992 resultados para surface failure


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The New Zealand White rabbit has been widely used as a model of limbal stem cell deficiency (LSCD). Current techniques for experimental induction of LSCD utilize caustic chemicals, or organic solvents applied in conjunction with a surgical limbectomy. While generally successful in depleting epithelial progenitors, the depth and severity of injury is difficult to control using chemical-based methods. Moreover, the anterior chamber can be easily perforated while surgically excising the corneal limbus. In the interest of creating a safer and more defined LSCD model, we have therefore evaluated a mechanical debridement technique based upon use of the AlgerBrush II rotating burr. An initial comparison of debridement techniques was conducted in situ using 24 eyes in freshly acquired New Zealand White rabbit cadavers. Techniques for comparison (4 eyes each) included: (1) non-wounded control, (2) surgical limbectomy followed by treatment with 100% (v/v) n-heptanol to remove the corneal epithelium (1-2 minutes), (3) treatment of both limbus and cornea with n-heptanol alone, (4) treatment of both limbus and cornea with 20% (v/v) ethanol (2-3 minutes), (5) a 2.5-mm rounded burr applied to both the limbus and cornea, and (6) a 1-mm pointed burr applied to the limbus, followed by the 2.5-mm rounded burr applied to the cornea. All corneas were excised and processed for histology immediately following debridement. A panel of four assessors subsequently scored the degree of epithelial debridement within the cornea and limbus using masked slides. The 2.5-mm burr most consistently removed the corneal and limbal epithelia. Islands of limbal epithelial cells were occasionally retained following surgical limbectomy/heptanol treatment, or use of the 1-mm burr. Limbal epithelial cells were consistently retained following treatment with either ethanol or n-heptanol alone, with ethanol being the least effective treatment overall. The 2.5-mm burr method was subsequently evaluated in the right eye of 3 live rabbits by weekly clinical assessments (photography and slit lamp examination) for up to 5 weeks, followed by histological analyses (hematoxylin & eosin stain, periodic acid-Schiff stain and immunohistochemistry for keratin 3 and 13). All 3 eyes that had been completely debrided using the 2.5-mm burr displayed symptoms of ocular surface failure as defined by retention of a prominent epithelial defect (~40% of corneal surface at 5 weeks), corneal neovascularization (2 to 3 quadrants), reduced corneal transparency and conjunctivalization of the corneal surface (demonstrated by the presence of goblet cells and/or staining for keratin 13). In conclusion, our findings indicate that the AlgerBrush II rotating burr is an effective method for the establishment of ocular surface failure in New Zealand White rabbits. In particular, we recommend use of the 2.5-mm rotating burr for improved efficiency of epithelial debridement and safety compared to surgical limbectomy.

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The literature relating to road surface failure and design is briefly reviewed and the conventional methods for assessing the road damaging effects of dynamic tire forces are examined. A new time domain technique for analyzing dynamic tire forces and four associated road damage criteria are presented. The force criteria are used to examine the road damaging characteristics of a simple tandem-axle vehicle model for a range of speed and road roughness conditions. It is concluded that for the proposed criteria, the theoretical service life of road surfaces that are prone to fatigue failure may be reduced significantly by the dynamic component of wheel forces. The damage done to approximately five per cent of the road surface area during the passage of a theoretical model vehicle at typical highway speeds may be increased by as much as four times.

