Fig. 2.
Fig. 2. The cellular origin of circulating microparticles in peripheral blood samples from PNH individuals and control subjects. The capture procedure involved insolubilized MoAbs to human glycophorin A, human GPIb, and irrelevant IgG1, the latter yielding control values that never exceeded 3 nmol/L phosphatidylserine equivalent and were subtracted from those reported in this figure. The assay of the phosphatidylserine content of captured particles is based on the ability of this phospholipid to promote the assembly of the prothrombinase enzyme complex. Each value is the mean of triplicate determinations. The means corresponding to the PNH samples were not significantly different from their control counterparts at the .05 level using the Student’s two-tailed t-test. Variances were also compared (using the ratio method) and the distribution of the values was shown to be different between the PNH and the control samples at the .002 level.

The cellular origin of circulating microparticles in peripheral blood samples from PNH individuals and control subjects. The capture procedure involved insolubilized MoAbs to human glycophorin A, human GPIb, and irrelevant IgG1, the latter yielding control values that never exceeded 3 nmol/L phosphatidylserine equivalent and were subtracted from those reported in this figure. The assay of the phosphatidylserine content of captured particles is based on the ability of this phospholipid to promote the assembly of the prothrombinase enzyme complex. Each value is the mean of triplicate determinations. The means corresponding to the PNH samples were not significantly different from their control counterparts at the .05 level using the Student’s two-tailed t-test. Variances were also compared (using the ratio method) and the distribution of the values was shown to be different between the PNH and the control samples at the .002 level.

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