Proliferation kinetics of bone marrow cells in congenital dyserythropoietic anemia type II

1985 ◽  
Vol 50 (4) ◽  
pp. 219-224 ◽  
Author(s):  
G. Ucci ◽  
A. Riccardi ◽  
P. D�rmer ◽  
M. Cazzola ◽  
M. Danova
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Type Ii ◽  
Congenital Dyserythropoietic Anemia ◽  
Proliferation Kinetics ◽  
Kinetics Of ◽  
Marrow Cells

The kinetics of in vivo sister chromatid exchange induction in mouse bone marrow cells by ethylnitrosourea and methylnitrosourea

1986 ◽  
Vol 84 (1) ◽  
pp. 56-65 ◽  
Author(s):  
James L. Charles ◽  
David Jacobson-Kram ◽  
Lyman W. Condie ◽  
Joseph F. Borzelleca ◽  
Richard A. Carchman
Keyword(s):  
Bone Marrow ◽  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Bone Marrow Cells ◽  
Mouse Bone Marrow ◽  
Kinetics Of ◽  
Mouse Bone Marrow Cells ◽  
Marrow Cells

scholarly journals Monocyte-derived recruiting activity: kinetics of production and effects of endotoxin

Blood ◽  
1985 ◽  
Vol 65 (3) ◽  
pp. 689-695 ◽  
Author(s):  
E McCall ◽  
GC Jr Bagby
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Bone Marrow Cells ◽  
Umbilical Vein ◽  
Calf Serum ◽  
Fold Increase ◽  
Umbilical Vein Endothelial Cells ◽  
Kinetics Of ◽  
Marrow Cells

Abstract Cultured monocytes release a factor, monocyte-derived recruiting activity (MRA), which stimulates fibroblasts, endothelial cells, and T lymphocytes to produce colony-stimulating activity (CSA). We studied the kinetics of MRA production using a technique in which MRA levels were measured in a two stage bioassay. We used umbilical vein endothelial cells as the MRA-responsive (CSA-producing) cells, and normal colony-forming unit granulocyte-macrophage (CFU-GM)-enriched bone marrow cells (T lymphocyte- and monocyte-depleted, low density bone marrow cells) as the CSA-responsive cells. MRA stimulated a 30- fold increase in CSA production by endothelial cells. MRA production was detected in supernatants from as few as 10(3) monocytes per milliliter, required the presence of fetal calf serum, and was inhibited by cycloheximide (10 to 100 micrograms/mL) and puromycin (10 to 50 micrograms/mL). Production was detectable after 24 hours of monocyte incubation, was maintained for three days, and fell to undetectable levels by seven days. With the addition of bacterial endotoxin (lipopolysaccharide [LPS]) (50 micrograms per 10(6) cells), MRA was detectable after only three hours of incubation, and levels peaked at 24 hours. Further, maximum MRA levels in the supernatants of LPS-stimulated monocytes were up to ten times greater than peak levels in the supernatants of unstimulated monocytes. Endotoxin augmented monocyte production of MRA to a greater extent than it did CSA production, indicating that the stimulation of CSA production by endotoxin may be at least partly indirect. The responsiveness of MRA production to endotoxin in vitro is consistent with the notion that MRA may be a biologically relevant regulator of CSA production by cells of the hematopoietic microenvironment.

scholarly journals In vivo investigations of clastogenic effect of levamisole hydrochloride on bone marrow cells of BALB/c mice

2005 ◽  
Vol 59 (5-6) ◽  
pp. 549-556
Author(s):  
Milan Kulic ◽  
Zoran Stanimirovic ◽  
Sinisa Ristic ◽  
Biljana Markovic
Keyword(s):  
Bone Marrow ◽  
Mitotic Activity ◽  
Opposite Effect ◽  
Bone Marrow Cells ◽  
The Other ◽  
Control Group ◽  
Clastogenic Effect ◽  
Kinetics Of ◽  
Marrow Cells

Cytotoxic and genotoxic examinations were performed of the effect of levamisole hydrochloride (2.2 mg/kg bm, 4.4 mg/kg bm, LD50-25% mg/kg bm and LD50-75% mg/kg bm) on bone marrow cells of mice of the BALB/c strain. The effect of levamisole hydrochloride on kinetics of the cellular cycle and the appearance of structural and numerical changes in chromosomes of bone marrow cells were followed. The therapeutic dose of levamisole of 2.2 mg/kg bm showed the ability to increase the mitotic activity of the observed cells, thus confirming knowledge of the immunostimulative effect of this dose of the medicine under in vivo conditions. The other tested doses of levamisole in this experiment, observed in comparison with the control group, had an opposite effect, i.e. they caused a reduction in the mitotic activity of bone marrow cells. All the examined doses in vivo showed the ability of inducing numeric (aneuloid and polyploid) and structural (lesions, breaks and insertions) chromosomal aberrations. On this basis, it can be concluded that the examined doses have a genotoxic effect.

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