The blood-surface interaction can be studied from two prospective, first the blood can cause deterioration of the implant which consequently will result in device performance failure, second the material can cause blood clotting and plasma activation.
The 3rd passage of cells highly expressed the MSCs surface marker molecules, CD29 and CD90, and negatively expressed the blood cell surface molecules, c-kit, CD34, and CD45.
The blood vessel surface area per tumor volume was estimated from the CD31 stained slides using the method of Hilmas and Gilette[45].
Based on CD31 staining, the blood vessel surface area to tumor volume was ∼260 cm2/cm3 in this outer region, whereas it was ∼120 cm2/cm3 in the middle of the tumor.
They identified two bacterial enzymes that cleave only A- or B-type sugars, leaving other sugars on the blood cells' surfaces intact.
Despite the therapeutic benefits of both mechanical circulatory assist devices and nitinol stents with titanium (Ti) outer surfaces, problems remain with thrombosis at the blood-contacting surface.
Biphasic scaffolds with PGS as the blood-contacting surface were successfully fabricated.
The blood-contacting surface should simultaneously prevent thrombus formation and promote formation of a confluent endothelial cell layer, to achieve sustained haemostasis.
The interfacial tension (γs·blood) between PLLA surface and blood decreased by chain extension and molecular orientation, indicating the weakened interaction between bioactive substance in the blood and the surface of PLLA.
One with a dowel stirred the blood, for the surface had congealed into a spongy foam, and accidentally sloshed some onto the floor in bright starbursts.
Feasting inside red blood cells, it is invisible to the body's immune defenses except for an anchor protein it inserts into the blood cell's surface to tether the cell to a vessel wall.
