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Biomedical subjects

F Walker

Publications and source records attributed to F Walker.

At least 91 records · Page 5Linked to original sources
PubMed1985

Specific binding of radioiodinated granulocyte-macrophage colony-stimulating factor to hemopoietic cells.

The hemopoietic growth factor granulocyte-macrophage colony-stimulating factor, GM-CSF, specifically controls the production of granulocytes and macrophages. This report describes the binding of biologically-active 125I-labeled murine GM-CSF to a range of hemopoietic cells. Specific binding was restricted to murine cells and neither rat nor human bone marrow cells appeared to have surface receptors for 125I-labeled GM-CSF. 125I-Labeled GM-CSF only appeared to bind specifically to cells in the myelomonocytic lineage. The binding of 125I-labeled GM-CSF to both bone marrow cells and WEHI-3B(D+) was rapid (50% maximum binding was attained within 5 min at both 20 degrees C and 37 degrees C). Unlabeled GM-CSF was the only polypeptide hormone which completely inhibited the binding of 125I-labeled GM-CSF to bone marrow cells, however, multi-CSF (also called IL-3) and G-CSF partially reduced the binding of 125I-labeled GM-CSF to bone marrow cells. Interestingly, the binding of 125I-labeled GM-CSF to a myelomonocytic cell line, WEHI-3B(D+), was inhibited by unlabeled GM-CSF but not by multi-CSF or G-CSF. Scatchard analysis of the binding of 125I-labeled GM-CSF to WEHI-3B(D+) cells, bone marrow cells and peritoneal neutrophils indicated that there were two classes of binding sites: one of high affinity (Kd1 = 20 pM) and one of low affinity (Kd2 = 0.8-1.2 nM). Multi-CSF only inhibited the binding of 125I-labeled GM-CSF to the high affinity receptor on bone marrow cells: this inhibition appeared to be a result of down regulation or modification of the GM-CSF receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Hierarchical down-modulation of hemopoietic growth factor receptors.

Granulocytes and macrophages can be produced in vitro when progenitor cells from mouse bone marrow are stimulated by any of four distinct colony stimulating factors, Multi-CSF (IL-3), GM-CSF, G-CSF, and M-CSF (CSF-1). At 0 degrees C the four CSFs do not cross-compete for binding to bone marrow cells, indicating that each has a specific cell surface receptor. However, at 21 degrees C or 37 degrees C, Multi-CSF inhibits binding of the other three CSFs and GM-CSF inhibits binding of G-CSF and M-CSF. Rather than competing directly for receptor binding, the binding of Multi-CSF, GM-CSF, or G-CSF to their own receptor induces the down-modulation (and thus activation) of other CSF receptors at 37 degrees C. The pattern and potency of down-modulation activity exhibited by each type of CSF parallels the pattern and potency of its biological activity. We propose a model in which the biological interactions of the four CSFs are explained by their ability to down-modulate and activate lineage-specific receptors.

Animals↗
PubMed1985

Malignant transformation of a growth factor-dependent myeloid cell line by Abelson virus without evidence of an autocrine mechanism.

Abelson virus has been used to transform cells of a murine, factor-dependent myeloid cell line (FD). Factor-independent (FI) cell lines were derived, which expressed the viral genome and were tumorigenic in syngeneic mice. Karyotypic analysis of FI cells before and after passage in vivo indicated that the tumorigenic cells were derived from FD cells. Northern gel analysis of mRNA, bioassay of culture supernatants, and the density-independent growth of the FI cells indicated that the transformation had not induced the synthesis of the hemopoietic growth factors normally required to support the FD cells, that is, granulocyte-macrophage CSF or Multi-CSF. The FD and FI cells displayed similar numbers of cell surface receptors for Multi-CSF (IL-3) and GM-CSF. We conclude that Abelson virus transformation of this line from factor-dependence to factor-independence and tumorigenicity did not involve autocrine stimulation.

Abelson murine leukemia virus↗
PubMed1984

Age related detection of tissue amyloid P in the skin.

The presence of tissue amyloid P component in normal skin from fetuses and children was studied using direct, fluorescent, immunohistochemical techniques on frozen sections. Tissue amyloid P is not detected in fetuses or in children up to the age of 2 years but from the age of 4 years upwards it is readily detected and invariably present. Though the function of human amyloid P is unknown its role appears to be age or maturity related.

Adolescent↗
PubMed1984

Amyloid P component in human thyroid.

The distribution of amyloid P component in the adult human thyroid was studied by direct immunofluorescence on frozen sections of surgically removed tissue. Amyloid P component shows a striking fibrillary and broken linear distribution in the interfollicular areas. This pattern corresponds to that of reticulin fibres. Amyloid P is also localised to the small amount of elastic tissue in blood vessels but is not demonstrable within cells or in acinar basement membranes.

Amyloid↗
PubMed1983

The distribution of amyloid P component in normal human cervix.

The distribution of amyloid P component in normal human adult cervix was studied using fluorescent immunohistochemical techniques on frozen sections. Amyloid P component is associated with elastic fibres which are particularly concentrated in a sub-epithelial plexus in the ectocervix. This plexus does not extend into the endocervix but terminates at, or just caudal to, the squamocolumnar junction. Amyloid P component was not demonstrated in any of the epithelial basement membranes.

Amyloid↗
PubMed1983

Nephrotic syndrome in Hodgkins disease.

A case of nephrotic syndrome due to minimal lesion glomerulonephritis associated with Hodgkins disease is described. The course of the nephrotic syndrome was relapsing, preceeding the development of lymphoma by eighteen months. Treatment of this nephrotic syndrome with repeated courses of Prednisone and Cyclophosphamide resulted only in partial improvement of his proteinuria. However, complete absence of proteinuria only occurred with successful therapy of Hodgkins disease.

Child↗
PubMed1982

The distribution of amyloid P component in normal human skin.

The distribution of amyloid P component in normal human adult skin was studied using fluorescent immunohistochemical techniques on frozen sections. Amyloid P component is associated with elastic fibres of all sizes, and is present in the basement membrane of sweat gland ducts. It is not demonstrable in the basement membrane at the epidermo-dermal junction or in the secretory portion of the sweat glands. In the latter site there is however a spiral, fibrillar, elastic plexus closely related to the basement membrane.

Adult↗