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D W Golde

Publications and source records attributed to D W Golde.

At least 361 records · Page 20Linked to original sources
PubMed1972

Identification of the colony-stimulating cell in human peripheral blood.

Bone marrow colony formation in soft gel culture may be stimulated by substances elaborated by human peripheral blood leukocytes. In order to determine the cell type responsible for colony stimulation, peripheral leukocytes were separated by Ficoll-Hypaque gradients and differential glass adhesion. Morphologic, histochemical, and functional criteria were applied to determine the purity of the monocyte, lymphocyte, and neutrophil fractions. Using these cells as feeder layers and as a source of conditioned medium, evidence was obtained that the monocyte is the colony-stimulating cell of human peripheral blood. Activity greater than that of mixed white cells was obtained with monocyte underlayers, and only monocyte- and macrophage-conditioned media were shown to have significant colony-stimulating activity.

Bone Marrow↗
PubMedDate not supplied

Molecular characterization of genome of a novel human T-cell leukaemia virus.

A novel human retrovirus (HTLV-II) was previously found associated with a T-cell variant of hairy-cell leukaemia. Molecular cloning demonstrates that the complete provirus genome is 8.8 kilobase pairs in size and is transmissible to uninfected cells. Two types of infectious deleted provirus were also characterized. The sequences of HTLV-II are distinct from those of HTLV-I.

Base Sequence↗
PubMedDate not supplied

Long terminal repeats of human T-cell leukaemia virus II genome determine target cell specificity.

Human T-cell leukaemias and lymphomas associated with the human T-cell leukaemia viruses (HTLV) are invariably neoplasms of cells with mature T-lymphocyte phenotype. Epstein-Barr virus-transformed B- lymphoycte lines which are productively infected with HTLV may be isolated from patients with HTLV malignancies, but no non-lymphoid tissues seem to be involved. Here, to investigate the basis for this tissue specificity, we introduced type II HTLV (HTLV-II) into a variety of human cells by infection and also by transfection of recombinant genomes. We found no HTLV-II expression in non-lymphoid tissues although expression and correct initiation of transcription was observed in B and T lymphocytes. Our results using recombinant genomes indicate that the restriction of expression is at least partly due to cis-acting functions of the long terminal repeats which lie at each end of the HTLV genome.

Base Sequence↗
PubMedDate not supplied

Human granulocyte-macrophage colony-stimulating factor is a neutrophil activator.

The polymorphonuclear leukocyte (PMN), or neutrophil, is the major host defence cell protecting the body against invasion by bacteria and fungi. Products of oxidative metabolism mediate PMN microbicidal and tumoricidal activity but the mechanisms by which these pathways become activated are not well understood. We have previously described a human granulocyte-macrophage colony-stimulating factor (GM-CSF) of relative molecular mass (Mr) 22,000 that also inhibits neutrophil motility (NIF-T activity). Because of its direct action on granulocytes, this lymphokine is a candidate for a neutrophil-activating factor. We have studied the effect of GM-CSF/NIF-T on superoxide anion generation in response to the bacterial chemo-attractant N-formylmethionyl-leucylphenylalanine (f-MLP), and report here that PMNs preincubated with either purified natural GM-CSF or biosynthetic (recombinant) GM-CSF showed increased (as much as fourfold) superoxide anion production in response to f-MLP. These results indicate that human GM-CSF is a neutrophil-activating factor.

Colony-Stimulating Factors↗
PubMedDate not supplied

Molecular characterization and expression of the gene encoding human erythroid-potentiating activity.

Erythropoietin is the primary physiological regulator of erythropoiesis; however, in vitro studies have identified another class of mediators which appear to be important in stimulating erythroid progenitors. These factors have generally been referred to as burst-promoting activities (BPA), because they stimulate the growth of early erythroid progenitors referred to as burst-forming units-erythroid (BFU-E) which give rise to colonies of up to thousands of haemoglobinized cells. We recently reported purification of a burst-promoting activity from medium conditioned by the Mo T-lymphoblast cell line infected with human T-cell lymphotropic virus type II (HTLV-II). This purified glycoprotein of relative molecular mass (Mr) 28,000 also stimulates colony formation by more mature erythroid precursors (CFU-E) and is therefore referred to as erythroid-potentiating activity (EPA). Purified EPA specifically stimulates human and murine cells of the erythroid lineage, unlike murine interleukin-3 (IL-3) which stimulates precursor cells from all haematopoietic lineages. We report here the isolation of a complementary DNA molecular clone encoding EPA and its use in producing EPA in COS (monkey) cells and CHO (Chinese hamster ovary) cells. We also define the organization of the EPA gene in human DNA.

Animals↗