In the first approach we utilize a model-based, reduced, composite representation of the electric conductivity that is highly flexible, even for a moderate number of degrees of freedom.
We utilize a simulation model able to integrate both point mutations and recombination in the generated viral population depending on the amount of diversity required.
In order to investigate the number of chains and the contact resistance between the particles in the CM, we utilized a model of the effective electric resistance.
To demonstrate effective repression of HIF-1α in these cell lines, we utilized a model of ambient hypoxia.
To test our hypothesis, we utilized a model of canine obesity based on feeding dogs a hypercaloric, high-fat diet to induce the development of insulin resistance.
We utilized a model of mesangial proliferative glomerulonephritis, known as anti-Thy1-induced glomerulonephritis (Thy1 GN), which exhibits sclerosis in the glomeruli.
We utilized a model similar to that used for the analysis of the multiple-cycle viral yield assay, but allowed for a normal distribution of the latent infection period among cells rather than a fixed value for all cells, as assumed previously (see Materials and Methods).
We utilized a model of arteriogenesis in the rat hindlimb that allowed us to identify and isolate a single collateral vessel early after induction of collateral growth [ 8].
In contrast, we utilized a model of moderate overexpression of GLO1 activity and investigated the natural course of vascular aging without additional induction of disease.
