Figure 6.
iMer inhibits stable aggregate formation under conditions of physiologic shear. (A) Human WB was pulled vertically (bottom to top) across horizontally oriented fibrillar collagen by vacuum syringe at a venous shear rate of 750 s−1. Plts were stained with anti-CD41 antibody (blue), then counterstained with anti–P-selectin antibody (green). (B) Surface area coverage was calculated by densitometry and circularity measurements and was significantly higher in vehicle-treated human platelets (green, n = 7), compared with iMer-treated platelets (red, n = 7 independent experiment samples; P < .05, Wilcoxon signed pairs rank test). (C) Quantitation of brightfield images of platelets showing a higher proportion of small aggregates (1-2 and 3-10 platelets per aggregate) after pretreatment with iMer than samples pretreated with vehicle control, which contained higher proportions of large aggregates (11-50, 50-100, and >100 platelets per aggregate). plts, platelets.

iMer inhibits stable aggregate formation under conditions of physiologic shear. (A) Human WB was pulled vertically (bottom to top) across horizontally oriented fibrillar collagen by vacuum syringe at a venous shear rate of 750 s−1. Plts were stained with anti-CD41 antibody (blue), then counterstained with anti–P-selectin antibody (green). (B) Surface area coverage was calculated by densitometry and circularity measurements and was significantly higher in vehicle-treated human platelets (green, n = 7), compared with iMer-treated platelets (red, n = 7 independent experiment samples; P < .05, Wilcoxon signed pairs rank test). (C) Quantitation of brightfield images of platelets showing a higher proportion of small aggregates (1-2 and 3-10 platelets per aggregate) after pretreatment with iMer than samples pretreated with vehicle control, which contained higher proportions of large aggregates (11-50, 50-100, and >100 platelets per aggregate). plts, platelets.

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