Adherent cells were eluted by high shear, calcium-free buffer, and air embolism.

Therefore, rigid-walled analyses may be acceptable for identifying high shear regions of arteriovenous fistulae.

This decrease was lost under high shear and pulsatile flow.

Anfibatide also inhibited thrombus growth at low shear conditions, though less than at high shear.

Platelet adhesion to collagen was studied in an ex vivo whole-blood perfusion system under high shear conditions.

Injectable hydrogels are investigated for cell encapsulation and delivery as they can shield cells from high shear forces.

The fast flow generates high shear stress that has been demonstrated in vitro to activate and aggregate platelets.

These quantities show a universal dependence on a concentration- and functionality-dependent Weissenberg number with slight deviations at high shear rates.

This process may function as a protective mechanism to prevent in vivo irreversible platelet activation and aggregation under temporary high shear.

Anfibatide strongly inhibited platelet adhesion, aggregation, and thrombus formation in perfusion chambers at high shear conditions and efficiently dissolved preformed thrombi.

It also markedly reduced thrombus growth in human and murine blood in perfusion chambers at both low and high shear rates.

Depletion of polymers in the gap region due to the high shear rates involved is a possible cause for such a variation.

Here, we present results of a microfocus X-ray scattering experiment on spherical silica colloids in a liquid jet at high shear rates.

Here, we show that miR-126-5p sustains endothelial integrity in the context of high shear stress and autophagy.

Ex vivo platelet activation, platelet aggregation, and thrombus formation were measured following blood perfusion of low shear and high shear stress chambers.

Platelet aggregation under this condition requires a low shear exposure immediately after a high shear pulse, suggesting that post-stenosis low flow enhances platelet aggregation.