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Results for “ERYTHROBLASTOSIS”

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At least 1,207 records · Page 67Linked to original sources
PubMed1978

Erythrokinetics and ferrokinetics of a viral-induced murine erythroblastosis.

A variant of Rauscher leukemia virus, designated RLV-A, induced a slow progressive impairment of erythropoiesis in BALB/c mice. Identified in this study were a shortened red cell 51-cr half-time, anemia with indices showing minimal but significant hypochromia, ineffective erythropoiesis, and infiltration of the liver, spleen, and peripheral blood with erythroid pecursors. Ferrokinetic studies indicated a normal plasma iron turnover in infected mice but a decreased red cell iron turnover. Large amounts of 59Fe were taken up by the enlarged liver and spleen. Peak splenic heme 59Fe synthesis was delayed 12 hr in the infected mice. The substantial increase in the splenic intraerythrocytic nonheme iron pool and the hypochromic indices indicate a process analogous to that seen in the sideroblastic anemias. The disease produced by this RLV-A variant may prove useful for studying various aspects of the preleukemic sideroblastic anemias and DiGuglielmo syndrome.

Anemia↗
PubMed1978

[Antigenic marker of human erythrokaryocytes similar to mouse erythroblastosis antigen].

Identical antigenic determinants are discovered on the surface of human erythrokaryocytes with antibodies against specific antigen of murine erythroblasts (Ag-Ed), previously revealed in study of Rauscher leukemia, in the immunofluorescent and cytotoxic tests. The antigen is present on the membranes of the majority of human embryonic liver and adult bone marrow nuclear erythroid cells, but is not found in fetal thymocytes, newborn kidney cells, adult human hepatic cells and in peripheral blood erythrocytes. Ag-Eb appears to possess an inter-species determinant, shared by mammalian nuclear erythroid cells, and may be used as their specific marker.

Animals↗
PubMed1976

[Haemolytic disease of the newborn (fetus) (author's transl)].

Haemolytic disease of the newborn is mostly caused by Rh antibody anti-D (Rh erythroblastosis) and antibodies of the ABO system anti-A and anti-B (ABO erythroblastosis). Because of possible fetal death in utero prenatal diagnosis and treatment of Rh erythroblastosis is necessary. Prophylactic administration of anti-Rh-gammaglobulin prevents the induction of Rh antibodies. In contrast to Rh erythroblastosis prenatal diagnosis and treatment of ABO erythroblastosis is not necessary. Postnatally, however, hyperbilirubinemia due to ABO erythroblastosis should be treated to avoid Kernicterus. Our results with diagnosis and treatment of haemolytic diseases of the newborn are presented and related to the literature. Furthermore, immunofluorescence studies are reported, which could possibly explain the differences between Rh and ABO erythroblastosis.

ABO Blood-Group System↗