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Biomedical subjects

B Sallerfors

Publications and source records attributed to B Sallerfors.

23 records · Page 2Linked to original sources
PubMed1989

Cell-mediated inhibition of granulopoiesis in vitro in patients with acute myeloid leukemia in remission.

We investigated the in vitro granulopoiesis in 11 patients with acute myeloid leukemia (AML) in complete remission 3-80 months after diagnosis (median 8.5 months). 3 of the patients had subnormal levels of bone marrow-derived CFU-GM. 6 of 10 patients tested had defective recloning capacity of d-7 CFU-GM, suggesting a stem cell defect. Most patients (7/11) showed an increased colony growth of bone marrow-derived CFU-GM after T-cell depletion by E-rosetting, while readdition of isolated autologous T cells to T-cell depleted marrow caused a dose-dependent inhibition of colony formation; bone marrow T cells were more effective in this inhibition than peripheral blood T cells. Experiments using cells depleted of either CD4- or CD8-positive cells and CD4/CD8-enriched cell populations showed that both CD4- and CD8-positive cells had the capacity to inhibit colony growth. Long-term culture of bone marrow cells in suspension showed that the production of CFU-GM declined at about the same rate as in normal controls. Our findings suggest that there are persisting stem cell defects in patients with AML in remission and that the cell growth regulatory systems may be altered. These abnormalities could possibly be an effect of residual damage to the hematopoietic system caused by intensive chemotherapy.

Bone Marrow↗
PubMed1987

Modulation of the production of leukemia associated inhibitor (LAI) and its interaction with granulocyte-macrophage colony-forming cells.

Leukemia associated inhibitor, LAI, reversibly inhibits DNA synthesis in normal human granulocyte-macrophage colony-forming units (CFU-GM). LAI is produced by myeloid leukemia cells, a subpopulation of normal nonadherent low-density mononuclear cells in peripheral blood and bone marrow, as well as by the human promyelocytic cell line HL-60. Normal low-density marrow cell absorbed LAI at 37 degrees C from HL-60 cell-conditioned medium. When normal marrow cells were treated with trypsin or chymotrypsin they lost their capacity to absorb LAI and also became insensitive to the inhibitory effect of LAI. These observations were taken as circumstantial evidence for the existence of a trypsin-sensitive LAI receptor on normal marrow cells, including CFU-GM. Glucocorticoid steroids (hydrocortisone, prednisolone, and dexamethasone) inhibited LAI production by acute myeloid leukemia (AML) cells, normal LAI-producing cells, and HL-60 cells. The fact that prostaglandin E1 (PGE) totally inhibited LAI production by normal cells and that indomethacin abrogated the inhibitory effect of adherent cells on LAI production suggested a role for adherent monocytic cells and PGE in the regulation of LAI production.

Bone Marrow↗
PubMed1984

Venous volume in offspring of hypertensive patients.

Twenty normotensive healthy male offspring of hypertensive patients were compared to 20 adequate controls regarding venous volume, the effect of ouabain on venous volume and signs of left ventricular hypertrophy. Among offspring there were slightly increased amplitudes in the orthogonal ECG as compared to controls but the differences were not statistically significant. Using a plethysmographic technique we found a significantly lower venous volume of the forearm in the offspring than in controls. There was, however, no effect of ouabain on the venous volume. The decreased venous distensibility among normotensive offspring might be an early manifestation of essential hypertension.

Adult↗