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Biomedical subjects

A E Irvine

Publications and source records attributed to A E Irvine.

26 records · Page 2Linked to original sources
PubMed1989

CFU-GM inhibitors in neutropenia.

Peripheral blood lymphocytes from 20 patients with neutropenia not consistent with aplastic anaemia were tested for their ability to inhibit the proliferation of normal granulopoietic precursor cells (CFU-GM) in agar culture. Two patients, both with features of an autoimmune disorder, had lymphocytes which were more inhibitory than normal lymphocytes to both normal and their own CFU-GM. Two other patients had lymphocytes which were more inhibitory than normal lymphocytes to either their own CFU-GM or normal CFU-GM but not both. Eight patients had lymphocytes which were significantly less inhibitory than normal lymphocytes to either normal or their own CFU-GM, but only one showed this feature against both normal and their own CFU-GM. One patient had a highly potent plasma inhibitor of CFU-GM--this patient had received multiple transfusions and had a leucocyte antibody of a broad specificity. No clinical or haematological features were common to any of these groups of patients which reflects the heterogeneity of patients studied and stresses the importance of controls.

Adolescent↗
PubMed1987

Evidence following splenic radiotherapy for a highly dynamic traffic of CFU-GM between the spleen and other organs in chronic granulocytic leukaemia.

Five patients with Ph1 +ve chronic granulocytic leukaemia and massive splenomegaly were given induction therapy with splenic irradiation, and their peripheral blood leucocyte count and granulocyte macrophage progenitor (CFU-GM) concentration monitored during the following six hours. In each patient there was a greater fall in CFU-GM than would have been expected from the fall in leucocyte count, but no evidence of a plasma inhibitor was found to explain the disproportionate reduction in CFU-GM. The difference between the estimated and observed decrease in CFU-GM/1 following splenic irradiation indicates a highly dynamic traffic of CFU-GM from the spleen to other organs in chronic granulocytic leukaemia.

Adult↗
PubMed1987

T-lymphocyte colony formation by lymphocytes from patients with aplastic anaemia.

T-lymphocyte colonies were cultured using lymphocytes from patients with aplastic anaemia and normal donors to assess their respective proliferative activities. Colony numbers from aplastic patient's cells were lower than from normal donors', though this was not significant. When lymphocytes from patients were co-cultured with normal lymphocytes, inhibition of T-colony formation was observed in 8 out of 12 experiments. As the degree of inhibition was greater than if patient cells grew no colonies, then, clearly, normal T-colony formation was inhibited. This ability of patients' lymphocytes to suppress lymphopoiesis might account for the low levels of patient T-colony formation, as well as low in vivo numbers of lymphocytes found in patients with aplastic anaemia. The role of patients' lymphocytes in causing marrow aplasia was investigated. Although the incorporation of patients' lymphocytes in normal granulocyte-macrophage (GM) colony-forming systems inhibited colony growth, in only 1 out of 8 patients was this inhibition significantly greater than that caused by the addition of normal lymphocytes to GM colony systems. Therefore, lymphocytes may not be the primary cause of aplastic anaemia, except for a few rare cases.

Adolescent↗
PubMed1986

Lymphocytes from patients receiving lithium do not inhibit CFU-C growth.

Lymphocyte subset levels and function were examined in 12 patients on lithium therapy and in 11 healthy hospital personnel. Co-culture of allogeneic human bone marrow cells with monocyte-depleted lymphocyte preparations revealed that CFU-C formation was significantly reduced (mean 43% inhibition) in the presence of normal lymphocytes but not with the patients' lymphocytes (less than 5% inhibition). This did not reflect numerical changes in lymphocyte subsets, since these were similar for control and lithium subjects. T colony formation was significantly depressed in the patient group (P less than 0.05), whereas B colony numbers were similar in both groups (P greater than 0.1). The possible role of HLA-incompatibility affecting CFU-C growth was investigated in co-culture experiments, using lymphocytes from HLA-identical twins, one of whom was receiving lithium. In four separate co-culture experiments, the inhibitory effect was shown with lymphocytes from the non-lithium twin but was not demonstrated by the lithium subject. Addition of lithium in vitro to co-cultures of normal marrow and lymphocytes was found to negate the inhibitory phenomenon in a dose-related manner. It is postulated that granulocytosis induced by the administration of lithium may be a manifestation of changes in a lymphocytic control system.

Adult↗
PubMed1984

Human umbilical cord conditioned medium: a stimulus for human CFU-G.

Segments of human umbilical cord have been used to prepare a highly active conditioned medium (HUCCM) for in vitro human granulopoiesis and have been compared with human placenta conditioned medium (HPCM) and feeder layers. The HUCCM produced more colonies on day 7 than HPCM (P less than 0.001), and colonies consisted almost exclusively (over 98%) of granulocytic cells by both morphological and cytochemical analysis. The HUCCM-stimulated colonies have a short culture life, the number of colonies being maximal on day 7 of culture with few colonies remaining on day 10. The main source of the colony-stimulating activity in the umbilical cord was found in the Wharton's Jelly component.

Colony-Forming Units Assay↗
PubMed1983

Ticarcillin-induced neutropenia corroborated by in vitro CFU-C toxicity.

A patient developed a drug rash and neutropenia while receiving tobramycin, ticarcillin and flucloxacillin intravenously for osteomyelitis. Incorporation of these antibiotics into in vitro cultures of bone marrow granulocyte macrophage precursors (CFU-C) showed no inhibition of the patient's marrow or normal marrow by tobramycin. The patient's marrow was more sensitive to ticarcillin than were control cultures, and all cultures incorporating flucloxacillin failed to show growth of CFU-C. Drugs of the penicillin group appear to be responsible for the patient's neutropenia.

Adolescent↗