Proliferation of Myeloid Cells

Perry, S. Scott

doi:10.1146/annurev.me.22.020171.001131

Cited by 8 publications

(4 citation statements)

References 33 publications

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“…The control of release of cells from the marrow reserve compartment to the blood is achieved in the model by permitting the reserve release rate 7 to depend on the number of cells in the blood compartment Nn (t), as follows, [8,70 . NB(t_tR)> ~8" (4) Here ?0, Yl, NB, P and t R are positive constants. The existence of a time delay t R is indicated by various experiments, for example, the response to leukopheresis N~ represents the steady state value of the population in the blood compartment, so that in the steady state, 7 = 7o.…”

Section: L\ N (T) /mentioning

confidence: 99%

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A mathematical model of neutrophil production and control in normal man

1975

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A comprehensive mathematical model of neutrophil production in normal man is presented. The model incorporates three control elements which regulate homeostatically the rates of release of marrow cells to proliferation, maturation, and to the blood. The steady state properties of the model are demonstrated analytically. The basic equations of the model, which are nonlinear, have been integrated numerically. The solutions so obtained display graphically the dynamical response of the system to various perturbations, which simulate experimental investigations that have been made in the past of granulocytopoiesis. By an appropriate choice of values of the parameters characterizing the system, it is shown how most of the principal kinetic properties of the neutrophil production and control system are represented in a quantitative manner.

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Section: L\ N (T) /mentioning

confidence: 99%

“…Based on this interpretation and the inferred value of TA + t = 50 hr, we infer that l/Co =20 hr, and so =0.05/hr. It should 4 ~o be noted that the maximum value T A could approach is 50 hr. However, this would be at the expense of making :% very large.…”

Section: Determinations Of the Values Of The Parametersmentioning

confidence: 99%

A mathematical model of neutrophil production and control in normal man

1975

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“…King-Smith & Morley (1970) have postulated that the size of the total blood granulocyte pool is regulated by two nonlinear feedback loops, one governing the rate of production of granulocytes through either stem cell pool size or turnover rate, the other governing the rate of release of mature granulocytes from the marrow. Factors controlling the release rate of granulocytes from the bone marrow may include circulating releasing factor(s) (Perry 1971), characteristics of the granulocytes themselves such as their deformability (Lichtman 1970) or alterations of the cell periphery (Lichtman & Weed 1972), and intrinsic marrow structure (Weiss 1970). Alterations in marrow fine structure, exemplified by intrasinusoidal foci of haematopoiesis in myeloid metaplasia with myelosclerosis (Rappaport 1966) and disruption of sinusoidal walls in experimental myelogenous leukaemia in rats (Chen 1972) have been described.…”

Section: Commentmentioning

confidence: 99%

Leukaemoid Reactions in Myeloproliferative Diseases

White¹,

George²,

Sears³

1975

Scandinavian Journal of Haematology

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The occurrence of transient extreme neutrophilic leucocytosis, with white blood cell counts exceeding 100,000/μl in two adult patients with myeloproliferative diseases, polycythaemia vera and acute myelocytic leukaemia in remission, is reported. The reaction was transient, and the subsequent course of the patient's disease did not differ from that prior to the episode. Such extreme leucocytosis is rare in adults, despite the frequency of provoking conditions, and factors which predispose an individual to develop a leukaemoid reaction remain unknown. An increase in the size of the pool of proliferating granulocyte precursors accompanied by a loss of the restraining function of the marrow sinusoidal walls in myeloproliferative diseases may explain the augmented release of myeloid cells in our patients.

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“…There are two main lineages of white blood cells: myeloid and lymphoid 99 . Both of these branches have a common pluripotent hematopoietic stem cell progenitor, which may be found in the bone marrow 100 .…”

Section: White Blood Cell Developmentmentioning

confidence: 99%

The role of mitochondrial superoxide in the development of the mammalian hematopoietic system

Case¹

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The SOD2 gene encodes the mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD), which converts superoxide (O 2 •-) to hydrogen peroxide (H 2 O 2). Down-regulation of SOD2 has been reported in many cancer cells of diverse tissue origins, and forced over expression of this enzyme in carcinoma cells decreases their tumorigenicity. These findings suggest that SOD2 functions as an initiation or promotion tumor suppressor; however, it remains to be determined whether loss of SOD2 expression is sufficient for tumor formation since homozygous SOD2 knockout mice die within weeks after birth. Additionally, due to the shortened lifespan of the constitutive SOD2 knockout mouse limited studies have been performed in assessing the role of SOD2 in tissue-specific development in vivo. Using Cre-loxP genetics, we now have the capability to generate mice in which SOD2 may be knocked out in a cell type-specific manner and these mice can be used to query the effect of loss of SOD2 expression in tissue development, function, and oncogenesis. We primarily focused our studies on the hematopoietic system, but expanded our research to solid organs such as the liver and mammary gland as well. Our findings demonstrate that SOD2 does not act as an initiating tumor suppressing enzyme in any of these unchallenged systems, and in fact the loss of SOD2 may act to delay tumor formation. T-cell specific SOD2 knockout demonstrated significant immunodeficiency as illustrated by a decreased immune response to influenza challenge secondary to decreased T-cell populations. Furthermore, hematopoietic stem cell specific SOD2 knockout showed a severe anemia in the red blood cell population due to increased mitochondrial superoxide. Additional analysis revealed the anemia to be a result of a porphyria due to the inactivation of the heme synthesis enzyme ferrochelatase. The observed phenotypes in all conditional hematological SOD2 knockout models were rescued by the addition of mitochondrially targeted anti-oxidants. In conclusion, the tissue specific loss of SOD2 in various hematological organs appeared to ACKNOWLEDGMENTS I would first like to thank the following core facilities for their expertise and help in processing and interpreting various experiments:

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Proliferation of Myeloid Cells

Cited by 8 publications

References 33 publications

A mathematical model of neutrophil production and control in normal man

A mathematical model of neutrophil production and control in normal man

Leukaemoid Reactions in Myeloproliferative Diseases

The role of mitochondrial superoxide in the development of the mammalian hematopoietic system

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