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Biomedical subjects

R J Fallon

Publications and source records attributed to R J Fallon.

At least 73 records · Page 4Linked to original sources
PubMed1988

How to deal with a hospital outbreak of Legionnaires' disease.

The outbreak of Legionnaires' disease in Glasgow Royal Infirmary is discussed together with the problems such an outbreak poses to the microbiologist. The importance of early diagnosis is stressed. The outbreak was managed by a team drawn up from various disciplines within the hospital. Frank daily reports to the press, together with regular staff meetings with staff representatives helped to allay public anxiety. The subsequent maintenance and monitoring of the wet cooling tower required for the hospital ventilation system have resulted in considerable additional work for the microbiology department but especially for the hospital engineers.

Bacteriological Techniques↗
PubMed1988

Assessment of antimicrobial treatment of acute typhoid and paratyphoid fevers in Britain and The Netherlands 1971-1980.

The response of 310 patients with typhoid or paratyphoid fevers to current antibiotic therapy was studied retrospectively. Most patients were of Asian or European origin, thus reflecting the areas in which they were infected. Of the 244 patients with well-recorded therapy 63% were treated with chloramphenicol, 22% with co-trimoxazole and the remainder with various penicillins. There was little difference in response in terms of resolution of fever. Symptoms persisted in only two of 153 (1.3%) patients given chloramphenicol but side-effects led to a change of treatment in nine of these patients. Co-trimoxazole was not significantly inferior and amoxycillin performed well, but the small number of cases treated with ampicillin or mecillinam did not respond as well as those treated with the other drugs.

Acute Disease↗
PubMed1988

Legionella pneumophila serogroup 14 isolated from patients with fatal pneumonia.

Two Legionella-like organisms, one isolated from postmortem lung tissue and the other from a bronchial aspirate, were shown by growth, physiologic, and genetic characteristics to belong to the species Legionella pneumophila. Subsequent serologic testing indicated that both strains belonged to a new serogroup, serogroup 14.

Bronchi↗
PubMed1987

Golgi galactosyltransferase contains serine-linked phosphate.

In HeLa and HepG2 cells the Golgi complex enzyme galactosyltransferase became phosphorylated following incubation with 32Pi-Analysis on sodium dodecyl sulphate/polyacrylamide gel electrophoresis revealed incorporation of 32P into the mature 54-kDa form. This phosphorylation was independent of protein synthesis. Serine was identified as the sole phosphorylated amino acid; no radioactive phosphate was detected on N-linked oligosaccharide. The phosphate-labelled galactosyltransferase has the same turnover as [35S]methionine-labelled polypeptides (t1/2 = 20 h). Soluble enzyme, released by the cells, contained very little phosphate relative to that which remained cell-associated. Charge heterogeneity arising from phosphorylation contributes in part to the heterodispersed appearance of the enzyme on two-dimensional gels, as the degree of radioactive phosphate differs among the different iso-enzymes.

Amino Acids↗
PubMed1987

Macrophage membrane interleukin 1 regulates the expression of acute phase proteins in human hepatoma Hep 3B cells.

To assess the potential role of membrane interleukin 1 (mIL-1) in modulating expression of acute phase proteins, we studied the effect of fixed mouse peritoneal macrophages and isolated cell membranes on the synthesis of C3 and albumin in human hepatoma Hep 3B cells. An increase in C3 synthesis and decrease in albumin synthesis were detected after incubation of Hep 3B cells with fixed stimulated macrophages or with membrane preparations. Estimates of hepatocellular C3 and albumin mRNA indicated that the mIL-1 regulation was exerted at a pretranslational level. The changes in C3 and albumin expression induced by mIL-1 were inhibited by addition of anti-interleukin 1 (IL-1) antiserum to the macrophages, supporting the hypothesis that a form of IL-1 is present on the outer cell membrane of macrophages. Moreover, cell-surface iodination of macrophages allowed the detection of a 33-kDa IL-1 molecule, suggesting that an IL-1 species, similar to the intracellular precursor of IL-1 is present at the outer cell surface of macrophages. The expression of mIL-1 was temporally dissociated from IL-1 release, indicating that the cell-surface associated IL-1 activity is not the result of adsorbed soluble IL-1. These studies provide a basis for further investigation of the role of mIL-1 in modulating monocytes and macrophages function via cell-cell interactions.

Acute-Phase Proteins↗
PubMed1987

Heterogeneity of antibody response in infection with Legionella pneumophila serogroup 1.

The antibody response of patients infected with Legionella pneumophila serogroup 1 in a common source outbreak was investigated. Heat-killed antigens from L pneumophila serogroups 1-3 and 6-10, plus several other strains of L pneumophila, together with 13 other species of legionellas were used in an indirect fluorescence antibody test. Formolised yolk sac antigens made from L pneumophila serogroups 1, 6, and 7 were also used. Although antibodies were produced to several L pneumophila serogroups or Legionella species by individuals, there was no constant pattern, suggesting that the response is a characteristic of the infected individual and not of the infecting strain of Legionella. There is evidence that heat-killed antigen made from L pneumophila serogroup 7 may give unreliable results.

Antibodies, Bacterial↗
PubMed1987

Rapid diagnosis of an outbreak of Legionnaires' disease at Glasgow Royal Infirmary.

