Hematologic analysis of clinical bone marrow grafting evaluated by in vitro cultures.
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Biomedical subjects
Publications and source records attributed to M A Moore.
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Cells from patients with acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) can be grown and their properties analyzed in agar gel cultures. Levels of the glycoprotein regulator colony stimulating factor (CSF) were found to be elevated in 19-66% of plasmas tested from patients with various types of granulocytic leukemia, and the growth of AML and CML cells in vitro was observed to be dependent on, and responsive to, stimulation by CSF-containing material. In both diseases, the leukemic cells appear to be in a responsive state with respect to normal growth regulators, and potentially alterations in regulator levels may therefore be able to achieve sustained arrest of the growth of leukemic populations.
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89Sr treatment was used to determine if stem cells in young fetal liver could differentiate to mature B lymphocytes in adult animals that lacked functional bone marrow. Isotope injection alone resulted in a severe and lasting depletion of bone marrow cells and particularly lymphocytes, multipotential stem cells, and progenitors for granulocytes and macrophages. The latter two functional populations of cells expanded in number in the spleen but not the liver after their destruction in bone marrow. The total body content of stem cells did not, however, return to normal. Spleen B cells and lymphocytes lacking B or T cell markers were reduced by 89Sr treatment and possible reasons for this depletion are discussed. B lymphocytes were formed in lethally x-irradiated mice that had less than 1% of normal bone marrow function after reconstitution with fetal liver cells. These cells were immunologically mature by virtue of their ability to mount a primary immune response and function in a thymus-independent adoptive anti-hapten response.
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In studies on seven anephric patients, glucose and insulin administration before hemodialysis produced a significant reduction in plasma potassium concentration (mean reduction = 1.3, 1.7, and 1.4 meq/liter at 60, 120, and 180 min, respectively) which was accompanied by a significant and sustained reduction in plasma aldosterone concentration. There was a significant correlation between plasma aldosterone and plasma potassium concentration (r = +0.74, P < 0.001) and between changes in the concentration of plasma aldosterone occurring in individual patients and the corresponding changes in plasma potassium concentration (r = +0.52, P < 0.01). There was no significant change in plasma sodium concentration, and plasma corticoid concentration, which was monitored as an index of ACTH elaboration, was reduced at 60 min but increased subsequently as symptoms attributable to hypoglycemia were observed. These studies demonstrate that plasma aldosterone concentration can be modulated acutely by transitory changes in plasma potassium concentration without a change in potassium balance. The effect of glucose and insulin administration on intracellular potassium in the adrenal cortex is uncertain, and although increased net movement of potassium into cells is the presumptive mechanism of the reduction in plasma potassium concentration, whether the potassium content of the adrenal cortex may have increased or decreased or remained essentially unchanged, cannot be inferred from our data.