Figure 2.
Altered thrombus formation in the blood of index patients with confirmed genetics. Whole blood from patients and control subjects was perfused over microspots from M1 to M6 for 3.5 minutes at a wall-shear rate of 1000/s. Brightfield and fluorescence images were captured using an EVOS-FL microscope and a 60× oil objective and analyzed for platelet phenotypes. Shown are representative brightfield and fluorescence (FITC α-fibrinogen mAb for integrin αIIbβ3 activation) images at the end stage (scale bar, 20 μm) for microspots M1 (collagen 1) and M3 (collagen 3). Results for a control subject (CCF01), index patients with a defect in RASGRP2 (Pat01∗) or P2RY12 (Pat06∗), SPD with TCP (SPD, VWD, and TCP) (Pat10∗), δ-SPD (no variant identified, Pat13∗), or compound heterozygous variants of HPS3 (Pat19∗) or HSP1 (Pat29∗) genes. FITC, fluorescein isothiocyanate.

Altered thrombus formation in the blood of index patients with confirmed genetics. Whole blood from patients and control subjects was perfused over microspots from M1 to M6 for 3.5 minutes at a wall-shear rate of 1000/s. Brightfield and fluorescence images were captured using an EVOS-FL microscope and a 60× oil objective and analyzed for platelet phenotypes. Shown are representative brightfield and fluorescence (FITC α-fibrinogen mAb for integrin αIIbβ3 activation) images at the end stage (scale bar, 20 μm) for microspots M1 (collagen 1) and M3 (collagen 3). Results for a control subject (CCF01), index patients with a defect in RASGRP2 (Pat01∗) or P2RY12 (Pat06∗), SPD with TCP (SPD, VWD, and TCP) (Pat10∗), δ-SPD (no variant identified, Pat13∗), or compound heterozygous variants of HPS3 (Pat19∗) or HSP1 (Pat29∗) genes. FITC, fluorescein isothiocyanate.

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