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dc.contributor.authorLoeffler, M
dc.contributor.authorHerkenrath, P
dc.contributor.authorWichmann, H E
dc.contributor.authorLord, Brian I
dc.contributor.authorMurphy, M J
dc.date.accessioned2011-03-08T12:20:41Z
dc.date.available2011-03-08T12:20:41Z
dc.date.issued1984-12
dc.identifier.citationThe kinetics of hematopoietic stem cells during and after hypoxia. A model analysis. 1984, 49 (6):427-39 Bluten
dc.identifier.issn0006-5242
dc.identifier.pmid6509215
dc.identifier.doi10.1007/BF00320485
dc.identifier.urihttp://hdl.handle.net/10541/123938
dc.description.abstractA previously described mathematical model of the hematopoietic stem cell system has been extended to permit a detailed understanding of the data during and after hypoxia. The model includes stem cells, erythroid and granuloid progenitors and precursors. Concerning the intramedullary feedback mechanisms two basic assumptions are made: 1) The fraction "a" of CFU-S in active cell cycle is regulated. Reduced cell densities of CFU-S, progenitors or precursors lead to an accelerated stem cell cycling. Enlarged cell densities suppress cycling. 2) The self renewal probability "p" of CFU-S is also regulated. The normal steady state is described by p = 0.5, indicating that on statistical average each dividing mother stem cell is replaced by one daughter stem cell, while the second differentiates. Diminished cell densities of CFU-S or enlarged densities of progenitors and precursors induce a more intensive self renewal (p greater than 0.5), such that the stem cell number increases. The self renewal probability declines (p less than 0.5) if too many CFU-S or too few progenitors and precursors are present. The model reproduces bone marrow data for CFU-S, BFU-E, CFU-C, CFU-E, 59 Fe-uptake and nucleated cells in hypoxia and posthypoxia. Although the ratio of differentiation into the erythroid and granuloid cell lines is kept constant in the model, a changing ratio of CFU-E and CFU-C results. The model suggests that stem cells and progenitor cells are regulated by a regulatory interference of erythropoiesis and granulopoiesis.
dc.language.isoenen
dc.subject.meshAnoxia
dc.subject.meshCell Differentiation
dc.subject.meshErythropoiesis
dc.subject.meshHematopoiesis
dc.subject.meshHematopoietic Stem Cells
dc.subject.meshHumans
dc.subject.meshKinetics
dc.subject.meshModels, Biological
dc.subject.meshThymidine
dc.titleThe kinetics of hematopoietic stem cells during and after hypoxia. A model analysis.en
dc.typeArticleen
dc.contributor.departmentMedizinische Universitätsklinik, Joseph-Stelzmann-Stasse 9, D-5000 Köln 41, Federal Republic of Germany.en
dc.identifier.journalBluten
html.description.abstractA previously described mathematical model of the hematopoietic stem cell system has been extended to permit a detailed understanding of the data during and after hypoxia. The model includes stem cells, erythroid and granuloid progenitors and precursors. Concerning the intramedullary feedback mechanisms two basic assumptions are made: 1) The fraction "a" of CFU-S in active cell cycle is regulated. Reduced cell densities of CFU-S, progenitors or precursors lead to an accelerated stem cell cycling. Enlarged cell densities suppress cycling. 2) The self renewal probability "p" of CFU-S is also regulated. The normal steady state is described by p = 0.5, indicating that on statistical average each dividing mother stem cell is replaced by one daughter stem cell, while the second differentiates. Diminished cell densities of CFU-S or enlarged densities of progenitors and precursors induce a more intensive self renewal (p greater than 0.5), such that the stem cell number increases. The self renewal probability declines (p less than 0.5) if too many CFU-S or too few progenitors and precursors are present. The model reproduces bone marrow data for CFU-S, BFU-E, CFU-C, CFU-E, 59 Fe-uptake and nucleated cells in hypoxia and posthypoxia. Although the ratio of differentiation into the erythroid and granuloid cell lines is kept constant in the model, a changing ratio of CFU-E and CFU-C results. The model suggests that stem cells and progenitor cells are regulated by a regulatory interference of erythropoiesis and granulopoiesis.


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