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Myron L. Mills, MD

JAMA. 1985;254(11):1487-1491.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

SINCE 1910, when sickle cell anemia (SCA) was first described by Dr James Herrick, a Chicago cardiologist, a prodigious amount of clinical and laboratory investigation has taken place in an effort to elucidate the pathogenesis, etiology, and treatment of SCA.¹ In 1949, Pauling and Itano² published their findings relating to the different electrophoretic properties of hemoglobin from patients with SCA. Later, in 1957, Ingram³ published the results of his work detailing the biochemical defect in hemoglobin S. From the early 1950s to the present time, the sickle erythrocyte and hemoglobin S molecule have been studied by sophisticated techniques that have revealed their structure and function at the molecular level. Techniques employed for these studies have included low-resolution x-ray crystallography, electron microscopy with image reconstruction, hemoglobin S polymerization kinetics, high-resolution proton nuclear magnetic resonance spectroscopy, and fiber x-ray diffraction.

The basic defect in hemoglobin S is the substitution . . . [Full Text PDF of this Article]

Author Affiliations
From the Division of Emergency Medicine, University Hospital of Jacksonville, University of Florida.

Footnotes
Reprint requests to Section of Emergency Medicine, Arizona Health Sciences Center, Tucson, AZ 85724 (Dr Mills).

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