Figure 4.
Figure 4. LHR-A, but not LHR-B, prolongs the survival of transfused RBCs in vivo. (A) Survival of human group A RBCs in mice treated with LHR-A (administered at 2.5 mg/kg, n = 9, ⋄) is significantly greater than in mice treated with LHR-B (administered at 2.5 mg/kg, n = 5, ○)(P < .05 at all time points). For comparison, the survival of transfused RBCs from mice treated with mock (n = 15, □) and sCR1 (10 mg/kg, n = 9, ▪) from Figure 3A are shown. (B) Survival of human group O RBCs in mice treated with LHR-A (2.5 mg/kg, n = 4, ⋄) is significantly greater than in mice treated with LHR-B (2.5 mg/kg, n = 6, ○)(P < .05 at all time points). For comparison, the survival curves of mock (n = 8, ▵) and sCR1 (n = 8, ▴) from Figure 3C are included.

LHR-A, but not LHR-B, prolongs the survival of transfused RBCs in vivo. (A) Survival of human group A RBCs in mice treated with LHR-A (administered at 2.5 mg/kg, n = 9, ⋄) is significantly greater than in mice treated with LHR-B (administered at 2.5 mg/kg, n = 5, ○)(P < .05 at all time points). For comparison, the survival of transfused RBCs from mice treated with mock (n = 15, □) and sCR1 (10 mg/kg, n = 9, ▪) from Figure 3A are shown. (B) Survival of human group O RBCs in mice treated with LHR-A (2.5 mg/kg, n = 4, ⋄) is significantly greater than in mice treated with LHR-B (2.5 mg/kg, n = 6, ○)(P < .05 at all time points). For comparison, the survival curves of mock (n = 8, ▵) and sCR1 (n = 8, ▴) from Figure 3C are included.

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