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Article
February 1956

Studies on the Destruction of Red Blood Cells: X. The Biophysics and Biology of Sickle-Cell Disease

Author Affiliations

Cleveland; Boston

From the Thorndike Memorial Laboratory, The Second and Fourth Medical Services (Harvard), Boston City Hospital, and the Department of Medicine, Harvard Medical School. Research Fellow of the American College of Physicians for 1951-1952, present address: City Hospital, Cleveland (Dr. Harris); present address: University Hospitals, Cleveland (Dr. Brewster); present address: School of Medicine, Western Reserve University, Cleveland (Dr. Ham).

AMA Arch Intern Med. 1956;97(2):145-168. doi:10.1001/archinte.1956.00250200021002
Abstract

In 1927, in a classic paper, Hahn and Gillespie 19 clearly defined the basis of the anomalous physical behavior of the sickle cell as an abnormality of its hemoglobin when in the deoxygenated state and pointed to the affected cells as the primary cause of the characteristic hemolytic anemia. From microscopic observations of drops of blood suspended in a gas chamber and from the results of the removal of a large spleen from a child with sicklemia, they were led to make the following statement: Sickle cell formation is a reversible phenomenon depending on the free or combined state of the hemoglobin of the susceptible corpuscles. When the hemoglobin is in the combined state, the discoid form is stable; when in the uncombined state, the distorted form is stable. The behavior of the susceptible corpuscles toward oxygen asphyxia thus constitutes a special application of a hypothesis correlating contour with

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