He demonstrated that SCD and sickle cell trait were due to the presence of abnormal 8-globin polypeptides in red blood cells. He demonstrated that the electrophhoretic mobility of B-globin from patients with SCD was different from that of healthy individuals. He demonstrated that both parents of multiple patients with SCD had low levels of sickled red blood cells. He hypothesized that SCD was a recessive trait and that the parents of patients with SCD would be heterozygous carriers. He demonstrated that the difference between B-globin polypeptides in individuals who were healthy and those with SCD is an amino acid substitution. He performed a peptide fingerprint analysis on B-globin from individuals with 84 84 and 89 88, which identified the segment of B-globin that was changed by the BS mutation. James Neel Linus Pauling Vernon Ingram
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