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Biomedical subjects

D L Coleman

Publications and source records attributed to D L Coleman.

189 records · Page 11Linked to original sources
PubMedDate not supplied

Granulocyte-macrophage colony-stimulating factor: pleiotropic cytokine with potential clinical usefulness.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a 23-kDa glycoprotein with remarkably diverse effects on immune and nonimmune cells. GM-CSF induces differentiation of granulocyte, macrophage, and eosinophil precursor cells. Proliferation of monocyte-macrophages, T lymphocytes, keratinocytes, and endothelial cells is also stimulated by GM-CSF. In addition, GM-CSF alters the functional properties of mature granulocytes, macrophages, eosinophils, and basophils. GM-CSF is produced by T lymphocytes, macrophages, and several cell types in extramedullary sites, where it may act in a paracrine manner to regulate the local response to antigenic challenge. Clinical trials of GM-CSF have been conducted in patients with AIDS, aplastic anemia, myelodysplastic syndromes, and sarcoma and following bone marrow transplantation and accidental radiation exposure. GM-CSF significantly increased circulating numbers of several myeloid cells and produced dose-dependent toxicity consisting primarily of myalgias, fever, fluid retention, and serosal effusions. Additional studies are needed to define the role of GM-CSF in treatment of patients with qualitative and quantitative dysfunction of immune cells.

Animals↗
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Fat (fat) and tubby (tub): two autosomal recessive mutations causing obesity syndromes in the mouse.

This report describes the development of obesity syndromes in mice caused by two autosomal recessive mutations, fat (fat), located on chromosome 8, and tubby (tub), located on chromosome 7. Both mutations cause slowly developing but ultimately severe obesity conditions. Although hyperinsulinemia, hyperactivity of the beta cell of the islets of Langerhans, and beta-cell degranulation are consistent features, these obesity syndromes do not progress to severe diabetes. The many different single-gene mutations in the mouse that produce obesity-diabetes syndromes of varying degrees of severity make the mutant mouse a powerful tool for analyzing the number and nature of the primary defects than can cause obesity states.

Aging↗
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An unusual pontine mass lesion.

A 27-year-old Puerto Rican man presented to Yale-New Haven Hospital with a six-week history of left-sided headache, diplopia, and drooping of the left side of his face. Cerebrospinal fluid examination showed a lymphocytic pleocytosis and a CT scan of the brain revealed an unusual intrapontine mass lesion requiring systemic antifungal therapy. This case emphasizes many of the diagnostic and therapeutic considerations required for effective therapy of fungal disease in the central nervous system.

Adult↗
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Analysis of Egr-1 protein induction in murine peritoneal macrophages treated with granulocyte-macrophage colony-stimulating factor.

Transcription of early growth response gene-1 (Egr-1) is required for macrophage differentiation. Since granulocyte-macrophage colony-stimulating factor (GM-CSF) induces macrophage proliferation as well as the transcription of Egr-1 mRNA, we characterized the induction of Egr-1 protein in murine peritoneal macrophages following treatment with GM-CSF. As determined by Western blot analysis, the concentration of GM-CSF required to induce detectable Egr-1 protein in macrophages was 50 units/ml, and the inducible Egr-1 protein species was 80 kDa. Following stimulation of macrophages with GM-CSF, Egr-1 protein was detected within 25 min and reached maximum level at 70 min. The concentration of GM-CSF that was required to induce Egr-1 protein in macrophages was similar to that required to induce macrophage proliferation. A similar concentration has been detected previously in mouse serum exposed to bacterial endotoxin in vivo, suggesting that the 80 kDa Egr-1 protein may be induced in macrophages under the physiologic circumstances of pathogen invasion. Thus, our data support further study on the role of Egr-1 protein in mediating GM-CSF induction of macrophage proliferation.

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