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This thesis focuses on the tribological performance of tool surfaces in two steel working operations, namely wire drawing and hot rolling. In all forming operations dimensions and surface finish of the products are of utmost importance. Forming basically includes three parts – forming conditions excluded – that may be changed; work material, tool and (possibly) lubricant. In the interface between work material and tool, the conditions are very aggressive with – generally or locally – high temperatures and pressures. The surfaces will be worn in various ways and this will change the conditions in the process. Consequently, the surface finish as well as the dimensions of the formed product may change and in the end, the product will not fulfil the requirements of the customer. Therefore, research and development in regard to wear, and consequently tribology, of the forming tools is of great interest. The investigations of wire drawing dies focus on coating adhesion/cohesion, surface characteristics and material transfer onto the coated steel both in laboratory scale as well as in the wire drawing process. Results show that it in wire drawing is possible to enhance the tribological performance of drawing dies by using a lubricant together with a steel substrate coated by a polished, dual-layer coating containing both hard and friction-lowering layers. The investigations of hot rolling work rolls focus on microstructure and hardness as well as cracking- and surface characteristics in both laboratory scale and in the hot strip mill. Results show that an ideal hot work roll material should be made up of a matrix with high hardness and a large amount of complex, hard carbides evenly distributed in the microstructure. The surface failure mechanisms of work rolls are very complex involving plastic deformation, abrasive wear, adhesive wear, mechanical and thermal induced cracking, material transfer and oxidation. This knowledge may be used to develop new tools with higher wear resistance giving better performance, lower costs and lower environmental impact.

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The surface failure characteristics of different work roll materials, i.e. High Speed Steel, High Chromium Iron and Indefinite Chill Iron, used in the finishing stands of a hot strip mill have been investigated using stereo microscopy, 3D optical profilometry, scanning electron microscopy and energy dispersive X-ray spectroscopy. The results show that the surface failure mechanisms of work rolls for hot rolling are very complex, involving plastic deformation, abrasive wear, adhesive wear, mechanical and thermal induced cracking, material transfer and oxidation. Despite the differences in chemical composition and microstructure, the tribological response of the different work roll materials was found to be strongly dependent on the material microstructure and especially the presence and distribution of microstructural constituents, such as the different carbide phases and graphite (in the case of Indefinite Chill Iron). Cracking and chipping of the work roll surfaces, both having a negative impact on work roll wear, are strongly influenced by the presence of carbides, carbide networks and graphite in the work roll surface. Consequently, the amount of carbide forming elements as well as the manufacturing process must be controlled in order to obtain an optimised microstructure and a predictable wear rate.

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This paper presents the response of pile foundations to ground shocks induced by surface explosion using fully coupled and non-linear dynamic computer simulation techniques together with different material models for the explosive, air, soil and pile. It uses the Arbitrary Lagrange Euler coupling formulation with proper state material parameters and equations. Blast wave propagation in soil, horizontal pile deformation and pile damage are presented to facilitate failure evaluation of piles. Effects of end restraint of pile head and the number and spacing of piles within a group on their blast response and potential failure are investigated. The techniques developed and applied in this paper and its findings provide valuable information on the blast response and failure evaluation of piles and will provide guidance in their future analysis and design.

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Using a combination of a logarithmic spiral and a straight line as a failure surface, comprehensive charts have been developed to determine the passive earth pressure coefficients and the positions of the critical failure surface for positive as well as negative wall friction angles. Translational movement of the wall has been examined in detail, considering the soil as either an associated flow dilatant material or a non-dilatant material, to determine the kinematic admissibility of the limit equilibrium solutions.

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As an alternative to externally bonded FRP reinforcement, near-surface mounted (NSM) FRP reinforcement can be used to effectively improve the flexural performance of RC beams. In such FRP strengthened RC beams, end cover separation failure is one of the common failure modes. This failuremode involves the detachment of the NSM FRP reinforcement together with the concrete cover along the level of the tension steel reinforcement. This paper presents a new strength model for end cover separation failure in RC beams strengthened in flexure with NSM FRP strips (i.e. rectangular FRP bars with asectional height-to-thickness ratio not less than 5), which was formulated on the basis of extensive numerical results from a parametric study undertaken using an efficient finite element approach. The proposed strength model consists of an approximate equation for the debonding strain of the FRP reinforcement at the critical cracked section and a conventional section analysis to relate this debondingstrain to the moment acting on the same section (i.e. the debonding strain). Once the debonding strain is known, the load level at end cover separation of an FRP-strengthened RC beam can be easily determined for a given load distribution. Predictions from the proposed strength model are compared with those of two existing strength models of the same type and available test results, which shows that the proposed strength model is in close agreement with test results and is far more accurate than the existing strength models.

