trial than after both the moderate-intensity and downhill running trials. Therefore, following exercise up to 1 h duration, exercise intensity appears to have a greater effect on anti-inflammatory cytokine production than exercise-induced muscle damage
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Introduction: Unaccustomed eccentric exercise often results in muscle damage and neutrophil activation. We examined changes in plasma cytokines stress hormones, creatine kinase activity and myoglobin concentration, neutrophil surface receptor expression, degranulation, and the capacity of neutrophils to generate reactive oxygen species in response to in vitro stimulation after downhill running. Methods: Ten well-trained male runners ran downhill on a treadmill at a gradient of -10% for 45 min at 60% V̇O2max. Blood was sampled immediately before (PRE) and after (POST), 1 h (1 h POST), and 24 h (24 h POST) after exercise. Results: At POST, there were significant increases (P < 0.01) in neutrophil count (32%), plasma interleukin (IL)-6 concentration (460%), myoglobin (Mb) concentration (1100%), and creatine kinase (CK) activity (40%). At 1 h POST, there were further increases above preexercise values for neutrophil count (85%), plasma Mb levels (1800%), and CK activity (56%), and plasma IL-6 concentration remained above preexercise values (410%) (P < 0.01). At 24 h POST, neutrophil counts and plasma IL-6 levels had returned to baseline, whereas plasma Mb concentration (100%) and CK activity (420%) were elevated above preexercise values (P < 0.01). There were no significant changes in neutrophil receptor expression, degranulation and respiratory burst activity, and plasma IL-8 and granulocyte-colony stimulating factor concentrations at any time after exercise. Neutrophil count correlated with plasma Mb concentration at POST (r = 0.64, P < 0.05), and with plasma CK activity at POST (r = 0.83, P < 0.01) and 1 h POST (r = 0.78, P < 0.01). Conclusion: Neutrophil activation remains unchanged after downhill running in well-trained runners, despite increases in plasma markers of muscle damage.
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Anisotropic damage distribution and evolution have a profound effect on borehole stress concentrations. Damage evolution is an irreversible process that is not adequately described within classical equilibrium thermodynamics. Therefore, we propose a constitutive model, based on non-equilibrium thermodynamics, that accounts for anisotropic damage distribution, anisotropic damage threshold and anisotropic damage evolution. We implemented this constitutive model numerically, using the finite element method, to calculate stress–strain curves and borehole stresses. The resulting stress–strain curves are distinctively different from linear elastic-brittle and linear elastic-ideal plastic constitutive models and realistically model experimental responses of brittle rocks. We show that the onset of damage evolution leads to an inhomogeneous redistribution of material properties and stresses along the borehole wall. The classical linear elastic-brittle approach to borehole stability analysis systematically overestimates the stress concentrations on the borehole wall, because dissipative strain-softening is underestimated. The proposed damage mechanics approach explicitly models dissipative behaviour and leads to non-conservative mud window estimations. Furthermore, anisotropic rocks with preferential planes of failure, like shales, can be addressed with our model.
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In eukaryotes, genomic DNA is tightly compacted into a protein-DNA complex known as chromatin. This dense structure presents a barrier to DNA-dependent processes including transcription, replication and DNA repair. The repressive structure of chromatin is overcome by ATP-dependent chromatin remodelling complexes and chromatin-modifying enzymes. There is now ample evidence that DNA double-strand breaks (DSBs) elicit various histone modifications (such as acetylation, deacetylation, and phosphorylation) that function combinatorially to control the dynamic structure of the chromatin microenvironment. The role of these mechanisms during transcription and replication has been well studied, while the research into their impact on regulation of DNA damage response is rapidly gaining momentum. How chromatin structure is remodeled in response to DNA damage and how such alterations influence DSB repair are currently significant questions. This review will summarise the major chromatin modifications and chromatin remodelling complexes implicated in the DNA damage response to DSBs.
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Load bearing Light Gauge Steel Frame (LSF) walls made of cold-formed steel studs and tracks are commonly used in residential and commercial buildings. Fire safety of these walls is essential to minimize the damage caused by fire related accidents. Past investigations on the fire performance of load bearing LSF wall systems have been limited to LSF walls made of conventional lipped channel section studs. Although structurally efficient hollow flange steel sections are available in the building industry, they are not used as LSF wall studs due to the lack of fire performance data for such walls. The hollow flange sections have torsionally rigid hollow flanges that eliminate the occurrence of local and distortional buckling to an extent, thereby increasing their structural efficiency. The weaknesses of hollow flange sections such as lower lateral distortional buckling capacity are also eliminated when they are used as studs of LSF walls as the plasterboard restraints will prevent any lateral movement. Therefore hollow flange sections can be considered as structurally more efficient studs for use in LSF wall systems. This paper reports the full scale fire tests of LSF walls made of hollow flange section studs under standard fire conditions. The frames were made of 1.6 mm thick and 150 mm deep hollow flange section studs with two closed rectangular flanges of 45 mm width x 15 mm depth. Dual plasterboards were attached on both sides of the test wall panels. The load ratio was varied and the failure times, the lateral deflections and the axial displacements of the test walls were obtained. The failure behaviour of LSF walls made of hollow flange section studs was found to be different to that of LSF walls made of conventional lipped channel section studs. The results of these fire tests show that hollow flange section studs have a higher potential in being used in load bearing LSF Walls.
