Tentative evidence for 3?4 haematopoetic stem cells in man

Hitzeroth, H. W.; Bender, Klaus; Ropers, Hans‐Hilger; Geerthsen, J. M. P.

doi:10.1007/bf00393967

Cited by 11 publications

(3 citation statements)

References 7 publications

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“…Increasing experimental evidence suggests that this pool of stem cells is heterogenous, comprising of a number of sub-populations (Duplan and Legrand, 1979;Samarut et al, 1976;Hitzeroth, 1977). The radiosensitivities of these subpopulations are not known but they may be expected not to differ significantly from one another.…”

Section: Resultsmentioning

confidence: 96%

Haemopoietic recovery during radiation disease: Comments on combined-injuries

Stevenson

1981

Radiat Environ Biophys

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The regenerative ability of haemopoietic organs during combined radiation injuries has not been adequately investigated. Interactions among individual factors can critically influence the processes involved in haemopoietic recovery. An overview of radiation injuries is given, and a concept towards a hypothetical mode of action at the cellular level is presented. The influence which interacting factors can have on the concentration of pluripotential haemopoietic stem cells (HSC) is demonstrated by results from an initial experiment. The importance of synergistic and antagonistic reactions is emphasised and commented upon.

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Section: Resultsmentioning

confidence: 96%

Haemopoietic recovery during radiation disease: Comments on combined-injuries

Stevenson

1981

Radiat Environ Biophys

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“…The primary information about ARCH was collected from the study of hematopoietic stem cells. The very first study used hematopoietic stem cells collected from the South African Negro population, using the marker of X-linked enzyme glucose-6-phosphate dehydrogenase (G6PD) [ 43 ]. The study demonstrated that the reduced heterozygosity in blood stem cells was increasing with aging [ 44 ].…”

Section: Age-related Clonal Hematopoiesismentioning

confidence: 99%

Epithelial Cell Transformation and Senescence as Indicators of Genome Aging: Current Advances and Unanswered Questions

Kitakaze

Chijimatsu

Vecchione³

et al. 2021

IJMS

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The recent advances in deciphering the human genome allow us to understand and evaluate the mechanisms of human genome age-associated transformations, which are largely unclear. Genome sequencing techniques assure comprehensive mapping of human genetics; however, understanding of gene functional interactions, specifically of time/age-dependent modifications, remain challenging. The age of the genome is defined by the sum of individual (inherited) and acquired genomic traits, based on internal and external factors that impact ontogenesis from the moment of egg fertilization and embryonic development. The biological part of genomic age opens a new perspective for intervention. The discovery of single cell-based mechanisms for genetic change indicates the possibility of influencing aging and associated disease burden, as well as metabolism. Cell populations with transformed genetic background were shown to serve as the origin of common diseases during extended life expectancy (superaging). Consequently, age-related cell transformation leads to cancer and cell degeneration (senescence). This article aims to describe current advances in the genomic mechanisms of senescence and its role in the spatiotemporal spread of epithelial clones and cell evolution.

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“…For glucose-6-phosphate dehydrogenase B/A heterozygotes, Fialkow [34] estimated that at the time of inactivation the primordial cell pool size was sixteen (ten to twenty-four cells) for various tissues, including haemopoietic system. Other authors calculated less than eight [35] or even less than four [36] cells, using also glucose-6-phosphate dehydrogenase variants as an example. On the basis of enzyme activity, we computed for PGK Miinchen a precursor pool of three cells.…”

Section: Inheritancementioning

confidence: 99%

Hereditary deficiency of phosphoglycerate kinase: a new variant in erythrocytes and leucocytes, not associated with haemolytic anaemia

Krietsch

Kaiser

et al. 1977

Eur J Clin Investigation

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An X-chromosome linked phosphoglycerate kinase deficiency in erythrocytes and leucocytes was discovered in a large German kindred. Seven males of two generations were found to have only 21% of the normal enzyme activity in their erythrocytes, and twelve females of three generations showed various degrees of this defect. The differences in the expression of the deficiency in heterozygote females are explained by the Lyon hypothesis. The deficiency is caused by a variant enzyme, named phosphoglycerate kinase München. Although it differs from the normal enzyme electrophoretically, the two enzymes resemble one another closely in many respects. They have essentially the same Km for the substrates of the backward reaction, identical pH optima and similar rates of thermal inactivation. In contrast to the nine previously described phosphoglycerate kinase deficiencies, all of which are associated with haemolytic anaemia, the carriers of phosphoglycerate kinase München show no overt clinical symptoms. The erythrocyte concentrations of adenine nucleotides and 2,3-diphosphoglycerate are normal.

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Tentative evidence for 3?4 haematopoetic stem cells in man

Cited by 11 publications

References 7 publications

Haemopoietic recovery during radiation disease: Comments on combined-injuries

Haemopoietic recovery during radiation disease: Comments on combined-injuries

Epithelial Cell Transformation and Senescence as Indicators of Genome Aging: Current Advances and Unanswered Questions

Hereditary deficiency of phosphoglycerate kinase: a new variant in erythrocytes and leucocytes, not associated with haemolytic anaemia

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