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Biomedical subjects

I Hall

Publications and source records attributed to I Hall.

At least 37 records · Page 2Linked to original sources
PubMed1995

Circulating human IgG autoanti-IgE antibodies in asthma patients block the binding of IgE to its high affinity receptor.

Aims-To investigate the ability of circulating human IgG autoanti-IgE antibodies from asthma patients to block the binding of IgE to the alpha chain of the high affinity receptor (FcepsilonRI).Methods-This involved the use of a well validated flow cytometric method to detect inhibition of FITC labelled IgE binding to a fibroblast cell line (CHK1E1) transfected with the alpha chain of FcepsilonRI.Results-IgG autoanti-IgE-containing sera blocked the binding of IgE-FITC to the CHK1E1 cells. No such inhibition was demonstrable with rheumatoid sera containing autoanti-IgG (that is, rheumatoid factor) but lacking autoanti-IgE. Percentage inhibition (up to 50%) of IgE binding to the CHK1E1 cells was directly related to the titre of IgG1, but not IgG4, autoanti-IgE in the sera tested (correlation coefficient 0.66, probability 0.003).Conclusions-The capacity of anti-IgE to block the binding of IgE to FcepsilonRI has important clinical implications, particularly in terms of downregulation of allergic reactions.

Journal Article↗
PubMed1994

Effect of 443c81, an inhaled mu-opioid receptor agonist in asthma.

Stimulation of exposed C-fibre afferent nerve endings by inflammatory mediators may contribute to airway inflammation and bronchoconstriction in asthma through the release of neuropeptides from collateral nerve endings. The polar opioid peptide 443c81 is a mu-opioid receptor agonist which inhibits C-fibre activation and non-cholinergic neurally mediated bronchoconstriction in animal models. We have compared the effect of 443c81 (5 ml of a 4 mg/ml solution nebulized) four times daily for 7 days with placebo on asthma control in a double-blind parallel group study of 40 subjects with mild asthma. Twenty subjects (12 male, mean FEV1 83% predicted) received placebo and 20 (15 male, mean FEV1 91% predicted) 443c81 after a 1 week run-in. Efficacy was assessed by comparing changes from baseline values in FEV1, provocative dose of histamine causing a 20% fall in FEV1 (PD20), symptom scores, bronchodilator use and home peak flow readings. 443c81 had no acute effect on FEV1 and the mean changes in FEV1 after 1 week of treatment were not significantly different (placebo -0.9%; 443c81-3.8%). One hour after the first dose of 443c81 PD20 increased from a geometric mean of 0.88 to 1.48 mumol (mean change 0.76 doubling doses; 95% CI 0.23, 1.29) but this did not differ significantly from the change with placebo (mean difference between 443c81 and placebo 0.63 doubling doses; 95% CI -0.2, 1.5; P = 0.095). After 1 week's treatment, PD20 was similar to baseline values with 443c81 (0.78 mumol) and placebo (baseline 0.71, post-treatment 0.93 mumol).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1992

The effect of the enantiomers of ibuprofen and flurbiprofen on the beta-oxidation of palmitate in the rat.

The effects of the enantiomers of ibuprofen (0.25 and 0.50 mmol/kg b.w.) and flurbiprofen (0.01, 0.03, and 0.06 mmol/kg b.w.) on the beta-oxidation of palmitate were investigated in the rat. The mean cumulative exhalation of 14CO2 after ip administration of [U-14C]palmitic acid was significantly reduced over 6 h by ibuprofen at the higher dose but not at the lower dose for either enantiomer. There was no difference between the enantiomers, the reduction over 6 h being 31.3 and 33.0% for (R)- and (S)-ibuprofen, respectively. There was also a significant inhibition of beta-oxidation by flurbiprofen at all 3 doses. Again, there was no stereoselectivity evident in this inhibition. Flurbiprofen was much more potent than ibuprofen in eliciting this effect, the 0.01mmol/kg dose giving a similar reduction in beta-oxidation as observed for the 0.50 mmol/kg dose of ibuprofen. The data support the hypothesis that inhibition of the in vivo beta-oxidation of palmitate by ibuprofen and flurbiprofen is primarily via a nonstereoselective noncoenzyme A-dependent mechanism.

Animals↗
PubMed1986

Chronic dermal sinuses as a manifestation of histiocytosis X.

Two young patients presented with generalised lymphadenopathy, otorrhoea, otitis, and rash. Over the next few years chronically discharging sinuses began to form over enlarged nodes and histological appearances were typical of histiocytosis X. In neither case were micro-organisms isolated from the lesions, and in both patients healing occurred with immunosuppressive agents. Chronic dermal sinus formation secondary to lymph node disease has never before been recorded as a manifestation of histiocytosis X. Histiocytosis X should therefore be considered in the differential diagnosis of "suppurative" lymphadenopathy so that appropriate treatment may be given without delay.

Adult↗
PubMed1984

In vitro activity of ticarcillin plus clavulanic acid (BRL 28500, 'Timentin') against ticarcillin-resistant gram-negative rods.

A study was carried out to investigate the in vitro susceptibility of 211 clinical isolates of ticarcillin resistant (MICs greater than 128 micrograms/ml) Gram-negative rods to a combination of ticarcillin plus clavulanic acid. The combination demonstrated superior activity; 90% of the Proteus spp. and 50% of E. coli and Klebsiella spp. isolates were inhibited at a concentration of 64 micrograms/ml. It was 2 to 8-times more active than ticarcillin alone against E. coli, Proteus and Klebsiella spp. in half to three-quarters of the strains under test. This enhanced activity was only marginal, however, against Enterobacter, Acinetobacter, Citrobacter, Serratia and Pseudomonas spp. Against 161 ticarcillin sensitive strains the combination did not have any potentiation effect.

Clavulanic Acid↗
PubMed1983

Comparative in vitro activity of ticarcillin, piperacillin, azlocillin and mezlocillin.

The in vitro activity of ticarcillin, piperacillin, azlocillin and mezlocillin was determined against 403 clinical isolates. At MIC50, piperacillin was 2 to 8 times more active than the other three compounds against Pseudomonas, Escherichia coli, Proteus, Citrobacter, Acinetobacter and Salmonella species. Against Klebsiella, Enterobacter, Haemophilus, Bacteroides spp. and non-beta-lactamase producing Staphylococcus aureus the activity of piperacillin was similar to one or more of the most effective agents. However, azlocillin and mezlocillin were more active than piperacillin against enterococci. Ticarcillin was the least active in vitro. Despite these significant differences at MIC50 amongst the four compounds, they became much less discernible at MIC90, obviously due to beta-lactamase producing strains under study. The spectrum of activity of piperacillin encompasses those of azlocillin and mezlociLlin together except for Gram-positive organisms.

Azlocillin↗