Erosion in bubbling fluidized-bed combustors is a serious issue that may affect their reliability and economics. Available evidence suggests that the key to understanding this erosion is detailed knowledge of the coupled and complex phenomena of solids circulation and bubble motion. A thin transparent "two-dimensional" rectangular fluidized bed with an obstacle served as a rough model for a fluidized-bed combustor. This model was studied experimentally and computationally using two hydrodynamic equation sets. The computed hydrodynamic results agree reasonably well with experimental data. Bubble frequencies and sizes compare well with those obtained from analyzing a high-speed motion picture frame-by-frame. Time-averaged porosities computed from both models agree with time-averaged porosity distributions rneasured with a gamma-ray densitometer. The principal differences between the data and the computations in this paper are due to asymmetries present in the experiment and to the simplified solids rheology used in the hydrodynamic models.
Hemodynamic data on the roles of physiologically critical blood particulates are needed to better understand cardiovascular diseases. The blood flow patterns and particulate buildup were numerically simulated using the multiphase non-Newtonian theory of dense suspension hemodynamics in a realistic right coronary artery (RCA) having various cross sections. The local hemodynamic factors, such as wall shear stress (WSS), red blood cell (RBC) buildup, viscosity, and velocity, varied with the spatially nonuniform vessel structures and temporal cardiac cycles. The model generally predicted higher RBC buildup on the inside radius of curvature. A low WSS region was found in the high RBC buildup region, in particular, on the area of maximum curvature of a realistic human RCA. The complex recirculation patterns, the oscillatory flow with flow reversal, and vessel geometry resulted in RBC buildup due to the prolonged particulate residence time, specifically, at the end of the diastole cycle. The increase of the initial plasma viscosity caused the lower WSS. These predictions have significant implications for understanding the local hemodynamic phenomena that may contribute to the earliest stage of atherosclerosis, as clinically observed on the inside curvatures and torsion of coronary arteries.
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