The well-known phenomena of Plateau-Rayleigh instability has been simulated using computational fluid dynamics (CFD). The breakup of a liquid film into an array of droplets on a cylindrical element was simulated using a volume-of-fluid (VOF) solver and compared to experimental observations and existing theory. It is demonstrated that the VOF method can correctly predict the breakup of thins films into an array of either axisymmetric droplets or clam-shell droplets, depending on the surface energy. The existence of unrealistically large films is precluded. Droplet spacing was found to show reasonable agreement with theory. Droplet motion and displacement under fluid flow was also examined and compared to that in previous studies. It was found that the presence of air flow around the droplet does not influence the stable film thickness; however, it reduces the time required for droplet formation. Novel relationships for droplet displacement were derived from the results.
This work presents a theoretical model describing the force required to move a coalesced liquid droplet along an oleophilic filter fiber. Measurements have been made using the atomic force microscope (AFM) to examine these forces over a range of fiber and droplet diameters as well as oil properties. Good agreement between measured and modeled forces was found. The influence of droplet displacement perpendicular to the fiber on the force required to move the droplet has also been determined experimentally and theoretically. It was found that fiber surface inhomogeneities are likely to influence results. This work has also established empirical relationships that can be used to predict the force, based on a known droplet volume, for the liquid types used.
This work experimentally examines the detachment of liquid droplets from both oleophilic and oleophobic fibres, using an atomic force microscope. The droplet detachment force was found to increase with increasing fibre diameter and forces were higher for philic fibres than phobic fibres. We also considered the detachment of droplets situated on the intersection of two fibres and arrays of fibres (such as found in fibrous mats or filters) and found that the required detachment forces were higher than for similarly sized droplets on a single fibre, though not as high as expected based on theory. A model was developed to predict the detachment force, from single fibres, which agreed well with experimental results. It was found that the entire dataset (single and multiple fibres) could be best described by power law relationships.
Increasing use of biodiesel has prompted research into the potential health effects of biodiesel exhaust exposure. Few studies directly compare the health consequences of mineral diesel, biodiesel, or blend exhaust exposures. Here, we exposed human epithelial cell cultures to diluted exhaust generated by the combustion of Australian ultralow-sulfur-diesel (ULSD), unprocessed canola oil, 100% canola biodiesel (B100), and a blend of 20% canola biodiesel mixed with 80% ULSD. The physicochemical characteristics of the exhaust were assessed and we compared cellular viability, apoptosis, and levels of interleukin (IL)-6, IL-8, and Regulated on Activation, Normal T cell Expressed and Secreted (RANTES) in exposed cultured cells. Different fuel types produced significantly different amounts of exhaust gases and different particle characteristics. All exposures resulted in significant apoptosis and loss of viability when compared with control, with an increasing proportion of biodiesel being correlated with a decrease in viability. In most cases, exposure to exhaust resulted in an increase in mediator production, with the greatest increases most often in response to B100. Exposure to pure canola oil (PCO) exhaust did not increase mediator production, but resulted in a significant decrease in IL-8 and RANTES in some cases. Our results show that canola biodiesel exhaust exposure elicits inflammation and reduces viability of human epithelial cell cultures in vitro when compared with ULSD exhaust exposure. This may be related to an increase in particle surface area and number in B100 exhaust when compared with ULSD exhaust. Exposure to PCO exhaust elicited the greatest loss of cellular viability, but virtually no inflammatory response, likely due to an overall increase in average particle size.
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