Geoffrey M. Brittin
National Institutes of Health
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Featured researches published by Geoffrey M. Brittin.
Human Pathology | 1974
Kenneth B. McCredie; Jeane P. Hester; Emil J. Freireich; Geoffrey M. Brittin; Carlos Vallejos
Abstract The development of effective supportive therapy for myelosuppression could be expected to protect patients with hematological malignant disease against morbidity and mortality and to expand the potential of therapeutic agents. Although the technique of plateletpheresis has largely solved the problem of obtaining enough platelets from donors, available techniques for short and long term platelet preservation are inadequate. Refractoriness to platelet transfusions has been shown to result from development of antibodies to the HL-A system, and by HL-A matching of platelet donors and recipients it may be possible to reduce the numbers of units of platelets necessary to maintain thrombocytopenic patients and thereby to decrease the incidence of isosensitization and transfusion hepatitis. Both the NCI-IBM blood cell separator and the reversible adhesion of leukocytes to nylon fibers have been used to obtain sufficient quantities of granulocytes from normal donors for transfusion to neutropenic patients. Patients with chronic myelogenous leukemia still represent an important source of granulocytes for transfusion, and we have found that repeated leukapheresis of such patients produced good symptomatic improvement. Granulocyte transfusions have been effective in the treatment of infections in patients with acute leukemia. In our experience more of the administered granulocytes have been recovered in the peripheral blood of recipients when the donor and the recipient have been identical twins, but the clinical response to granulocyte transfusions has not been related to compatability of the HL-A or ABO systems or to the presence or absence of leukoagglutinins.
Experimental Biology and Medicine | 1966
Geoffrey M. Brittin; James E. Haley; George Brecher
Summary Rats with chronic PHH hemolysis developed severe anemia and marked increase in red cell size following splenectomy. The macrocytosis could not be explained by decreased destruction of macrocytes in splenectomized animals. The increased red cell size following splenectomy is believed to result from curtailment of the capability for compensatory expansion of erythropoiesis with a resulting increased stimulus per unit volume of remaining erythropoietic tissue. The macrocytosis sometimes seen in human myelofibrosis may be similarly explained.
Blood | 1964
Donald W. Kundel; George Brecher; Gerald P. Bodey; Geoffrey M. Brittin
Blood | 1963
Geoffrey M. Brittin; Yasukazu Tanaka; George Brecher
Archive | 1974
Shirley Ebbe; William Dameshek; J. W. Athens; Ford Bainton; Mario Baldini; R. I. Ernest Beutler; Dane R. Boggs; George Brecher; Geoffrey M. Brittin; Eugene P. Cronkite; Charles A. Doan; Frank Gardner; Albert S. Gordon; N. Y. Samuel Hellman; Victor Herbert; James G. Hirsch; Harry S. Jacob; Wallace N. Jensen; J. C. Levin; T. Makinodan; Aaron J. Marcus; Alvin M. Mauer; E. A. McCulloch; WilliamC. Moloney; Helen M. Ranney; N. Y. Richard Rosenfield; N. Y. JosEPH; F. D. Ross; Peter H. Schur; Sandor S. Shapiro
Blood | 1971
Geoffrey M. Brittin; George Brecher
Blood | 1963
Robert H. Levin; Geoffrey M. Brittin; Emil J. Freireich
Blood | 1971
Geoffrey M. Brittin; Shirley A. Dew; Elvi K. Fewell
American Journal of Pathology | 1963
Geoffrey M. Brittin; George Brecher; J. L. Steinfeld; Michael B. Shimkin
Technical bulletin of the Registry of Medical Technologists | 1969
Geoffrey M. Brittin; George Brecher; Carole A. Johnson; John Stuart