Extended nitric oxide analysis may improve personalized anti-inflammatory treatment in asthmatic children with intermediate FENO50

Item does not contain fulltextExhaled nitric oxide (FENO) is elevated in asthma, and a clinical practice guideline has been published with recommendations for anti-inflammatory treatment. It summarizes that a FENO at an expiratory flow rate of 50 ml s(-1) (FENO50) above 35 ppb in children indicates eosinophilic inflammation, and the most likely response is to use inhaled corticosteroids. Intermediate FENO50 between 20-35 ppb should be interpreted cautiously. The aim of the study was to investigate this guideline in a small group of asthmatic children. Thirty-seven asthmatic children; 23 boys and 14 girls, visited the outpatient clinic, and provided exhaled breath samples for offline NO measurement. These samples were analysed with chemiluminescence techniques. Three flow rates, namely 16, 90 and 230 ml s(-1) were used for the extended NO analysis (Hogman-Merilainen algorithm, HMA) to estimate the alveolar concentration (CANO), diffusion rate of the airway wall (DawNO) and airway wall content (CawNO). For accuracy of the HMA, the estimated value of FENO at 50 ml s(-1) (FENO50) was compared with measured FENO50. In nine children the difference was more than 5 ppb and the data were therefore excluded. Five children with FENO50 35 ppb had an allergy and had FENO50 of 56 (47;60) ppb and CawNO of 140 (121;172) ppb. Thirteen children with allergies, with intermediate FENO50, had FENO50 of 27 (25;30) ppb with a wide range of CawNO. In five of these children, values were comparable to healthy children, 44 (43;50) ppb while eight children had elevated CawNO values of 108 (95;129) ppb. Our data indicate the clinical potential use of extended NO analysis to determine the personal target value of FENO50 for monitoring the treatment outcome. Furthermore, for children with intermediate FENO50 more than half of them could possibly benefit from an adjustment of inhaled corticosteroids if the CawNO value was considered

Pulmonary infection, and not systemic inflammation, accounts for increased concentrations of exhaled nitric oxide in patients with septic shock

Nitric oxide (NO) is a key mediator in the pathophysiology of septic shock that can be measured in exhaled breath. To assess whether a pulmonary infection itself or systemic inflammation is responsible for NO production, we determined exhaled NO in ventilated patients with respiratory and non-respiratory septic shock and compared it with the concentration in ventilated intensive care patients without systemic inflammation. In addition, the change of NO production over time and correlations with haemodynamic instability were evaluated. The controls without systemic inflammation, as witnessed by the absence of systemic inflammatory response syndrome criteria and low levels of interleukin-6, had similar concentrations of NO as the patients with non-respiratory septic shock. The respiratory sepsis patients exhaled more NO than the non-respiratory sepsis patients (p = 0.05), and a time dependent decline in time in both groups (p = 0.04). Exhaled NO did not correlate with markers of disease severity, systemic inflammation and haemodynamic instability. These data indicate that the infected lungs are the source of exhaled NO

Position de consensus de la Société Française de Médecine du Sport concernant la directive n° 000149 du 3 avril 2001 sur les épreuves d'effort des sportifs de haut niveau

Réflexions et prise de position de la S.F.M.S. à partir des données épidémiologiques concernant l'incidence de la mort subite sur les terrains de sport, les données épidémiologiques concernant la morbidité lors des tests d'effort, sur la pertinence de l'épreuve cardiologique chez le jeune sportif, sur la limite du dépistage dans l'ensemble de la population

Real-time monitoring of hydrogen cyanide (HCN) and ammonia (NH3) emitted by Pseudomonas aeruginosa

Item does not contain fulltextWe present the real-time monitoring of hydrogen cyanide (HCN) production from Pseudomonas aeruginosa (P. aeruginosa) strains in vitro, using laser-based photoacoustic spectroscopy. Simultaneously, the production of ammonia (NH3) was measured, and the influence of different factors (e.g. the medium, temperature and antibiotics treatment) was assessed. Both reference strains and clinical isolates of patients with CF were studied, and compared to other pathogens commonly present in lungs/airways of CF patients. Hydrogen cyanide production starts to rise as soon as P. aeruginosa bacteria reach the stationary phase ((9.0-9.5) x 10(9) colony forming units, CFUs), up to concentrations of 14.5 microliters per hour (microl h(-1)). Different strains of P. aeruginosa produced HCN to varying degrees, and addition of tobramycin strongly reduced HCN production within 2 h from application. Burkholderia cepacia also produced HCN (up to 0.35microl h(-1) in 9.0 x 10(9) CFU) while other pathogens (Aspergillus fumigatus, Stenotrophomonas maltophilia, Mycobacterium abscessus) did not produce detectable levels. Our study reveals for the first time a broad overview of the dynamics of the HCN production in vitro

Dynamic changes of the ethylene biosynthesis in 'jonagold' apple

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