A tin dioxide (SnO 2) sensor was fabricated by inkjet printing onto polyimide foil. Gold electrodes and heater were printed on each side of the substrate. A SnO 2 based ink was developed by sol-gel method and jetted onto the electrodes. A final annealing at 400°C compatible with the polymeric transducers allowed to synthetize the SnO 2 sensing film. Electrical measurements were carried out to characterize the response of the fully printed sensors under oxidizing and reducing gases. The device was heated up at a temperature between 200 and 300°C using the integrated heater. The proper operation of the full printed metal-oxide gas sensors was validated under exposure to carbon monoxide and nitrogen dioxide, in dry and wet air.

We recommend performing AFB smears and cultures in CF children with severe lung disease and/or during a lung exacerbation. In these patients persistence of M. chelonae or M. abscessus in sputum should lead to consideration of treatment with clarithromycin.

To cite this version:Guy Tournier, Christophe Pijolat. Selective filter for SnO2 based gas sensors: application to hydrogen trace detection. Sensors and Actuators B: Chemical, Elsevier, 2005, 106 (2), pp.553-562.

The commonly held belief that adult onset wheezing illness is primarily nonatopic in nature suggests that the role of atopy in the pathophysiology of bronchial hyperresponsiveness (BHR) in adult onset wheeze may be minimal.This study examined risk factors for BHR (BHR: provocative dose causing a 20% fall in forced expiratory volume in one second PD20 #16.38 mmol methacholine) among 82 subjects with adult onset wheeze and among 191 subjects who had never wheezed. Subjects were identified from a cohort of subjects aged 39±45 yrs who were known to have had no childhood wheeze and who were involved in a 30 yr follow-up survey. Risk factors for BHR were examined among all subjects with BHR and among subjects with BHR stratified according to whether or not they had ever wheezed.The prevalence of BHR was 40% (33/82) among the subjects with adult onset wheeze and 11% (21/191) among the subjects who had never wheezed. Lower baseline lung function (odds ratio (OR) = 0.94; 95% confidence interval (CI) = 0.92±0.97 per unit forced expiratory volume (FEV1)% predicted) and atopy (OR = 7.23; Cl = 2.53± 20.64 for all three measures of atopic compared to nonatopic) were associated with BHR, while smoking and family history showed no statistically significant relation to BHR. This pattern was also apparent in analyses stratified by symptom status. A family history of atopy increased the risk that BHR was accompanied by wheezing symptoms (OR = 4.75; CI = 1.53±14.72 for more than one affected relative compared to no affected relatives).These findings suggest that atopy is associated with bronchial hyperresponsiveness in adults known to have had no childhood wheeze. A familial factor reflecting genetic influences and/or shared environmental factors may influence whether bronchial hyperresponsiveness is associated with symptoms. Eur Respir J 1999; 14: 335±338.

The commonly held belief that adult onset wheezing illness is primarily nonatopic in nature suggests that the role of atopy in the pathophysiology of bronchial hyperresponsiveness (BHR) in adult onset wheeze may be minimal.This study examined risk factors for BHR (BHR: provocative dose causing a 20% fall in forced expiratory volume in one second PD20 #16.38 mmol methacholine) among 82 subjects with adult onset wheeze and among 191 subjects who had never wheezed. Subjects were identified from a cohort of subjects aged 39±45 yrs who were known to have had no childhood wheeze and who were involved in a 30 yr follow-up survey. Risk factors for BHR were examined among all subjects with BHR and among subjects with BHR stratified according to whether or not they had ever wheezed.The prevalence of BHR was 40% (33/82) among the subjects with adult onset wheeze and 11% (21/191) among the subjects who had never wheezed. Lower baseline lung function (odds ratio (OR) = 0.94; 95% confidence interval (CI) = 0.92±0.97 per unit forced expiratory volume (FEV1)% predicted) and atopy (OR = 7.23; Cl = 2.53± 20.64 for all three measures of atopic compared to nonatopic) were associated with BHR, while smoking and family history showed no statistically significant relation to BHR. This pattern was also apparent in analyses stratified by symptom status. A family history of atopy increased the risk that BHR was accompanied by wheezing symptoms (OR = 4.75; CI = 1.53±14.72 for more than one affected relative compared to no affected relatives).These findings suggest that atopy is associated with bronchial hyperresponsiveness in adults known to have had no childhood wheeze. A familial factor reflecting genetic influences and/or shared environmental factors may influence whether bronchial hyperresponsiveness is associated with symptoms. Eur Respir J 1999; 14: 335±338.

Burkholderia cepacia, Stenotrophomonas maltophilia, and Alcaligenes xylosoxidans have been isolated with increasing frequency from the sputum of patients with cystic fibrosis in a pediatric hospital. In 1994-95, 27 of 120 patients were persistently colonized, 17 with Burkholderia cepacia, eight with Alcaligenes xylosoxidans, and five with Stenotrophomonas maltophilia. Genotyping of 220 clinical isolates revealed that most of the Burkholderia cepacia strains were clonally related, suggesting either cross-infection or a common source of exposure. In contrast, neither cross-infection nor a common source of exposure appear to have occurred in the cases of Alcaligenes xylosoxidans or Stenotrophomonas maltophilia.

Progression of pulmonary sarcoidosis in children remains poorly documented. The aim of this work was to gather follow-up information on pulmonary outcomes in children with sarcoidosis and to obtain data of relevance to a discussion of the optimal length and regimen of glucocorticoid therapy.In the present study, the authors experience of pulmonary sarcoidosis in 21 children referred to the paediatric pulmonary department over a 10-yr period is reported with a documented follow-up of at least 4 yr. Evaluation of the disease during the follow-up included analysis of clinical manifestations, chest radiographs, pulmonary function tests with measurements of the vital capacity (VC), dynamic lung compliance (CL,dyn), lung transfer for CO (TL,CO), and arterial blood gases, as well as bronchoalveolar lavage (BAL) with determination of total and differential cell counts.After initial evaluation the decision was a careful observation of four children without therapy. Corticosteroid treatment was initiated in 17 children. Analysis of results indicated that after 6±12 months of treatment most clinical manifestations of the disease and chest radiograph abnormalities disappeared, and bene®cial effects on VC and TL,CO were apparent. After 18 months of steroids no bene®t on pulmonary function tests could be noticed, with mainly persistence of alterations of CL,dyn. Results of BAL studies documented the presence of an alveolitis with increased lymphocyte populations throughout the follow-up. Relapses were observed in four children during tapering of prednisone; they were not reported after discontinuation of steroid therapy.Taken together data obtained in the presented population can lead to the following suggestions for the management of pulmonary sarcoidosis in children. BAL should be performed at the initial evaluation to document alveolitis; however, nothing seems to be gained from repeating this investigation during follow-up in the absence of speci®c reasons. Once the decision to initiate glucocorticoid therapy is made, 18 months may be a reasonable treatment duration. Discontinuation of therapy can be decided even if the pulmonary function tests remain abnormal, but the child should then be carefully monitored for a relapse.

No abstract