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Research Article Free access | 10.1172/JCI109654

Magnitude of the fetal hemoglobin response to acute hemolytic anemia in baboons is controlled by genetic factors.

J DeSimone, P Heller, J Amsel, and M Usman

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Published January 1, 1980 - More info

Published in Volume 65, Issue 1 on January 1, 1980
J Clin Invest. 1980;65(1):224–226. https://doi.org/10.1172/JCI109654.
© 1980 The American Society for Clinical Investigation
Published January 1, 1980 - Version history
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Abstract

When hemolytic anemia was induced in 26 baboons (Papio cynocephalus), aged 7-22 mo, they increased their production of fetal hemoglobin (HbF). Although the resulting reduction in hematocrits and increases of reticulocyte counts were similar in all stressed animals there was marked variability in the maximal rates of HbF synthesis. The maximal levels of HbF attained appeared to fall into three separate groups: low, intermediate, and high. These differences were not related to sex or several measures of erythrocyte metabolism. Animals exposed to repeated episodes of erythropoietic stress after full hematologic recovery demonstrated some variability in their maximal HbF levels attained from one episode to another, but these variations never extended to adjacent classes. The described biochemical and mating data suggest that the magnitude of the HbF response to hemolytic anemia is controlled by genetic factors.

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