Figure 4
Figure 4. Platelet aggregation and hemostasis are defective in platelets from Unc13dJinx mice. (A-G) Platelets from wild-type (WT, black) and Unc13dJinx mice (Unc13dJinx, gray) were prepared as described and diluted to approximately 3 × 108/mL. CaCl2 was added to each sample (0.7mM final) and platelets were activated with the indicated agonists. Increase in light transmittance (aggregation) and luminescence (ATP release) were monitored and plotted as a function of time. (H) The tails of wild-type (■) and Unc13dJinx (▴) mice were clipped and the duration of bleeding was measured (Bleeding Time) in seconds. The individual bleeding times (points) and averages (line) from n = 20 mice were plotted. A Student t test (SigmaPlot 9.0) was used to assess the statistical significance of the differences between groups.

Platelet aggregation and hemostasis are defective in platelets from Unc13dJinx mice. (A-G) Platelets from wild-type (WT, black) and Unc13dJinx mice (Unc13dJinx, gray) were prepared as described and diluted to approximately 3 × 108/mL. CaCl2 was added to each sample (0.7mM final) and platelets were activated with the indicated agonists. Increase in light transmittance (aggregation) and luminescence (ATP release) were monitored and plotted as a function of time. (H) The tails of wild-type (■) and Unc13dJinx (▴) mice were clipped and the duration of bleeding was measured (Bleeding Time) in seconds. The individual bleeding times (points) and averages (line) from n = 20 mice were plotted. A Student t test (SigmaPlot 9.0) was used to assess the statistical significance of the differences between groups.

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