In the late 1930s, William Bosworth Castle and his colleague Thomas Hale Ham were studying blood samples obtained from patients with sickle cell anemia and found that the viscosity of the blood increased dramatically as its oxygen content decreased. As Castle later reflected, “It immediately occurred to us that this was because the elongated, sickled red cells had become tangled up `like haywire.'”1 Castle and Ham went on to hypothesize about the pathophysiology of organ damage in sickle cell anemia in a way that still drives much of our thinking today: “a vicious cycle of erythrostasis may be set up . . .
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Orah S. Platt (2005) studied this question.
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