Figure 6.
Figure 6. Treatment with ε-aminocaproic acid does not reverse the hemostatic defect in f10 mutants. Offspring from f10+/− incrosses were treated with ε-aminocaproic acid at 24 hpf and tested for the ability to form a clot in the PCV in response to laser-mediated endothelial injury at 3 dpf, after which genotyping was performed. There was a slight increase in the percentage of occlusion in treated f10−/− larvae (12.8% vs 6.7% in controls). However, this increase was not statistically significant and likely represents background thrombus formation occasionally observed in homozygous mutants. Horizontal bars represent the median time to occlusion. ns, not significant; sec, second.

Treatment with ε-aminocaproic acid does not reverse the hemostatic defect in f10 mutants. Offspring from f10+/− incrosses were treated with ε-aminocaproic acid at 24 hpf and tested for the ability to form a clot in the PCV in response to laser-mediated endothelial injury at 3 dpf, after which genotyping was performed. There was a slight increase in the percentage of occlusion in treated f10−/− larvae (12.8% vs 6.7% in controls). However, this increase was not statistically significant and likely represents background thrombus formation occasionally observed in homozygous mutants. Horizontal bars represent the median time to occlusion. ns, not significant; sec, second.

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