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The flexural performance of RC beams can be improved using the near-surface mounted (NSM) FRP strengthening technique. A likely failure mode of such FRP-strengthened RC beams is bar-end cover separation which involves the detachment of the NSM FRP reinforcement together with the concrete cover along the level of the steel tension reinforcement. This paper presents a new analytical strength model for this failure mode. The proposed strength model and two existing strength models for this failure mode are compared with test results to demonstrate the superior performance of the new analytical model.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Background: The controversial effects promoted by cardiac resynchronization therapy (CRT) on the ventricular repolarization (VR) have motivated VR evaluation by body surface potential mapping (BSPM) in CRT patients. Methods: Fifty-two CRT patients, mean age 58.8 +/- 12.3 years, 31 male, LVEF 27.5 +/- 9.2, NYHA III-IV heart failure with QRS181.5 +/- 14.2 ms, underwent 87-lead BSPM in sinus rhythm (BASELINE) and biventricular pacing (BIV). Measurements of mean and corrected QT intervals and dispersion, mean and corrected T peak end intervals and their dispersion, and JT intervals characterized global and regional (RV, Intermediate, and LV regions) ventricular repolarization response. Results: Global QTm (P < 0.001) and QTcm (P < 0.05) were decreased in BIV; QTm was similar across regions in both modes (P = ns); QTcm values were lower in RV/LV than in Intermediate region in BASELINE and BIV (P < 0.001); only RV/Septum showed a significant difference (P < 0.01) in the BIV mode. QTD values both of BASELINE (P < 0.01) and BIV (P < 0.001) were greater in the Intermediate than in the LV region. CRT effect significantly reduced global/regional QTm and QTcm values. QTD was globally decreased in RV/LV (Intermediate: P = ns). BIV mode significantly reduced global T peak end mean and corrected intervals and their dispersion. JT values were not significant. Conclusions: Ventricular repolarization parameters QTm, QTcm, and QTD global/regional values, as assessed by BSPM, were reduced in patients under CRT with severe HF and LBBB. Greater recovery impairment in the Intermediate region was detected by the smaller variation of its dispersion.

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High energy is involved when a rider impacts a road surface in a crash. Rider speed, height of fall and road surface morphology all contribute to the level of initial impact energy. Impact can cause fabrics and seams of protective garments to burst rendering their protective value void. The Cambridge abrasion tester tests protective clothing with a fall height of 50mm and abrasive belt speed of 28km/hr, far below what can happen in a “high side” motorcycle crash at 100km/hr. This work addresses the mechanics of what occurs in the first few microseconds of an impact and provides insight into the effect that speed has on fabric burst. This work used a Cambridge impact abrasion test to evaluate two different protective motorcycle clothing fabrics (a denim and brushed fleecy fabric over a p-aramid protective liner). It measured their abrasion resistance at an abrasion speed of 28km/hr and standard impact height. It used a high speed camera to measure the impact displacement of the test head. Fabrics with high stretch were more prone to burst failure on initial impact. Fabric burst is caused by a high speed tensile stress between the fabric coupled with the abrasion surface and the inertia of the body dragging against it. Stretch fabrics are pushed into the abrasion surface for a longer period by the body before the tensile stress occurs so the coupling force is higher. If the transition to abrasion occurs early in the impact then a fabric is less likely to burst.

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The premature failure of an aluminium injection die with a duplex surface treatment (plasma nitriding and physical vapor deposition coating) was investigated, in an effort to identify the causes of such premature failure of the component. The manufacturing and the operating conditions were documented. Analytical tools were used, including scanning electron microscopy with energy dispersive X-ray capability, X-ray diffraction, and instrumented microhardness testing. Preliminary observations showed a microstructure of coarse tempered martensite, and a considerably rough surface with porosity and cracks. A detailed analysis of crack initiation sites identified sulfur inclusions in the subsurface, underneath the coating. A further revision of the processing conditions revealed that a sulfur-impregnated grinding stone had been used to polish the die. The chemical composition of such grinding stone matched that of the inclusions found in the subsurface of the failed component. Thus, searched causes of premature failure could be discussed on the lights of the present findings.

