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Biomedical subjects

M A Moore

Publications and source records attributed to M A Moore.

At least 451 records · Page 25Linked to original sources
PubMed1978

Limitation of excessive myelopoiesis by the intrinsic modulation of macrophage-derived prostaglandin E.

The clonal proliferation of the committed granulocyte-macrophage stem cell is controlled by a balance between mutually opposing factors, colony stimulating factor and prostaglandin E, both of monocyte-macrophage derivation. Increases beyond a critical concentration of colony stimulating factor within the local milieu of the mononuclear phagocyte induces the coincident elaboration of prostaglandin E, a self-regulated response which serves to limit the unopposed humoral stimulation of myelopoiesis.

Animals↗
PubMed1978

Evidence for distinct lymphocytic and monocytic populations in a patient with terminal transferase--positive acute leukemia.

Two distinct cell populations with lymphoblastic and monocytic characteristics were separated and characterized by multiple cell markers in a patient with terminal transferase-positive acute acute leukemia. The clinical course and sequential cell marker studies were consistent with the interpretation of a defect at the level of a common stem cell giving rise to a terminal transferase--positive lymphoblastic cell population at diagnosis and, following initial therapy, a terminal transferase--negative monocytic population.

Adult↗
PubMed1978

Induction of myeloid colony-stimulating activity in murine monocyte tumor cell lines by macrophage activators and in a T-cell line by concanavalin A.

Certain fibrosarcoma lines in culture and the WEHI-3 myelomonocytic leukemia cell line have previously been shown to secrete myeloid colony-stimulating activity (CSA) spontaneously. We describe here other hematopoietic tumor cell lines in which CSA is either produced constitutively or inducible by immunostimulators. CSA production in macrophage and monocyte tumor lines is induced by lipopolysaccharide, zymosan, Mycobacterium strain Bacillus Calmette-Guérin, tuberculin purified protein-derivative preparation from mycobacteria, and dextran sulfate. Myeloma, mastocytoma, and T-lymphoma lines do not produce CSA with or without these agents. In contrast, the T-lymphocyte mitogen concanavalin A (but not phytohemagglutinin) induces CSA synthesis in one of seven T-lymphomas tested. In most cases induction of CSA is correlated with conditions of cell growth inhibition by the immunomodulators. However, other drugs that cause cytostasis or cytotoxicity do not lead to CSA production. Leukemic cells thus may retain sensitivity to normal regulatory events with resultant effects on host hematopoietic cell functions.

Animals↗
PubMed1978

Regulation of megakaryopoiesis in long-term murine bone marrow cultures.

Megakaryocytes and their precursor cells were sustained in mouse bone marrow suspension cultures for over 4-6 wk. Megakaryocyte precursor cells were detected by their capacity to form colonies of megakaryocytes in semisolid agar cultures. Colony formation was dependent on the presence of medium conditioned by a myelomonocytic leukemic cell line (WEHI-3CM). Megakaryocytes from the liquid and semisolid cultures were identified by cytoplasmic acetylcholine esterase and by ultrastructural analysis. The suspension medium from the bone marrow liquid cultures which sustained megakaryopoiesis was not directly acitive in stimulating megakaryocyte colony formation in the semisolid agar cultures, but potentiated the number of colonies detected when WEHI-3CM was present. Bone marrow-conditioned medium increased the sensitivity of megakaryocyte progenitor cells to the stimulus in WEHI-3CM. Addition of the activities present in the two sources produced a quantitative assay for the detection of mouse megakaryocyte progenitor cells. These studies showed: (1) that no inductive regulator of in vitro clones of megakaryocytes was present in the supernatants from the long-term marrow cultures and, (2) that at least two factors were necessary for the induction of megakaryocyte progenitors to proliferate and differentiate in semisolid cultures in vitro.

Animals↗
PubMed1978

Effect of myleran on murine hemopoiesis. III. Changes in the density distribution of spleen colony forming (CFU-S) and agar gel colony forming cells (CFU-C).