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Considerate amount of research has proposed optimization-based approaches employing various vibration parameters for structural damage diagnosis. The damage detection by these methods is in fact a result of updating the analytical structural model in line with the current physical model. The feasibility of these approaches has been proven. But most of the verification has been done on simple structures, such as beams or plates. In the application on a complex structure, like steel truss bridges, a traditional optimization process will cost massive computational resources and lengthy convergence. This study presents a multi-layer genetic algorithm (ML-GA) to overcome the problem. Unlike the tedious convergence process in a conventional damage optimization process, in each layer, the proposed algorithm divides the GA’s population into groups with a less number of damage candidates; then, the converged population in each group evolves as an initial population of the next layer, where the groups merge to larger groups. In a damage detection process featuring ML-GA, as parallel computation can be implemented, the optimization performance and computational efficiency can be enhanced. In order to assess the proposed algorithm, the modal strain energy correlation (MSEC) has been considered as the objective function. Several damage scenarios of a complex steel truss bridge’s finite element model have been employed to evaluate the effectiveness and performance of ML-GA, against a conventional GA. In both single- and multiple damage scenarios, the analytical and experimental study shows that the MSEC index has achieved excellent damage indication and efficiency using the proposed ML-GA, whereas the conventional GA only converges at a local solution.
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This thesis investigated the viability of using Frequency Response Functions in combination with Artificial Neural Network technique in damage assessment of building structures. The proposed approach can help overcome some of limitations associated with previously developed vibration based methods and assist in delivering more accurate and robust damage identification results. Excellent results are obtained for damage identification of the case studies proving that the proposed approach has been developed successfully.
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BACKGROUND: Epidemiologic research has demonstrated that cutaneous markers of photo-damage are associated with risk of basal cell carcinoma (BCC). However there has been no previous attempt to calculate pooled risk estimates. METHODS: We conducted a systematic review and meta-analysis after extracting relevant studies published up to January 2013 from five electronic databases. Eligible studies were those that permitted quantitative assessment of the association between histologically-confirmed BCC and actinic keratoses, solar elastosis, solar lentigines, or telangiectasia. RESULTS: Seven eligible studies were identified and summary odds ratios (OR) were calculated using both random and quality effects models. Having more than ten actinic keratoses was most strongly associated with BCC, conferring up to a 5-fold increase in risk (OR: 4.97; 95% CI: 3.26, 7.58). Other factors, including solar elastosis, solar lentigines, and telangiectasia had weaker but positive associations with BCC with ORs around 1.5. CONCLUSIONS: Markers of chronic photo-damage are positively associated with BCC. The presence of actinic keratoses was the most strongly associated with BCC of the markers examined. IMPACT: This work highlights the relatively modest association between markers of chronic ultraviolet exposure and BCC.
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This study presents a segmentation pipeline that fuses colour and depth information to automatically separate objects of interest in video sequences captured from a quadcopter. Many approaches assume that cameras are static with known position, a condition which cannot be preserved in most outdoor robotic applications. In this study, the authors compute depth information and camera positions from a monocular video sequence using structure from motion and use this information as an additional cue to colour for accurate segmentation. The authors model the problem similarly to standard segmentation routines as a Markov random field and perform the segmentation using graph cuts optimisation. Manual intervention is minimised and is only required to determine pixel seeds in the first frame which are then automatically reprojected into the remaining frames of the sequence. The authors also describe an automated method to adjust the relative weights for colour and depth according to their discriminative properties in each frame. Experimental results are presented for two video sequences captured using a quadcopter. The quality of the segmentation is compared to a ground truth and other state-of-the-art methods with consistently accurate results.
