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R M Crapper

Publications and source records attributed to R M Crapper.

23 records · Page 2Linked to original sources
PubMed1983

P-cell stimulating factor: characterization, action on multiple lineages of bone-marrow-derived cells and role in oncogenesis.

T-cell hybridomas have allowed us to define unequivocally a group of 3 distinct molecules, TCGF, T-cell GM-CSF, and PSF, as the products of the activated T-cell. It is becoming increasingly evident that these T-cell-derived molecules, together with a fourth, interferon-gamma, (Wong et al. 1982, 1983), affect a wide range of cell-types. The molecule which we have studied in greatest detail, PSF, probably effects every lineage of non-lymphoid bone-marrow-derived cells. We have evidence that PSF acts in vivo as an important mediator in a pleotropic defence and repair response to antigens that involves all the non-lymphoid elements of the blood. Finally, there is evidence that PSF-dependent cells can become immortal, and that activation and functional expression of the PSF gene can occur in such cells and result in autonomy and tumorigenesis. Clonal sources of T-cell lymphokines and clonal targets for lymphokine assays, formed the basis of recent progress in defining the number and nature of non-antigen-specific T cell products; cloning of the genes coding for these lymphokines should result in a similar impetus to the investigation of the physiology and possible therapeutic role of T-cell lymphokines, and lead to new insights into the control of gene expression and the role of these factors in oncogenesis.

Animals↗
PubMed1983

Chronic active hepatitis in alcoholic patients.

The histologic appearances characteristic of chronic active hepatitis (CAH) were observed in liver biopsies of seven patients among whom alcohol abuse was the only identifiable determinant of liver disease. Clinical, hematologic, biochemical and histologic features in these patients were contrasted with those of 20 patients with typical alcoholic hepatitis. For the CAH group, the liver was less enlarged below the costal margin, a palpable spleen was more frequent, the mean neutrophil count was lower, and there was a lower mean level of transaminase enzymes. In both groups there was minimal evidence of the serologic markers of autoimmune CAH or antecedent hepatitis B virus (HBV) infection. Histologically, all liver biopsies in the CAH group showed perilobular "piecemeal" necrosis, "rosette" formation and dense portal and septal lymphoid infiltrates, in contrast to the fatty change, Mallory bodies and intralobular neutrophil clusters of the alcoholic hepatitis group. In the CAH group, a second liver biopsy was assessed after a period during which alcohol consumption was known; histologic improvement or deterioration correlated with abstinence or continuation of drinking. Thus "alcoholic" CAH has some clinical and histologic features distinct from those of typical alcoholic hepatitis, but the two types were similar in other respects including dependence of the course of disease on continuing use of alcohol.

Adult↗
PubMed1983

Frequency of mast cell precursors in normal tissues determined by an in vitro assay: antigen induces parallel increases in the frequency of P cell precursors and mast cells.

Persisting (P) cells, homogeneous populations of cells that grow in vitro for prolonged periods provided a specific growth factor is present, resemble mast cells in many respects. An in vitro assay based on limit dilution was used to determine the frequency of precursors capable of giving rise to P cells. The incidences of P cell precursors per 10(6) cells in tissues of CBA mice in representative experiments were as follows: bone marrow, 291; spleen, 30; mononuclear blood cells, 11; popliteal lymph node, 0.5; and mesenteric lymph node, 18. P cell precursors appeared to be relatively undifferentiated, non-granulated cells; no cells with metachromatically staining granules were detected in the bone marrow or peripheral blood. Furthermore, mice of the Wf/Wf genotype that were grossly deficient in mast cells had the same frequencies of P cell precursors in bone marrow and spleen as their normal +/+ littermates. In many tissues in which we found P cell precursors, pluripotential hemopoietic stem cells are present. Among nonepithelial cells from the gut mucosa, however, in which there was a 10-fold higher frequency of P cell precursors than in bone marrow cells, pluripotential hemopoietic stem cells were undetectable, indicating the existence of committed P cell precursors distinct from pluripotential hemopoietic stem cells. The frequency of P cell precursors in mesenteric lymph nodes was more than 30-fold higher than in the popliteal lymph nodes, suggesting that antigenic stimulation influences their numbers. This latter notion is supported by the observation that after immunization in the footpad, the number of P cell precursors in ipsilateral popliteal lymph nodes rose about 35-fold. Immunization was also accompanied by a rise in mast cell numbers in draining popliteal nodes. This correlation between P cell precursors and the local production of mast cells was strengthened by the observation that the frequency of P cell precursors in cells from the gut mucosa of mice of Wf/Wf genotype, which are unable to mount an intestinal mastocytosis, was more than 1000-fold lower than in wild type mice. Thus, the precursors of P cells and probably of at least the T cell-dependent subset of mast cells appear to be generated in the bone marrow and seed as non-granulated cells via the blood to peripheral tissues such as spleen, lymph node, and mucosal surfaces. P cells appear to be in vitro counterparts of the mucosal subset of mast cells.

Animals↗
PubMed1981

Fatal agranulocytosis attributable to cimetidine.

There exist some 12 reported cases of agranulocytosis or pancytopenia occurring after the use of cimetidine to reduce gastric acidity. Reported here is the case of a 74-year-old man with renal failure who, 21 days after treatment with cimetidine for peptic oesophagitis, developed severe granulocytopenia followed by fatal septicaemia.

Aged↗