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Research Article Free access | 10.1172/JCI107026
1Department of Health, Education and Welfare, National Institutes of Health, National Institute of Allergy and Infectious Diseases, Laboratory of Clinical Investigation, Bethesda, Maryland 20014
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1Department of Health, Education and Welfare, National Institutes of Health, National Institute of Allergy and Infectious Diseases, Laboratory of Clinical Investigation, Bethesda, Maryland 20014
Find articles by Ward, S. in: JCI | PubMed | Google Scholar
1Department of Health, Education and Welfare, National Institutes of Health, National Institute of Allergy and Infectious Diseases, Laboratory of Clinical Investigation, Bethesda, Maryland 20014
Find articles by Kimball, H. in: JCI | PubMed | Google Scholar
1Department of Health, Education and Welfare, National Institutes of Health, National Institute of Allergy and Infectious Diseases, Laboratory of Clinical Investigation, Bethesda, Maryland 20014
Find articles by Wolff, S. in: JCI | PubMed | Google Scholar
Published August 1, 1972 - More info
12 grey collie dogs had cyclic neutropenia with the neutropenia recurring at 11.8±0.1-day intervals. The recovery from neutropenia was accompanied by a single wave of myeloid proliferation, an increase in marrow myeloid-labeling indices, and an increase in serum muramidase levels. After recovery from neutropenia during the period when blood neutrophils (PMN) were normal or increased, marrow myeloid precursors became scarce. The decline in marrow precursors and marrow PMN reserves heralded the recurrence of neutropenia. Neither diisopropyl fluorophosphate (DF32P) leukokinetic studies nor the rate of development of neutropenia suggested shortened PMN survival as a mechanism for the neutropenia. These studies indicate that the cyclic neutropenia is due to a regularly recurring failure in PMN production.
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