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Biomedical subjects

J K Greenacre

Publications and source records attributed to J K Greenacre.

15 recordsLinked to original sources
PubMed1993

Chronic beryllium disease in a dental laboratory technician.

Workers involved in the manufacture of dental prostheses are exposed to a number of potentially harmful substances capable of inducing lung disease. In this report, we describe a dental laboratory technician who developed chronic beryllium disease as a result of exposure in the workplace. The diagnosis of chronic beryllium disease was suspected from the clinical, radiographic, and histologic features and confirmed by the in vitro proliferation of lung lymphocytes to beryllium salts. The potential risks of beryllium use in the dental industry have been recognized for some time, but this is the first documentation of chronic beryllium disease in this population of workers. Since chronic beryllium disease may be easily confused with sarcoidosis, awareness of this occupational association is essential in preventing misdiagnosis and in providing appropriate management.

Adult↗
PubMed1979

Comparison of four weeks' treatment with fenoterol and terbutaline aerosols in adult asthmatics. A double-blind crossover study.

Fenoterol and terbutaline, two long-acting beta 2-adrenoceptor agonists in aerosol form, were compared in an 8-wk randomized double-blind crossover study in 22 mild to moderately severe asthmatics. Patients completed diary cards, recorded peak expiratory flow rate (PEFR) twice daily, and attended a clinic for measurement of PEFR, 1-sec forced expiratory volume (FEV1), and forced vital capacity (FVC) twice during each treatment period. Fifteen patients completed the study; 5 dropped out while using fenoterol, and 2 while using terbutaline. At clinic attendances, the patients had a significantly higher mean PEFR after 4 wk on terbutaline (385 L/min) than after fenoterol (316 L/min) (p less than 0.001). Similar results were found on analysis of the morning and evening PEFR recordings. On comparing each individual's PEFR recordings during the 2 treatments, it was found that there was no significant difference among the treatments in 3 patients, while 9 patients had a better response to terbutaline, and 3 patients had a better response to fenoterol. While similar number expressed a subjective preference for each treatment, the lung function data suggested that the effectiveness of fenoterol appeared to decline during the trial period.

Adult↗
PubMed1978

Use of exercise challenge to investigate possible tolerance to beta-adrenoceptor stimulation in asthma.

The effect of prolonged salbutamol administration on beta-adrenoceptor function in asthma has been examined. Six adult patients received salbutamol tablets (16 mg daily) for between 4 and 20 weeks and six adolescents received salbutamol aerosol (800 microgram daily) for 2--5 weeks. Before and after the treatment period the acute bronchodilator response to inhaled salbutamol and the ability of inhaled salbutamol to protect against exercise-induced asthma were examined. Lymphocyte beta-adrenoceptor function was also measured in the patients on tablet therapy. Inhaled salbutamol was less effective in protecting against exercise-induced asthma at the end of the treatment period in the patients who had received tablet therapy, but otherwise there was no significant change in beta-receptor function of either airways or lymphocytes. This apparent loss of efficacy of inhaled salbutamol in the prevention of exercise-induced asthma in some subjects, even when its acute bronchodilator effect is preserved, might reflect differences in the susceptibility of different beta-adrenoceptors to desensitization after prolonged stimulation: its clinical importance remains uncertain.

Adolescent↗
PubMed1978

Desensitization of the beta-adrenoceptor of lymphocytes from normal subjects and patients with phaeochromocytoma: studies in vivo.

1 Following the observation that lymphocyte beta-adrenoceptor responsiveness was not depressed in asthmatics treated only with non-adrenergic drugs we have explored the effects of prolonged exposure to beta-adrenoceptor agonists in normal subjects. 2 Treatment with oral salbutamol (12-16 mg/kg/day for 10 days), or with inhaled salbutamol (3000 microgram/day for 8-10 days) resulted in a significant reduction in lymphocyte beta-adrenoceptor responsiveness. 3 A 48 h infusion of isoxsuprine (10 mg/h) resulted in a marked depression of lymphocyte beta-adrenoceptor responsiveness (P less than 0.001). 4 Prolonged elevation of endogenous catecholamines caused by phaeochromocytoma was also associated with a marked depression of lymphocyte beta-adrenoceptor responsiveness (P less than 0.001). 5 There was no evidence that an increase in phosphodiesterase activity could explain the reduced cyclic AMP response. 6 It is concluded that diminished beta-adrenoceptor response occurs as a response to prolonged exposure to beta-adrenoceptor agonists. It is likely that the diminished response seen in asthmatic subjects can be explained on a similar basis and does not indicate an inherent cellular defect. 7 The possible clinical significance of such changes in asthmatics are discussed.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1978

Desensitization of the beta-adrenoceptor of lymphocytes from normal subjects and asthmatic patients in vitro.

1 A lymphocyte culture method has been developed for studying in vitro the effect of prolonged exposure (24 h) to isoprenaline (10(-8) to 10(-6) mol/l) and prostaglandin E1 (PGE1; 2.8 x 10(-6) mol/l). 2 The cyclic AMP response to isoprenaline is reduced by prolonged exposure to isoprenaline. The degree of desensitization is in proportion to the concentration of isoprenaline in the culture medium. 3 Culture with isoprenaline does not reduce the cyclic AMP response to PGE1. 4 Culture for 24 h with PGE1 (2.8 x 10(-6) mol/l) reduces the cyclic AMP response to PGE1. It also significantly reduces the response to isoprenaline. 5 Lymphocytes from asthmatic patients show a similar degree of desensitization to isoprenaline (after 24 h culture with isoprenaline) to that seen in lymphocytes from normal subjects. 6 A modified assay for phosphodiesterase (PDE) activity was developed. PDE activity increased 24.5% (P less than 0.02) after culture with PGE1 but was not significantly affected by culture with isoprenaline. 7 It is concluded that desensitization caused by prolonged exposure to various stimulators of adenylate cyclase is an event dependent on several components, not all of which are yet defined.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1977

The beta-adrenoceptor of the human lymphocyte and human lung parenchyma.