In the last three months of 1985 there was an outbreak of legionnaires' disease at Glasgow Royal Infirmary affecting 15 patients and one surgeon; five patients died. Legionnaires' disease was first suspected when a second case of severe nosocomial pneumonia occurred in a high dependency unit. The application of the direct fluorescent antibody test to specimens obtained at bronchoscopy was responsible for the rapid diagnosis of legionnaires' disease, which led to the prescription of appropriate antibiotic treatment and the shutting down of the contaminated cooling tower, thereby containing the outbreak. It also led to a search for further cases. It is suggested that these diagnostic techniques should be included in the investigation of affected patients in an outbreak of pneumonia.

Aged↗
PubMed1987

Mechanism of the phorbol ester-mediated redistribution of asialoglycoprotein receptor: selective effects on receptor recycling pathways in Hep G2 cells.

We have investigated the effect of phorbol dibutyrate on intracellular routing of the asialoglycoprotein receptor (ASGP-R) in a human hepatoma cell line, Hep G2. We have previously shown that this agent causes a net redistribution of 50% of cell surface receptors to the cell interior (Fallon, R.J., and A.L. Schwartz, J. Biol. Chem. 261: 15081-15089 (1986)). To explore the mechanism of this effect, we measured the rate constants of receptor and ligand movement during internalization, ligand-receptor uncoupling, sorting of ligand to degradative sites or return to the extracellular medium, and return of receptor to the plasma membrane. The rate of internalization of bound asialoorosomucoid (ASOR) is identical in phorbol ester-treated and control cells, over a range of ASOR concentrations from 5 to 125 nM. The pathway of ligand recycling returns approximately 30% of internalized ASOR undegraded to the extracellular medium; phorbol esters do not modify the extent of this pathway in Hep G2 cells nor the kinetics of recovery of undegraded ASOR in the medium (t1/2 = 20 min). The rate of ligand-receptor uncoupling is similarly unaltered by phorbol esters, as measured by the amount of free ASOR that accumulates intracellularly and exits the cell after saponin permeabilization. In contrast, phorbol esters cause a rapid (less than 5 min) 50% decrease in receptor return to the cell surface from internal sites. This suggests that 1) phorbol esters interfere with selected specific sites in receptor and ligand pathways of receptor-mediated endocytosis and 2) the apparent net "internalization" of ASGP-R by phorbol esters results from an inhibition of receptor recycling to the cell surface and not from a direct stimulation of the internalization process.

Asialoglycoprotein Receptor↗
PubMed1986

Regulation by phorbol esters of asialoglycoprotein and transferrin receptor distribution and ligand affinity in a hepatoma cell line.

We have investigated the simultaneous regulation of cell surface distribution and ligand binding of the asialoglycoprotein (ASGP) receptor and the transferrin receptor in a hepatoma cell line by phorbol esters. One hour exposure to phorbol esters causes a redistribution of both receptors to the cell interior as shown by radioligand binding at 4 degrees C and selective immunoprecipitation from the plasma membrane. This effect is temperature- and dose-dependent and is not seen with 4-alpha-phorbol, an inactive tumor promoter. The mechanism and kinetics of the ASGP receptor response to phorbol esters appears to differ from that of the transferrin receptor in this cell line. Within the first 10 min there is a decrease in binding of iodinated ligands for both receptors to the HepG2 cell surface. For the transferrin receptor this results from a net internalization of receptor molecules from the plasma membrane pool, while for the ASGP receptor this decrease is accounted for by a 3.5-fold reduction in ligand binding affinity (6.6 X 10(-8) M to 24.0 X 10(-8) M), with essentially no change in the number of ASGP receptors recoverable from the plasma membrane pool by immunoprecipitation. The altered affinity of the ASGP-R is transient; the Kd returns to control levels by 20 min of continued exposure to the agent. The transferrin receptor shows no change in binding affinity during the course of exposure to phorbol esters. ASGP receptors in cells exposed to phorbol esters for 1 h maintain their competence to deliver exogenous ligand to intracellular sites of degradation and to participate in the recycling pathway of receptor-mediated endocytosis, although at a lower rate than in control cells. We conclude that under identical conditions phorbol esters modulate the binding capacity of two receptors at the cell surface by separate mechanisms. Furthermore, the transient nature of the altered ASGP-R binding affinity suggests that at least two mechanisms, receptor redistribution as well as decreased binding affinity, are operative in the modulation of ASGP-R cell surface binding during the first hour of exposure to the phorbol esters.

Asialoglycoprotein Receptor↗
PubMed1986

Outbreak of Legionnaires' disease in Glasgow Royal Infirmary: microbiological aspects.

The bacteriological investigation of an outbreak of Legionnaires' disease in Glasgow Royal Infirmary affecting 16 patients is described. Most of the patients had been treated in high-dependency areas on two floors of the hospital supplied by the same two air-conditioned ventilation systems. The source of infection was traced to contamination of a cooling tower from which a plume of spray discharged into the intake vents of the two ventilation systems. Rubber grommets within the cooling tower probably provided a nidus of infection there. The control and management of the outbreak are discussed: a policy of frankness about the course and progress of the investigations was adopted and helped to allay anxiety on the part of both staff and media.

Air Conditioning↗
PubMed1986

The Legionellaceae.

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Antibodies, Bacterial↗