PAUL HELLER, M.D., F.A.C.P.; VINCENT J. YAKULIS, B.S.; ARNOLD I. ROSENZWEIG, M.D.; CHARLES F. ABILDGAARD, M.D.; DONALD L. RUCKNAGEL, M.D., PH.D.
The genetic and biochemical basis of thalassemia is not known, but it is generally envisioned that the normally highly integrated chain of molecular events governing the synthesis of the polypeptide chains of normal adult hemoglobin (α2Aβ2A) is disturbed at a still unknown level resulting in a significant decrease in the rate of hemoglobin production (1-5). This disturbance may more or less selectively affect the synthesis of either the alpha- or the beta-polypeptide chain of hemoglobin, referred to as alpha- and beta-thalassemia, respectively. Beta-thalassemia is characteristically associated with a twofold increase in the relative proportion of hemoglobin A2. The chromosomal locus
PAUL HELLER, VINCENT J. YAKULIS, ARNOLD I. ROSENZWEIG, CHARLES F. ABILDGAARD, DONALD L. RUCKNAGEL. Mild Homozygous Beta-Thalassemia: Further Evidence for the Heterogeneity of Beta-Thalassemia Genes. Ann Intern Med. 1966;64:52–61. doi: 10.7326/0003-4819-64-1-52
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Published: Ann Intern Med. 1966;64(1):52-61.
Hematology/Oncology, Red Cell Disorders.
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