1 The response of the beta-adrenoceptors of human lymphocytes to selective agonists and antagonists has been studied quantitatively by measuring changes in cyclic adenosine-3',5'-monophosphate (cyclic AMP) levels. 2 The receptor was activated by isoprenaline and by salbutamol, and blocked by propranolol but not by practolol. A similar pattern of response was obtained with fragments of human lung tissue. 3 The mean value for pA2 for propranolol was 8.34 and for practolol was 3.95. 4 These findings indicate that the lymphocyte beta-adrenoceptor is a beta2-receptor and support the solidity of using lymphocytes to study beta-adrenoceptor function in bronchial asthma. It may also be of use in the evaluation of selective beta2-blocking drugs in man.

Albuterol↗
PubMed1976

Comparison of levodopa with carbidopa or benserazide in parkinsonism.

The therapeutic efficacy and side-effects of two preparations of levodopa with extracerebral decarboxylase inhibitors have been compared in 19 patients with idiopathic parkinsonism in a blind randomised crossover trial. The mean daily dose of levodopa was 658 +/- 64 mg/day (mean +/- S.E.M.) when given together with carbidopa 66 mg/day and 605 +/- 59 mg/day when levodopa was combined with benserazide 151 mg/day. There was no significant difference between the treatment regimens either in beneficial effects on parkinsonian symptoms and signs or in the adverse effects of levodopa assessed by a clinical observer unaware of the treatment given. Of the 19 patients studied, 9 preferred the carbidopa preparation, 8 preferred the benserazide preparation, and 2 had no preference. It is concluded that there is no significant difference in therapeutic effects or adverse reactions between the two commercially available decarboxylase inhibitor-containing preparations. Central-nervous-system actions and side-effects depend on the daily dose of levodopa, regardless of the different ratios of decarboxylase inhibitors to levodopa.

Aged↗
PubMed1976

The lymphocyte beta-adrenoceptor in normal subjects and patients with bronchial asthma: the effect of different forms of treatment on receptor function.

beta-Adrenoceptor function has been compared in lymphocytes of normal subjects, asthmatic patients taking large doses of beta-adrenergic bronchodilators, and comparable asthmatics treated exclusively with nonadrenergic medication. The effect of prolonged administration of beta-adrenoceptor agonists on receptor function in normal subjects has also been examined. beta-receptor response in each situation was quantitated by changes in levels of cyclic AMP, measured by a protein-binding assay. Dose response curves to isoproterenol (10 nM-0.1 mM) have been constructed for each group. Maximal increase in cyclic AMP in lymphocytes from normal subjects (393.2+/-44.0%) and in asthmatics on nonadrenergic preparations (408.3+/-46.7%) was significantly greater (P less than 0.001) than in asthmatics taking large doses of beta-sympathomimetics (67.5+/-24.2%). Depression of the cyclic AMP response appeared to correlate with the degree of exposure to beta-adrenergic agonists but not with the prevailing severity of the patient's asthma. Withdrawal of beta-adrenergic drugs was followed by a reversion of the cyclic AMP response to normal values, which suggests that the depression was drug-induced rather than an inherent feature of the disease. This interpretation was confirmed by the finding that prolonged exposure of normal subjects to high doses of a beta-adrenergic agonist caused a marked and significant (p less than 0.001) reduction in the cyclic AMP response, very similar to that seen in asthmatics on large doses of adrenergic bronchodilators. A possible link between drug-induced changes in the cyclic AMP response and the rise in the United Kingdom asthma death rate in the 1960's is discussed.

Adolescent↗
PubMed1975

Idiopathic parkinsonism treated with bromocriptine.

The efficacy and toxicity of bromocriptine, a drug which simulates dopamine, have been studied in twenty-eight patients with idiopathic parkinsonism. A double-blind, within-patient comparison between maximum tolerated doses of bromocriptine (mean 46-9 mg daily) and placebo revealed a substantial and statistically significant therapeutic response to the active drug. Adverse reactions were dose dependent, reversible, and similar to those encountered with levodopa. While taking bromocriptine fourteen patients were able to stop levodopa (with or without carbidopa); in five patients the dose of levodopa was reduced by 54% (mean). Eight patients could not tolerate bromocriptine; one patient failed to comply with prescribed adjustments of dosage.

Aged↗
PubMed1974

Bromocriptine in Parkinsonism.

Bromocriptine, a drug acting directly upon dopaminergic receptors, has been found to have a significant therapeutic action in a double-blind study of 20 patients with idiopathic Parkinsonism who were already receiving conventional therapy, including levodopa. Neurological deficits improved by almost 20% in severely disabled patients; amelioration of mildly affected patients was about 10%. Adverse reactions were similar to those encountered with levodopa-they were all dose-dependent and reversible. These observations are discussed in relation to certain theoretical advantages which might be expected from a drug which acts directly on dopaminergic receptors.

Aged↗