Spleen colony forming cells (CFU-S) and agar-gel colony forming cells (CFU-C) are separate but heterogeneous cell populations, as measured by buoyant density. Myleran (MY) abrogated the major (lighter density) components of the CFU-S and CFU-C compartments, thus shifting the surviving CFU-S and CFU-C density profiles into the higher density region. The normal spleen colony erythrocytic : granulocytic (E:G) ratio profile showed three density regions with different distributions of erythroid and granulocytic colonies. The preponderantly erythrocytic colony-generating CFU-S of the intermediate density regions were eradicated by MY. Comparison of the density distribution of erythrocytic and granulocytic colony-generating CFU-S of normal bone marrow showed that the erythrocytic CFU-S profile paralleled that of total CFU-S, while most of the granulocytic CFU-S were contained in the major (and lowest density) peak. MY eradicated the two main (and lowest density) peaks of CFU-S; surviving CFU-S occurred preponderantly in a minor (higher density) peak which has a high potential for generating erythrocytic colonies.

Animals↗
PubMed1977

Regulation of B-lymphocyte clonal proliferation by stimulatory and inhibitory macrophage-derived factors.

A functional subpopulation of murine B lymphocytes proliferate in semisolid agar culture in the presence of 2-mercaptoethanol to form colonies. The effects of diffusible macrophage-derived factors on this focal proliferation was investigated using a two-layer culture system which prevented macrophage-lymphocyte contact and permitted B-cell activation to be critically assessed under conditions of extremely low cell densities. Adherent peritoneal macrophages incorporated within underlayers of spleen or lymph node cell cultures potentiated both the number and size of developing B-cell colonies. These effects were most striking when low numbers of spleen or lymph node cells, or macrophage- depleted lymphoid cell suspensions were used. Thus, macrophage-depleted lymph node ceils gave rise to virtually no colonies, but colony-forming ability was restored by the presence of an optimal number of macrophages. When the number of macrophages exceeded that required for optimal stimulation, colony formation was suppressed; an effect which was largely prevented by indomethacin, an inhibitor of prostaglandin synthesis. Under these conditions, stimulation and inhibition of B-cell activation by macrophages could be dissociated, indicating that each signal is selectively controlled by individual molecules elaborated by the macrophage. With an appropriate number of macrophages required for B-cell activation, and sufficient indomethacin to inhibit the accumulation of macrophage-derived prostaglandin, B-lymphocyte clonal proliferation was a linear function of the number of B cells placed in culture. In the absence of macrophages, B-cell colony formation was potentiated by both lipopolysaccharide and intact sheep erythrocytes through a mechanism different from that of the macrophage-derived stimulatory factor. In addition to their direct stimulatory effect on B-cell proliferation, lipopolysaccharide and sheep erythrocytes were each capable of modulating the production and/or release of B-cell stimulatory and inhibitory factors by the macrophage. Parallel studies of conventional mitogen- stimulated lymphocyte cultures did not show a requirement for macrophages and confirm that the semisolid assay is uniquely suited to studies on the regulatory role of the macrophage in B-cell activation.

Animals↗
PubMed1977

Maintenance of hemopoietic stem cells and production of differentiated progeny in allogeneic and semiallogeneic bone marrow chimeras in vitro.

A culture system is described in which bone marrow-derived adherent cells can support prolonged proliferation and differentiation of genetically incompatible stem cells and precursor cells. The results suggest that the reactive cells responsible in vivo for host transplantation resistance and for graft-versus-host disease are selectively lost or inhibited in such cultures, which may provide a vehicle for studying some of the cellular mechanisms involved in transplantation resistance.

Animals↗
PubMed1977

Reversible renal hypertension secondary to renal arteriovenous fistula and renal cell carcinoma.

A 40-year-old woman with hypertension (179/100) and a massive renal arteriovenous fistula involving most of the right kidney is reported. A 131I hippuran renogram, split urinary function studies and renal vein renins were normal. The renal arteriovenous fistula was removed by total nephrectomy and blood pressure returned to normal. A renal cell carcinoma was found within the fistula. This case confirms the association of renal cell carcinoma with renal arteriovenous fistulas and demonstrates the potential curative effects of nephrectomy for the hypertension associated with and demonstrates the potential curative effects of nephrectomy for the hypertension associated with it. The normal split function studies, renogram and renal vein renins do not support the concept of secondary hyperreninemia as a causative factor in the hypertension seen with renal arteriovenous fistulas.

Adenocarcinoma↗