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Introduction: Nursing in the cardiac catheterisation laboratory (CCL) varies globally in terms of scope and deployment. In the US, all allied staff are cross-trained into all CCL roles. The Australian and New Zealand experience has legislative frameworks that reserves specific functions to nurses. Yet, the nursing role within the CCL is poorly researched and defined. Aim: This study sought to gain deeper understanding of the perceived role of CCL nurses in Australia and New Zealand. Method: A descriptive qualitative study using semi-structured in-depth interviews was used. A cross-sectional sample of 23 senior clinical nurses or nursing managers representing 16 CCLs across Australia and New Zealand was obtained. Data were digitally recorded and transcribed verbatim prior to analysis by three researchers. Results: Five major themes emerged from the data. These themes were: 1. The CCL is a unique environment; 2. CCL nursing is a unique and advanced cardiac nursing discipline; 3. The recruitment attributes for CCL nurses are advanced; 4. Education needs to be standardised; and 5. The evidence to support practice is poor. Discussion: The CCL environment is a dynamic, deeply interdisciplinary setting with CCL nursing seen to be a unique advanced practice role. Yet the time has come for a scope of practice, educational standards, guidelines and competencies was expressed by the participants. Conclusion: Nursing in the CCL is an advanced practice role working within a complex interdisciplinary environment. Further work is required to define the role of CCL nurses together with the evidence-base for their practice.
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Damage detection using modal properties is a widely accepted method. However, quantifying such damage using modal properties is still not well established. With this in mind, a research project is presently underway towards the development of a procedure to detect, locate and quantify damage in structural components using the variations in modal properties. A novel vibration based parameter called Vibration based Damage Index is introduced into the damage assessment procedure. This paper presents the early part of the research project which treats flexural members. The proposed procedure is validated using experimental data and/or theoretical techniques and illustrated through application. Outcomes of this research highlight the ability of the proposed procedure to successfully detect, locate and quantify damage in flexural structural components using the modal properties of the first few modes.
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Purpose: To develop, using dacarbazine as a model, reliable techniques for measuring DNA damage and repair as pharmacodynamic endpoints for patients receiving chemotherapy. Methods: A group of 39 patients with malignant melanoma were treated with dacarbazine 1 g/m2 i.v. every 21 days. Tamoxifen 20 mg daily was commenced 24 h after the first infusion and continued until 3 weeks after the last cycle of chemotherapy. DNA strand breaks formed during dacarbazine-induced DNA damage and repair were measured in individual cells by the alkaline comet assay. DNA methyl adducts were quantified by measuring urinary 3-methyladenine (3-MeA) excretion using immunoaffinity ELISA. Venous blood was taken on cycles 1 and 2 for separation of peripheral blood lymphocytes (PBLs) for measurement of DNA strand breaks. Results: Wide interpatient variation in PBL DNA strand breaks occurred following chemotherapy, with a peak at 4 h (median 26.6 h, interquartile range 14.75- 40.5 h) and incomplete repair by 24 h. Similarly, there was a range of 3-MeA excretion with peak levels 4-10 h after chemotherapy (median 33 nmol/h, interquartile range 20.448.65 nmol/h). Peak 3-MeA excretion was positively correlated with DNA strand breaks at 4 h (Spearman's correlation coefficient, r = 0.39, P = 0.036) and 24 h (r = 0.46, P = 0.01). Drug-induced emesis correlated with PBL DNA strand breaks (Mann Whitney U-test, P = 0.03) but not with peak 3-MeA excretion. Conclusions: DNA damage and repair following cytotoxic chemotherapy can be measured in vivo by the alkaline comet assay and by urinary 3-MeA excretion in patients receiving chemotherapy.
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In particle-strengthened metallic alloys, fatigue damage incubates at inclusion particles near the surface or at the change of geometries. Micromechanical simulation of inclusions such that the fatigue damage incubation mechanisms can be categorized. As micro-plasticity gradient field around different inclusions is different, a novel concept for nonlocal evaluation of micro-plasticity intensity is introduced. The effects of void aspects ration and spatial distributions are quantified for fatigue incubation life in the high-cycle fatigue regime. At last, these effects are integrated based on the statistical facts of inclusions to predict the fatigue life of structural components.
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Around lunchtime on 22 February 2011, the New Zealand city of Christchurch – the country’s second largest city – was hit by a magnitude 6.3 earthquake. Built on a geological faultline, like Los Angeles and Tokyo, Christchurch is no stranger to tremors; indeed, it had experienced a magnitude 7.1 quake just months before, in September 2010, and technically, this new earthquake was no more than an aftershock of the earlier tremor. That earlier quake had caused significant structural damage, but no fatalities, but the February earthquake was different: with its epicentre located no more than ten kilometres from the Christchurch city centre, at a depth of only five kilometres, it proved considerably more destructive – and it affected buildings whose structural integrity had already been severely compromised by the September quake, in the middle of a weekday when schools and city offices would have been fully occupied. While the full death toll has yet to be determined, it is estimated at close to 200.