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3 grees -thalassemia (S beta degrees ), sickle-hemoglobin C disease (SC), or sickle-beta(+)-thalassemia
4 obinopathy (sickle-cell disease, sickle-cell hemoglobin C disease, and sickle-cell thalassemia) and a
15 ous sickle cell anemia (HbSS), 7 with sickle hemoglobin C (HbSC), 7 with sickle/beta-thalassemia (HbS
16 melting curve analysis for factor V Leiden, hemoglobin C, hemoglobin S, the thermolabile mutation of
17 e findings indicate that schoolchildren with hemoglobin C mutation might contribute disproportionatel
18 hat G6PD deficiency, alpha+ thalassemia, and hemoglobin C protect against malaria mortality; the appl
20 b) three sheep received a bolus of 50 mg/kg hemoglobin; c) six sheep received 100 mg/kg of hemoglobi
22 laria in children, but it is unclear whether hemoglobin C trait also protects against uncomplicated m
24 t that the presence of sickle cell trait and hemoglobin C trait may explain, at least in part, prior
25 nts received 13.2% (P=0.003) higher dose and hemoglobin C trait patients exhibited a similar differen
26 We hypothesized that Malian children with hemoglobin C trait would have a lower risk of clinical m
27 2 patients (10.3% sickle cell trait and 2.4% hemoglobin C trait) receiving ESAs, demographic and clin
29 with SCT, six of 243 (2.5%) individuals with hemoglobin C trait, and 234 of 8927 (2.6%) noncarriers.
30 iants, including sickle cell trait (SCT) and hemoglobin C trait, have a role in kidney disease in bla
32 ckle cell trait, and 129 (2.4%) patients had hemoglobin C trait; no other hemoglobinopathy traits wer
33 um erythrocyte membrane protein-1 display is hemoglobin C, which may protect against malaria by impai
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