Numerical and Experimental Study of the Performance Effects of Varying Vaneless Space and Vane Solidity in Radial Inflow Turbine Stators.

An extensive experimental program has been carried out on a 135?mm tip diameter radial turbine using a variety of stator designs, in order to facilitate direct performance comparisons of varying stator vane solidity and the effect of varying the vaneless space. A baseline vaned stator was designed using commercial blade design software, having 15 vanes and a vane trailing edge to rotor leading edge radius ratio (Rte/rle) of 1.13. Two additional series of stator vanes were designed and manufactured; one series having varying vane numbers of 12, 18, 24, and 30, and a further series with Rte/rle ratios of 1.05, 1.175, 1.20, and 1.25. As part of the design process a series of CFD simulations were carried out in order to guide design iterations towards achieving a matched flow capacity for each stator. In this way the variations in the measured stage efficiency could be attributed to the stator passages only, thus allowing direct comparisons to be made. Interstage measurements were taken to capture the static pressure distribution at the rotor inlet and these measurements were then used to validate subsequent numerical models. The overall losses for different stators have been quantified and the variations in the measured and computed efficiency were used to recommend optimum values of vane solidity and Rte/rle.

Matrilysin-1 mediates bronchiolization of alveoli, a potential premalignant change in lung cancer

Matrilysin-1 (also called matrix metalloproteinase-7) is expressed in injured lung and in cancer but not in normal epithelia. Bronchiolization of the alveoli (BOA), a potential precursor of lung cancer, is a histologically distinct type of metaplasia that is composed of cells resembling airway epithelium in the alveolar compartment. We demonstrate that there is increased expression of matrilysin-1 in human lesions and BOA in the CC10-human achaete-scute homolog-1 transgenic mouse model. Forced expression of the matrilysin-1 gene in immortalized human normal airway epithelial BEAS-2B and HPLD1 cells, which do not normally express matrilysin-1, promoted cellular migration, suggesting a functional link for BOA formation via bronchiolar cell migration. In addition, matrilysin-1 stimulated proliferation and inhibited Fas-induced apoptosis, while a knockdown by RNA interference decreased cell growth, migration, and increased sensitivity to apoptosis. Western blotting demonstrated increased levels of phospho-p38 and phospho-Erk1/2 kinases after matrilysin-1 expression. Gene expression analysis uncovered several genes that were related to cell growth, migration/movement, and death, which could potentially facilitate bronchiolization. In vivo, the formation of BOA lesions was reduced when CC10-human achaete-scute homolog-1 mice were crossed with matrilysin-1 null mice and was correlated with reduced matrilysin-1 expression in BOA. We conclude that matrilysin-1 may play an important role in the bronchiolization of alveoli by promoting proliferation, migration, and attenuation of apoptosis involving multiple genes in the MAP kinase pathway.