Monitoring flow rates and retention of inhalation techniques using the in-check dial device in adult asthmatics.

The In-Check-Dial (Alliance Tech Medical, Granburg, TX) was used to determine adequacy of inhalation techniques and teaching of two different devices. Retention of adequate techniques, was assessed in 234 moderate to severe asthmatics. Inhalation techniques were assessed at periodic follow-ups divided into less than 1 month return visit, between 1 and 3 months, 3 to less than 6 months, and 6 months to less than 1 year.

Etiology of decreased gastric nitric oxide in the critically ill.

Background: Nitric oxide (NO) is present in the gas phase of the normal human stomach at a high concentration (1-10 ppm). The majority of this NO is produced from the reduction of dietary nitrate to nitrite and finally NO. Generation of this nonenzymatically produced gastric NO occurs only in an acidic environment.

Exhaled nitric oxide and bronchial wall thickening in asthmatics during and after acute exacerbation: evidence of bronchial wall remodeling.

To assess whether bronchial wall thickening during asthma exacerbations is due to active inflammation in severe asthmatics, we measured bronchial wall thickness and exhaled nitric oxide (FeNO) following treatment. Nine asthmatics were compared with seven controls with high-resolution computed tomography, spirometry, and FeNO measurements. The asthmatic bronchial wall area percent and FeNO was greater than controls.

Exhaled nitric oxide predicts asthma exacerbation.

The fraction of exhaled nitric oxide (FeNO) is elevated in asthmatics compared to normal subjects. Many studies have demonstrated that FeNO correlates with other markers of airway inflammation. The purpose of this study was to assess the clinical utility of routine monitoring of FeNO in determining its ability to predict future asthma exacerbations compared with other standard clinical measures of spirometry, peak flows, quality of life score, medication usage, and symptoms.

TNF-alpha-induced increase in intestinal epithelial tight junction permeability requires NF-kappa B activation.

Crohn's disease (CD) patients have an abnormal increase in intestinal epithelial permeability. The defect in intestinal tight junction (TJ) barrier has been proposed as an important etiologic factor of CD. TNF-alpha increases intestinal TJ permeability.

Regulation of CD23 in the chronic inflammatory response in asthma: a role for interferon-gamma and heat shock protein 70 in the TH2 environment.

Background: Monocytic cells and alveolar macrophages (AMs) are activated in patients with asthma, producing inflammatory cytokines. This occurs despite a TH2 environment that consists of the cytokines interleukin (IL) 4, IL-10, and IL-13. The mechanism by which this occurs may involve cross-linking of the low-alphaffinity IgE receptor CD23.