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Biomedical subjects

A C Louwagie

Publications and source records attributed to A C Louwagie.

At least 19 recordsLinked to original sources
PubMed1987

Bone marrow plasmocytosis in acute leukemia.

A quantitative evaluation of IgA, IgD, IgG and IgM plasmocytes in sequential bone marrow aspirates of patients with acute leukemia using the peroxidase-antiperoxidase method was undertaken. Plasmocytosis resembled that of normal controls or was slightly subnormal on admission. When remission was obtained, bone marrow plasmocytosis was similar to normal controls, irrespective of the type of acute leukemia and the cytostatic treatment. Occurrence of infection strongly augmented the number of plasmocytes, with an initial increase in IgM and later in IgG plasmocytes. This suggests that the immune response is preserved in patients with acute leukemia.

Acute Disease↗
PubMed1985

Discordances of cytoplasmic immunoglobulin G staining with the immunoperoxidase technic in plasma cells from bone marrow, tonsils, and appendix.

Plasma cell cytoplasmic immunoglobulin was stained using the peroxidase-antiperoxidase technic in Bouin-fixed, paraffin-embedded human tissues from different origins. Bone marrow (BM), tonsils, and appendices were examined. IgA-, IgD-, and IgM-secreting plasmocytes were easily studied using highly diluted rabbit antihuman antisera in all tissues, including BM. IgG plasmocytes showed good stainability in tonsils and appendices, but variable results were obtained in BM. Bone marrow IgG plasmocytes from persons without infection required a tenfold higher concentration of rabbit antihuman IgG than plasmocytes derived from patients with infection. Stainability of BM plasmocytes from patients with infection was equal to BM plasmocytes from myeloma patients. Because the same rabbit antihuman IgG concentration could be applied for staining plasmocytes derived from tonsils and appendices, it is most probable that the difference in staining ability is due to a difference in activity of the plasmocytes, i.e., a different IgG concentration in the plasmocytes.

Acute Disease↗
PubMed1977

II. Mechanism of increased colony formation of CFU-S and CFU-C after in vivo PHA administration in mice.

In vivo administration of 3 mg PHA-M results in an increase in spleen colonies due to an augmented seeding of CFU-S into the spleen. An increase in the number of CFU-S in the developing nine-day spleen colonies also occurred together with a slight increase in the number of CFU-S in DNA-S phase 24 hours after PHA-M administration. The increased colony formation was due to an increased number of CFU-C from the early culture period onwards but could not be explained by an increase in the number of CFU-C in DNA/S phase. The release of colony-stimulating substances was proved but this only partially accounted for the observed rise in bone marrow CFU-C.

Animals↗
PubMed1977

I. Increase in bone marrow CFU-S and CFU-C after in vivo phytohaemagglutinin (PHA) administration in mice.

An absolute increase in bone marrow CFU-S was observed within 4 hours after intraperitoneal administration of 3 mg PHA-M or 250 microgram PHA-P. At that time, there was no increase in spleen CFU-S, while a pronounced decrease in the number of circulating CFU-S was noted. A two to fourfold increase in bone marrow CFU-C was found within 12 hours after intraperitoneal administration of a similar dose of PHA-M or PHA-P. Addition of PHA-M or PHA-P at small concentrations resulted in a marked inhibition of granulocytic colony formation whereas macrophage colony growth became depressed only at very high concentrations.

Animals↗