75 research outputs found
Geometry of inertial manifolds probed via a Lyapunov projection method
A method for determining the dimension and state space geometry of inertial
manifolds of dissipative extended dynamical systems is presented. It works by
projecting vector differences between reference states and recurrent states
onto local linear subspaces spanned by the Lyapunov vectors. A sharp
characteristic transition of the projection error occurs as soon as the number
of basis vectors is increased beyond the inertial manifold dimension. Since the
method can be applied using standard orthogonal Lyapunov vectors, it provides a
simple way to determine also experimentally inertial manifolds and their
geometric characteristics
Artificial Compressibility Method Revisited: Asymptotic Numerical Method for Incompressible Navier-Stokes Equations
High-performance Implementations and Large-scale Validation of the Link-wise Artificial Compressibility Method
The link-wise artificial compressibility method (LW-ACM) is a recent formulation of the artificial compressibility method for solving the incompressible Navier-Stokes equations. Two implementations of the LW-ACM in three dimensions on CUDA enabled GPUs are described. The first one is a modified version of a stateof-the-art CUDA implementation of the lattice Boltzmann method (LBM), showing that an existing GPU LBM solver might easily be adapted to LW-ACM. The second one follows a novel approach, which leads to a performance increase of up to 1.8 compared to the LBM implementation considered here, while reducing the memory requirements by a factor of 5.25. Large-scale simulations of the lid-driven cubic cavity at Reynolds number Re = 2000 were performed for both LW-ACM and LBM. Comparison of the simulation results against spectral elements reference data shows that LW-ACM performs almost as well as multiple-relaxation-time LBM in terms of accurac
Simulation of fluid-structure interaction with the interface artificial compressibility method
Partitioned fluid–structure interaction simulations of the arterial system are difficult due to the incompressibility of the fluid and the shape of the domain. The interface artificial compressibility (IAC) method mitigates the incompressibility constraint by adding a source term to the continuity equation in the fluid domain adjacent to the fluid–structure interface. This source term imitates the effect of the structure's displacement as a result of the fluid pressure and disappears when the coupling iterations have converged. The IAC method requires a small modification of the flow solver but not of the black-box structural solver and it outperforms a partitioned quasi-Newton coupling of the two black-box solvers in a simulation of a carotid bifurcation. Copyright © 2009 John Wiley & Sons, Ltd
Simulation of fluid-structure interaction with the interface artificial compressibility method
Poly(I:C) induces intense expression of c-IAP2 and cooperates with an IAP inhibitor in induction of apoptosis in cancer cells
<p>Abstract</p> <p>Background</p> <p>There is increasing evidence that the toll-like receptor 3 (TLR3) is an interesting target for anti-cancer therapy. Unfortunately, most laboratory investigations about the impact of TLR3 stimulation on human malignant cells have been performed with very high concentrations - 5 to 100 μg/ml - of the prototype TLR3 ligand, poly(I:C). In a previous study focused on a specific type of human carcinoma - nasopharyngeal carcinoma - we have shown that concentrations of poly(I:C) as low as 100 ng/ml are sufficient to induce apoptosis of malignant cells when combined to a pharmacological antagonist of the IAP family based on Smac mimicry.</p> <p>Methods</p> <p>This observation prompted us to investigate the contribution of the IAP family in cell response to poly(I:C) in a variety of human malignant cell types.</p> <p>Results</p> <p>We report a rapid, intense and selective increase in c-IAP2 protein expression observed under stimulation by poly(I:C)(500 ng/ml) in all types of human malignant cells. In most cell types, this change in protein expression is underlain by an increase in c-IAP2 transcripts and dependent on the TLR3/TRIF pathway. When poly(I:C) is combined to the IAP inhibitor RMT 5265, a cooperative effect in apoptosis induction and/or inhibition of clonogenic growth is obtained in a large fraction of carcinoma and melanoma cell lines.</p> <p>Conclusions</p> <p>Currently, IAP inhibitors like RMT 5265 and poly(I:C) are the subject of separate therapeutic trials. In light of our observations, combined use of both types of compounds should be considered for treatment of human malignancies including carcinomas and melanomas.</p
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