Figure 3.
Figure 3. Annexin A5 binding assays for patient plasma groups. PS/PC-coated wells that had been preincubated with plasmas from the aPL syndrome with thromboembolism group (A) bound significantly less annexin A5 (mean ± SD, 26.7 ± 4.3 ng/well, n = 25) than wells preincubated with plasmas from the healthy control group (D) (30.5 ± 3.1 ng/well, n = 20, P < .01) and plasmas from non-aPL thromboembolism group (C) (29.9 ± 3.2 ng/well, n = 15, P < .05). Wells pretreated with plasmas from the aPL antibodies without thrombosis group (B) also bound significantly less annexin A5 (28.2 ± 3.7 ng/well, n = 26) than the healthy controls (D) (P < .05). There were no significant differences in the binding of annexin A5 between the wells pretreated with plasmas from the aPL syndrome with thromboembolism (A) and the aPL antibodies without thrombosis (B) groups, and plasmas from the non-aPL thromboembolism (C) and the healthy controls (D). Error bars are shown for mean ± 2 SD of healthy controls (D).

Annexin A5 binding assays for patient plasma groups. PS/PC-coated wells that had been preincubated with plasmas from the aPL syndrome with thromboembolism group (A) bound significantly less annexin A5 (mean ± SD, 26.7 ± 4.3 ng/well, n = 25) than wells preincubated with plasmas from the healthy control group (D) (30.5 ± 3.1 ng/well, n = 20, P < .01) and plasmas from non-aPL thromboembolism group (C) (29.9 ± 3.2 ng/well, n = 15, P < .05). Wells pretreated with plasmas from the aPL antibodies without thrombosis group (B) also bound significantly less annexin A5 (28.2 ± 3.7 ng/well, n = 26) than the healthy controls (D) (P < .05). There were no significant differences in the binding of annexin A5 between the wells pretreated with plasmas from the aPL syndrome with thromboembolism (A) and the aPL antibodies without thrombosis (B) groups, and plasmas from the non-aPL thromboembolism (C) and the healthy controls (D). Error bars are shown for mean ± 2 SD of healthy controls (D).

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