[Pleural calcifications associated with exposure to asbestos dust detected by examination of microsamples with the polarizing microscope (apropos of 2 cases)].
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Biomedical subjects
Publications and source records attributed to J Bignon.
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In 9 healthy subjects and 22 patients with chronic obstructive disease, we computed total lung capacity (TLC) using an integrated flow pressure-corrected body plethysmograph. During panting manoeuvre, TLC derived from oesophageal pressure (TLCes) was compared to TLC derived from mouth pressure (TLCm). In healthy subjects, TLCm was identical to TLCes. Patients with obstructive disease exhibited different behaviours according to experimental conditions: a) in free frequency panting with mouth occlusion close to functional residual capacity (FRC) (9 patients), TLCm appeared to be significantly higher than TLCes (mean difference: 0.25 1; p less than 0.05); b) in panting with both low (less than 1 Hz) and high (2 Hz) frequencies and mouth occlusion close to FRC (7 patients), TLCm appeared to be significantly higher than TLCes only at a high frequency (p less than 0.05); c) in panting with both low and high frequencies and mouth occlusion close to TLC (6 patients), no significant difference was observed between TLCm and TLCes. These results suggest that in patients with chronic obstructive disease plethysmographic lung volume measurements are subject to error, due to the influence of extrathoracic airways. During occlusion at FRC, panting frequency was found to influence the results obtained, the error being minimized with low frequencies. In contrast, by occluding at TLC, we found that panting frequency was less likely to influence the results. However, potential sources of error still exist: for instance, the influence of abdominal gas or the panting pattern.
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The purpose of this paper is to show the problems with family data collection in a pharmacogenetic study, the aim of which was to study the genetic polymorphism of inducibility of cytochromes P4501A by polycyclic aromatic hydrocarbon (PAH). Data were collected from 76 smoker nuclear families (315 volunteers). A caffeine test, a blood sample and answers to a questionnaire were obtained from each healthy volunteer. It was a crucial problem to recruit nuclear families with healthy smoker father and/or mother and 2 smoker children. On 127 answers, 22 families were not eligible, 27 refused and 10 had a single child, that meant secondary refusals. Problems differed with origin of the recruitment. Included were 40 families obtained from 3 antismoking outpatient departments, 29 from general practitioners but 6 only from students. The family rates with 2 parents/2 children were significantly higher with general practitioners (p < 0.01). This emphasized their part in epidemiologic studies. Problems with the use of methodology were bound to acceptability of the tests which were better in females (p < 0.05), and a change in caffeine form could improve this acceptability. Lastly, difficulties with laboratories constraints required a very good coordination between families, nurses and laboratories.
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The severity and type of clinical manifestations are variable in patients with cystic fibrosis (CF). The respiratory syndromes in these patients consist of lung infections associated with disseminated bronchiectasis (DB), asthma, and chronic obstructive pulmonary disease. To investigate the possible involvement of the cystic fibrosis transmembrane conductance regulator (CFTR) gene in chronic pulmonary disease in adults, we studied 32 DB patients with a clinically isolated respiratory syndrome. Careful analysis of all the CFTR gene exons and their flanking regions revealed a significantly increased frequency of CFTR gene mutations in these patients. Thirteen CFTR gene mutations were identified in sixteen different alleles. Six of these mutations, which have previously been reported as CF defects, were found on nine alleles. A further four, two of which had not previously been described (D192N and 406-2 AdeltaC), are potentially disease-causing mutations. We also identified three rare substitutions (R31C, L997F, T1220I), which could be involved in mild CFTR gene disease. Four patients were compound heterozygotes, one carried two CFTR gene mutations (possibly allelic) and six were heterozygous for a mutation. These results indicate that CFTR gene mutations may play a role in bronchiectatic lung disease, possibly in a multifactorial context. These findings have implications for genetic counselling of DB patients and their families.
Typically, the functional abnormalities in individuals exposed to asbestos dust take the form of a pulmonary fibrosis. Recently, several authors have stressed the early existence of small airways obstruction. In the present study, by measurement of closing volume, we have confirmed an obstructive factor in a certain number of exposed subjects, even if they were non-smokers, i.e. had no other apparent reason for small airways disease.
The authors study three groups of subjects with different exposures to asbestos dust. The lung content in asbestos fibres is measured by optical and electron microscopy, the latter technique revealing preferential concentration of asbestos fibres in the peripheral zones of the lung, in particular in individuals subject to a moderate degree of professional exposure.