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R J Fallon

Publications and source records attributed to R J Fallon.

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

Explore the source record for details and available documents.

Antibodies, Bacterial↗
PubMed1985

Illness associated with a package holiday in Romania.

A study of 370 holidaymakers returning from Romania revealed that 279 (75%) reported illness. Alimentary symptoms predominated and were recorded either alone or along with other symptoms by 71 per cent of the tourists. The highest illness rate (82%) occurred in those under 39 years of age and those over 60 years had least illness (38%). Most of the tourists attributed their illnesses to the supply, handling or preparation of food and drink. Twenty-six (21%) tourists had serological evidence of typhoid immunisation out of 121 from whom blood samples were obtained. Most of the tourists studied (85%) were immune to poliomyelitis.

Adolescent↗
PubMed1984

Meningococcal infections in Scotland 1972-82.

Strains of Neisseria meningitidis isolated from patients with meningitis or septicaemia without meningitis in Scotland during the years 1972-82 have been reviewed together with details of the age, sex, disease and outcome of the patients from whom they were isolated. A total of 1185 strains were isolated, of which 927 were examined at the Meningococcal Reference Laboratory (Scotland): 19.3% were of serogroup A, 63% of group B, 9.6% of group C, 6% of W135 and 1.6% of other groups. Non-groupable strains were rare. Disease was most common in the first years of life but there was a difference in the age distribution of disease due to the different serogroups, the proportion of disease due to group B being smaller in adults than that due to other serogroups. The overall mortality in meningitis was 7.5% and in septicaemia was 20.6%, although there were differences between the rates for the various serogroups. The serogroup distribution differed in disease as opposed to meningococci isolated from carriers although group B strains were predominant in both series. Overall, approximately 15% of strains were resistant to sulphadiazine, the proportion of resistant group A strains being higher than that of other serogroups.

Adolescent↗
PubMed1983

Ano-genital gonorrhoea and pharyngeal colonisation with meningococci: a serogroup analysis.

Among patients attending a clinic for sexually transmitted diseases, women without gonorrhoea were significantly less likely to be colonised with meningococci than were women with gonorrhoea, men with gonorrhoea and men without gonorrhoea: the respective carriage rates (per cent) for groupable plus non-groupable meningococci were 16, 26, 23 and 31. Considering groupable and non-groupable meningococci separately it was found that women without gonorrhoea were also significantly less likely to be colonised with groupable meningococci but there were no significant differences in the carriage rates of non-groupable meningococci. The association between ano-genital gonorrhoea and meningococcal colonisation of the pharynx observed previously with certain groups of patients most likely results from increased mouth-to-mouth contact in 'high-risk' patients rather than individual susceptibility to neisserial infection. The possibility that there is a difference in the predominant means of spread of groupable and non-groupable meningococci is discussed.

Anus Diseases↗