Biomedical subjects
Publications and source records attributed to A Lurie.
Interaction between macrolides and theophylline has given rise to numerous studies which are reviewed in this paper. The results of these studies are often conflicting. When such interactions occur, the question is whether they have clinical significance.
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This article describes a recent study of how social work staff in a large medical center spend their time--the tasks and activities performed regularly. The value of this kind of study, especially as a first step in the development of a comprehensive quality assurance program for a department of social work services, is discussed.
Health care delivery systems are under careful and systematic scrutiny. Particular concerns are the availability and access of health care to those in the lower and middle income groups and the escalating costs of health care which until quite recently have exceeded annual inflationary rates of increase. Efforts in social work in the health field have reflected these developments. Programmatic trends in health and social work now emphasize ambulatory care and are reflected in the concept of primary care medicine. Deinstitutionalization as a preferred program for patients is under review with particular emphas -is on providing adequate supportive services to maintain patients in a home care environment. Social work is a major discipline contributing to these programs through appropriate interventive measures. Moreover, the role of the social worker, because of involvement with front line community activities, is particularly suited to make a substantial contribution to this trend.
Lung function tests must distinguish a true drug-induced bronchial response from changes not related to the drug itself, mainly due to intra-individual variability. We compared the variability and ability to detect true drug-induced bronchodilation of 3 modes of expression of the increase in forced expiratory volume in 1 second (delta FEV1) following administration of a 0.25 mg single oral dose of RU 42 173, a new beta 2-agonist. The study was performed in 12 patients with reversible obstructive asthma in a double-blind, crossover, placebo-controlled, randomized manner. The variability of each index was assessed by calculating the coefficient of variation (SD/mean). True drug-induced bronchodilation was assessed by calculating the F value of each index corresponding to the ratio of between-treatment to within-group differences. Three modes of expression of delta FEV1 were compared: delta FEV1 (L) = the absolute increase in FEV1, delta FEV1 (% baseline) and delta FEV1 (% predicted) where delta FEV1 (L) is divided by baseline FEV1 or predicted FEV1, respectively. A statistically significant increase in FEV1 was found up to respectively 3, 2 and 4 hours after dosing when using delta FEV1 (L), delta FEV1 (% baseline) and delta FEV1 (% predicted). The highest F value was obtained for delta FEV1 (% predicted). The coefficient of variation was lower with delta FEV1 (% predicted) than delta FEV1 (L) and delta FEV1 (% baseline). In conclusion, RU 42 173 showed a bronchodilating effect which appears to be clinically relevant. delta FEV1 (% predicted) was to be the least variable and most powerful index and should be preferred to delta FEV1 (L) and even more to delta FEV1 (% baseline) to assess the acute airway response to a bronchodilator drug.
The pulmonary toxicity of antineoplastic drugs may be either direct or mediated by hypersensitivity. The aim of this study was to determine whether the mechanism by which cyclophosphamide (CY) damages the lung is direct and immediate or is the result of delayed immune toxicity. Pulmonary and immune changes following intraperitoneal injection of either CY (50 mg/kg) or NaCl (0.9%) in rats were assessed repeatedly over a period of 31 days by semi-quantitative histological studies, by measuring the pulmonary water/body weight ratio, dry lung weight/body weight ratio, heart weight and by assessing the transfer of [125I]-albumin in lung tissue. Lung damage was delayed and greatest at 11 (D11) and 14 (D14) days after CY injection. The pulmonary lesions were: (i) an infiltration of lymphocytes, plasma cells and histiocytes surrounding blood vessels and small airways, (ii) an alveolitis composed of macrophages, lymphocytes, a few neutrophils and a lymphoid infiltration of alveolar septa. Pulmonary water/body weight and dry lung weight/body weight ratios also increased and peaked at D11-D14 in CY-treated rats. No significant increase in [125I]-albumin in lung tissue or in heart weight was observed. It can be concluded that the mechanism by which CY induces a lymphoid lung infiltration is not direct and immediate but is the result of a delayed immune toxicity.
Paf-acether, whose role has been suggested in asthma, is a mediator released by stimulated neutrophils, platelets and other cells. Neutrophils and platelets are activated in vivo during exercise or allergen-induced asthma. Upon in vitro stimulation, macrophages from mice treated with an inflammatory stimulus, such as thioglycoccollate, release less paf-acether than macrophages from non-treated mice. We hypothesized that upon in vitro activation platelets and neutrophils should produce less paf-acether after exercise- or allergen-induced asthma. To test this hypothesis, we measured the production of paf-acether by neutrophils and platelets obtained before, 15 and 75 min after exercise in seven normal subjects and five asthmatic subjects with exercise-induced asthma, and in five other asthmatic subjects after specific challenge with Dermatophagoides Pteronyssinus. Purified neutrophils and washed platelets were incubated independently for 10 min at 37 degrees C with no specific activator, with a platelet activator (thrombin, 1 IU.ml-1), a neutrophil activator (opsonized zymosan, 1 mg.ml-1), and both together. We found no significant difference between asthmatic and normal subjects in the amount of paf-acether synthesized by platelets or neutrophils and no fall in the production of paf-acether after exercise- or allergen-induced asthma. However, our method may lack sensitivity in detecting partial activation of these cells and is based on the assumption that changes in peripheral blood cells are representative of changes of these cells in lungs.
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