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1 with other protective polymorphisms, such as hemoglobin C.
4 grees -thalassemia (S beta degrees ), sickle-hemoglobin C disease (SC), or sickle-beta(+)-thalassemia
5 obinopathy (sickle-cell disease, sickle-cell hemoglobin C disease, and sickle-cell thalassemia) and a
6 aused by compound heterozygosity for HbS and hemoglobin C genes, is the second most common genotype o
15 und heterozygosity of hemoglobin S (HbS) and hemoglobin C (HbC), comprising 30% of sickle cell diseas
19 ous sickle cell anemia (HbSS), 7 with sickle hemoglobin C (HbSC), 7 with sickle/beta-thalassemia (HbS
20 melting curve analysis for factor V Leiden, hemoglobin C, hemoglobin S, the thermolabile mutation of
21 e findings indicate that schoolchildren with hemoglobin C mutation might contribute disproportionatel
22 hat G6PD deficiency, alpha+ thalassemia, and hemoglobin C protect against malaria mortality; the appl
24 (SS) genotype, 113 (28%) showed sickle cell hemoglobin C (SC) genotype, and 77 (19%) showed trait ge
26 b) three sheep received a bolus of 50 mg/kg hemoglobin; c) six sheep received 100 mg/kg of hemoglobi
28 laria in children, but it is unclear whether hemoglobin C trait also protects against uncomplicated m
30 t that the presence of sickle cell trait and hemoglobin C trait may explain, at least in part, prior
31 nts received 13.2% (P=0.003) higher dose and hemoglobin C trait patients exhibited a similar differen
32 We hypothesized that Malian children with hemoglobin C trait would have a lower risk of clinical m
33 2 patients (10.3% sickle cell trait and 2.4% hemoglobin C trait) receiving ESAs, demographic and clin
35 with SCT, six of 243 (2.5%) individuals with hemoglobin C trait, and 234 of 8927 (2.6%) noncarriers.
36 iants, including sickle cell trait (SCT) and hemoglobin C trait, have a role in kidney disease in bla
38 ckle cell trait, and 129 (2.4%) patients had hemoglobin C trait; no other hemoglobinopathy traits wer
39 um erythrocyte membrane protein-1 display is hemoglobin C, which may protect against malaria by impai