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Heart failure is a complex disorder, characterized by activation of the sympathetic nervous system, leading to dysregulated Ca2+ homeostasis in cardiac myocytes and tissue remodeling. In a variety of diseases, cardiac malfunction is associated with aberrant fluxes of Ca2+ across both the surface membrane and the internal Ca2+ store, the sarcoplasmic reticulum (SR). One prominent hypothesis residues is that in heart failure, the activity of the ryanodine receptor (RyR2) Ca2+ release channel in the SR is increased due to excess phosphorylation and that this contributes to excess SR Ca2+ leak in diastole, reduced SR Ca2+ load and decreased contractility (Huke & Bers, 2008). There is controversy over which serine residues in RyR2 are hyperphosphorylated in animal models of heart failure and whether this is via the CaMKII or the PKA-linked signaling pathway. S2808, S2814 and S2030 in RyR2 have been variously claimed to be hyperphosphorylated. Our aim was to examine the degree of phosphorylation of these residues in RyR2 from failing human hearts. The use of human tissue was approved by the Human Research Ethics Committee, The Prince Charles Hospital, EC28114. Left ventricular tissue samples were obtained from an explanted heart of a patient with endstage heart failure (Emery Dreifuss Muscular Dystrophy with cardiomyopathy) and non-failing tissue was from a patient with cystic fibrosis undergoing heart-lung transplantation with no history of heart disease. SR vesicles were prepared as described by Laver et al. (1995) and examined with SDS-Page and Western Blot. Transferred proteins were probed with antibodies to detect total protein phosphorylation, phosphorylation of RyR2 serine residues S2808, S2814, S2030 and for the key proteins calsequestrin, triadin, junctin and FKBP12.6. To avoid membrane stripping artifact, each membrane was exposed to one phosphorylation-specific antibody and signal densities quantified using Bio-Rad Quantity One software. We found no distinguishable difference between failing and healthy hearts in the protein expression levels of RyR2, triadin, junctin or calsequestrin. We found an expected upregulation of total RyR2 phosphorylation in the failing heart sample, compared to a matched amount of RyR2 (quantified using densiometry) in healthy heart. Probing with antibodies detecting only the phosphorylated form of the specific RyR2 residues showed that the increase in total RyR2 phosphorylation in the failing heart was due to hyperphosphorylation of S2808 and S2814. We found that S2030 phosphorylation levels were unchanged in human heart failure. Interestingly, we found that S2030 has a basal level of phosphorylation in the healthy human heart, different from the absence of basal phosphorylation recently reported in rodent heart (Huke & Bers, 2008). Finally, preliminary results indicate that less FKBP 12.6 is associated with RyR2 in the failing heart, possibly as a consequence of PKA activation. In conclusion, residues S2808 and S2814 are hyperphosphorylated in human heart failure, presumably due to upregulation of the CaMKII and/or PKA signaling pathway as a result of chronic activation of the sympathetic nervous system. Such changes in RyR2 phosphorylation are believed to contribute to the leaky RyR2 phenotype associated with heart failure, which increases the incidence of arrhythmia and contributes to the severely impaired contractile performance of the failing heart. Huke S & Bers DM. (2008). Ryanodine receptor phosphorylation at serine 2030, 2808 and 2814 in rat cardiomyocytes. Biochemical and Biophysical Research Communications 376, 80-85. Laver DR, Roden LD, Ahern GP, Eager KR, Junankar PR & Dulhunty AF. (1995). Cytoplasmic Ca2+ inhibits the ryanodine receptor from cardiac muscle. Journal of Membrane Biology 147, 7-22. Proceedings