Improvements in Modeling 90 degree Bleed Holes for Supersonic Inlets

The modeling of porous bleed regions as boundary conditions in computational fluid dynamics (CFD) simulations of supersonic inlet flows has been improved through a scaling of sonic flow coefficient data for 90deg bleed holes. The scaling removed the Mach number as a factor in computing the sonic flow coefficient and allowed the data to be fitted with a quadratic equation, with the only factor being the ratio of the plenum static pressure to the surface static pressure. The implementation of the bleed model into the Wind-US CFD flow solver was simplified by no longer requiring the evaluation of the flow properties at the boundary-layer edge. The quadratic equation can be extrapolated to allow the modeling of small amounts of blowing, which can exist when recirculation of the bleed flow occurs within the bleed region. The improved accuracy of the bleed model was demonstrated through CFD simulations of bleed regions on a flat plate in supersonic flow with and without an impinging oblique shock. The bleed model demonstrated good agreement with experimental data and three-dimensional CFD simulations of bleed holes

VEGF regulates the proliferation of acid-exposed alveolar lining epithelial cells

Methods: A549 cells were incubated in 24 well culture dishes 24 hours before exposure to acid, then incubated with serum free medium containing various concentrations of HCl for 30 minutes at 37°C in 5% CO(2). The acidified medium was changed to normal complete medium; at specified incubation periods the supernatants were collected and the VEGF concentration measured and the number of adherent cells counted. Results: Proliferation of A549 cells and VEGF production were suppressed for at least 48 hours in HCl at a concentration of 50 mM. Restoration of cellular proliferation occurred following exogenous administration of VEGF (concentration of 1–250 ng/ml) and was inhibited by co-incubation with neutralising anti-VEGF antibody, indicating an interaction between VEGF molecules and A549 cells. Control cells were not influenced by administration of exogenous VEGF or anti-VEGF antibody. Treatment with neutralising anti-VEGF receptor (VEGFR) antibodies against VEGFR-1 and VEGFR-2 suppressed proliferation of acid exposed A549 cells but had no effect on control cells. Conclusions: Exogenous VEGF interacts with VEGFR-1 and VEGFR-2 on the surface and regulates the proliferation of injured alveolar lining epithelial cells in an autocrine or paracrine fashion