Outstanding issues are concerned with production of anatomical models, simulation of arterial disease, refinement of blood mimics to account for non-Newtonian behavior and validation of velocity measurements against an independent technique such as particle image velocimetry.
In this study, we investigated the effect of bindarit on neointima formation using two animal models of arterial injury: rat carotid artery balloon angioplasty and wire-induced carotid injury in apolipoprotein E-deficient (apoE−/−) mice.
Here, we investigated the effect of bindarit on neointima formation in vivo using two well-known animal models of arterial injury: rat carotid artery balloon angioplasty and wire-induced carotid injury in apolipoprotein E-deficient (apoE−/−) mice.
We examined whether NRPs play a role in neointimal remodelling induced by balloon angioplasty in the rat carotid artery, a well-characterized model of arterial remodelling following endothelial denudation.
These findings are relevant to the development of mathematical models of arterial mechanics, particularly for mouse models of arterial diseases involving elastic tissue.
In this study, a computational model of arterial tissue response to stenting is applied to three clinically relevant stent designs.
UHRA-9 and UHRA-10 specifically inhibit polyP and prove antithrombotic effects without increasing bleeding in a mouse model of arterial thrombosis [158].
The present study was designed to assess the antithrombotic effect of both dual antiplatelet regimens using a human ex vivo model of arterial thrombosis.
In doing so, we are testing the hypothesis that a mechanobiological model of arterial tissue response to injury could predict the long-term outcomes of stent design.
