Analysis of two-dimensional incompressible flow past airfoils using unsteady Navier-Stokes equations

The conservative form of the unsteady Navier-Stokes equations in terms of vorticity and stream function in generalized curvilinear coordinates are used to analyze the flow structure of steady separation and unsteady flow with massive separation. The numerical method solves the discretized equations using an ADI-BGE method. The method is applied to a symmetric 12 percent thick Joukowski airfoil. A conformal clustered grid is generated; several 1-D stretching transformations are used to obtain a grid that attempts to resolve many of the multiple scales of the unsteady flow with massive separation, while maintaining the transformation metrics to be smooth and continuous in the entire flow field. Detailed numerical results are obtained for three flow configurations (1) Re = 1000, alpha = 5 deg., (2) Re =1000, alpha = 15 deg., (3) Re = 10,000, alpha = 5 deg. No artificial dissipation was added; however, lack of a fine grid in the normal direction has presently led to results which are considered qualitative, especially for case (3)

Simulation of self-induced unsteady motion in the near wake of a Joukowski airfoil

The unsteady Navier-Stokes analysis is shown to be capable of analyzing the massively separated, persistently unsteady flow in the post-stall regime of a Joukowski airfoil for an angle of attack as high as 53 degrees. The analysis has provided the detailed flow structure, showing the complex vortex interaction for this configuration. The aerodynamic coefficients for lift, drag, and moment were calculated. So far only the spatial structure of the vortex interaction was computed. It is now important to potentially use the large-scale vortex interactions, an additional energy source, to improve the aerodynamic performance

Characterization of dynamic stall phenomenon using two-dimensional unsteady Navier-Stokes equations

Among the new significant aspects of the present work are: (1) the treatment of the far-field boundary; (2) the use of C-grid topology, with the branch-cut singularity treated analytically; (3) evaluation of the effect of the envelope of prevailing initial states, and finally; (4) the ability to employ streakline/pathline 'visualization' to probe the unsteady features prevailing in vortex-dominated flows. The far-field boundary is placed at infinity, using appropriate grid stretching. This contributes to the accuracy of the solutions, but raised a number of important issues which needed to be resolved; this includes determining the equivalent time-dependent circulation for the pitching airfoil. A secondary counter-clockwise vortex erupts from within the boundary layer and immediately pinches off the energetic leading-edge shear layer which then, through hydrodynamic instability, rolls up into the dynamic stall vortex. The streakline/pathline visualization serves to provide information for insight into the physics of the unsteady separated flow

Iron causes lipid oxidation and inhibits proteasome function in multiple myeloma cells: A proof of concept for novel combination therapies

Adaptation to import iron for proliferation makes cancer cells potentially sensitive to iron toxicity. Iron loading impairs multiple myeloma (MM) cell proliferation and increases the efficacy of the proteasome inhibitor bortezomib. Here, we defined the mechanisms of iron toxicity in MM.1S, U266, H929, and OPM-2 MM cell lines, and validated this strategy in preclinical studies using Vk*MYC mice as MM model. High-dose ferric ammonium citrate triggered cell death in all cell lines tested, increasing malondialdehyde levels, the by-product of lipid peroxidation and index of ferroptosis. In addition, iron exposure caused dose-dependent accumulation of polyubiquitinated proteins in highly iron-sensitive MM.1S and H929 cells, suggesting that proteasome workload contributes to iron sensitivity. Accordingly, high iron concentrations inhibited the proteasomal chymotrypsin-like activity of 26S particles and of MM cellular extracts in vitro. In all MM cells, bortezomib-iron combination induced persistent lipid damage, exacerbated bortezomib-induced polyubiquitinated proteins accumulation, and triggered cell death more efficiently than individual treatments. In Vk*MYC mice, addition of iron dextran or ferric carboxymaltose to the bortezomib-melphalan-prednisone (VMP) regimen increased the therapeutic response and prolonged remission without causing evident toxicity. We conclude that iron loading interferes both with redox and protein homeostasis, a property that can be exploited to design novel combination strategies including iron supplementation, to increase the efficacy of current MM therapies