Effects of human recombinant erythropoietin on differentiation and distribution of erythroid progenitor cells on murine medullary and splenic erythropoiesis during hypoxia and post-hypoxia.

Hemopoietic cells, the extracellular matrix, growth factors and the microenvironment are involved in the regulation of hemopoiesis. Although the regulation of erythropoiesis is well understood at the cellular level in vivo and in vitro, the role of hemopoietic sites of erythroid progenitors production has not been well defined in both steady state conditions and in stress erythropoiesis. In this study we examined the qualitative erythroid differentiation and quantitative changes of the erythroid progenitors in different erythropoietic organs during erythropoiesis of stress in a hypoxia-induced polycythemia and post-hypoxic changes in a mice model.

Impaired response of polycythemic mice to erythropoietin induced by protein starvation imposed after hormone administration.

The present study was performed to determine the stage of the erythropoietic pathway which is affected by starvation or protein deprivation and whose manifestation is a depressed response to exogenous erythropoietin (EPO). The response to recombinant human EPO was measured in post-hypoxic polycythemic mice by determination of 59Fe uptake into red cells, spleen and femur and/or erythroid colony forming units (CFU-E) and erythroid precursor cell concentrations in femoral marrow. Experimental mice were either starved or fed one of seven different diets whose protein (casein) content ranged from 0 to 20%.

[T lymphoma of immature phenotype associated with polycythemia vera].

A 20-year old patient is presented with generalized lymphadenopathy, splenomegaly, hyperleukocytosis and a bone marrow biopsy showing panmyelosis with predominance of immature granulocytes. Lymph node biopsy showed a histopathological feature that was diagnosed as a chronic granulocytic leukemia in blast crisis. The cell surface phenotype of these blast cells showed predominance of immature CD1+, CD7+ T lymphocytes.