38 resultados para Pyrolytic and oxidative thermal degradation


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The thermal degradation of high density polyethylene has been modelled by the random breakage of polymer bonds, using a set of population balance equations. A model was proposed in which the population balances were lumped into representative sizes so that the experimentally determined molecular weight distribution of the original polymer could be used as the initial condition. This model was then compared to two different cases of the unlumped population balance which assumed unimolecular initial distributions of 100 and 500 monomer units, respectively. The model that utilised the experimentally determined molecular weight distribution was found to best describe the experimental data. The model fits suggested a second mechanism in addition to random breakage at slow reaction rates. (c) 2005 Elsevier Ltd. All rights reserved.

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Molecular dynamics simulations are used to study the interaction of low-energy Ar atoms with the Ni(001) surface, Angular scattering distributions, in and out of the plane of incidence, are investigated as a function of incident energy, angles of incidence, crystallographic orientation of the incident beam and surface temperature. The results show a clear transition to the structure scattering regime at around 2 eV. However, at lower energies, two sub-regimes are revealed by the simulations, Far energies up to 250 meV, scattering is mainly diffuse, and significant trapping on the surface is observed, At energies above this level, lobular patterns start to form and trapping decreases with the increase in energy, Generally, there is a weak temperature dependence, but variations in the angle of incidence and/or changes in the crystallographic direction, generate significant changes in the scattering patterns.

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Renal transplant recipients (RTRs) have elevated oxidative stress and a high incidence of cardiovascular morbidity and mortality. Although recent studies do not support the use of antioxidant supplements as a cardioprotectant in the general population, evidence suggests that RTRs may represent individuals that would benefit from this therapy. RTRs have elevated oxidative stress probably caused by the immunosuppressive therapy, and although only a small number of studies have examined the effects of antioxidant supplementation in these patients, most have reported beneficial findings. This review discusses these studies along with the rationale for the use of antioxidant supplements in RTRs and a call for more research to investigate this important topic.

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Purpose: The impact of acute weight loss on rowing performance was assessed when generous nutrient intake was provided in 2 h of recovery after making weight. Methods: Competitive rowers (N = 17) completed four ergometer trials, each separated by 48 h. Two trials were performed after a 4% body mass loss in the previous 24 h (WT) and two were performed after no weight restrictions, that is, unrestricted (UNR). In addition, two trials (I X WT, I X UNR) were in a thermoneutral environment (NEUTRAL, mean 21.1 +/- SD 0.7 degrees C, 29.0 +/- 4.5% RH) and two were in the heat (HOT 32.4, +/- 0.4 degrees C, 60.4 +/- 2.7% RH). Trials were performed in a counterbalanced fashion according to a Latin square design. Aggressive nutritional recovery strategies (WT 2.3 g(.)kg(-11) carbohydrate, 34 mg-kg(-1) Na, 28.4 mL(.)kg(-1) fluid; UNR ad libitum) were employed in the 2 h after weigh-in. Results: Both WT (mean 2.1, 95% CI 0.7-3.4 s; P = 0.003) and HOT (4.1, 2.7 - 5.4 s; P < 0.001) compromised 2000-m time-trial performance. Whereas WT resulted in hypohydration, the associated reduction in plasma volume explained only part of the performance compromise observed (0.2 s for every 1% decrement) Moreover, WT did not influence core temperature or indices of cardiovascular function. Conclusions: Acute weight loss compromised performance, despite generous nutrient intake in recovery, although the effect was small. Performance decrements were further exacerbated when exercise was performed in the heat.

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At least 30 minutes of moderate-intensity physical activity accumulated on most, preferably all days is considered the minimum level necessary to reduce the risk of developing cardiovascular disease. Despite an unclear explanation, some epidemiological data paradoxically suggest that a very high volume of exercise is associated with a decrease in cardiovascular health. Although ultra-endurance exercise training has been shown to increase antioxidant defences (and therefore confer a protective effect against oxidative stress), an increase in oxidative stress may contribute to the development of atherosclerosis via oxidative modification of low-density lipoprotein (LDL). Research has also shown that ultra-endurance exercise is associated with acute cardiac dysfunction and injury, and these may also be related to an increase in free radical production. Longitudinal studies are needed to assess whether antioxidant defences are adequate to prevent LDL oxidation that may occur as a result of increased free radical production during very high volumes of exercise. In addition, this work will assist in understanding the accrued effect of repeated ultra-endurance exercise-induced myocardial damage.

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