PubMed Health⌕ Search

Biomedical subjects

J Felber

Publications and source records attributed to J Felber.

5 recordsLinked to original sources
PubMed2004

Airway inflammation in children with tracheostomy.

We hypothesised that long-term tracheostomy in infants and children may perpetuate chronic airway inflammation and airway remodeling due to easier access to the lungs for microorganisms. Pulmonary surfactant represents an important part of the initial host defense, and in particular, the surfactant proteins (SP) A and D may directly interact with invading microorganisms and also modulate the activity of local immune cells. The goals of this study were to determine the presence and intensity of a peripheral airway inflammation and of potential deficiency states of surfactant proteins in nonsymptomatic children with tracheostomy. Bronchoalveolar lavage (BAL) cell pattern, bacteria and viruses recovered, and concentrations of SP-A, SP-B, SP-C, and SP-D were assessed in 46 children (4.3 years (1.6-6)) median (range) carrying a tracheostomy for 2.4 years (1.3-4.9), and were compared to 16 children with no lung disease. Children with tracheostomy had an increased total number of cells, increased neutrophils, and more frequently bacteria, but no viruses were recovered. SP-D concentration was reduced by 50% on average (P = 0.0002). SP-A, SP-B, and SP-C were not different between the two groups. SP-D was inversely correlated to neutrophils, and high numbers of bacteria were associated with lower SP-D concentrations. We suggest that bacteria and low SP-D support neutrophilic inflammation in the lower respiratory tract of nonsymptomatic with children with tracheostomy.

Bronchoalveolar Lavage↗
PubMed1986

Effect of trestatin, a new inhibitor of pancreatic alpha-amylase, on starch metabolism in man.

The effect of two doses (3 mg and 10 mg) of the inhibitor of pancreatic alpha-amylase trestatin on the metabolism of an oral load of 75 g of starch was observed in healthy human subjects. The mean elevation of plasma glucose over the 4 h following the load was markedly reduced both with 10 mg (mean +/- s.e.m.: 1.4 +/- 1.2 mg/dl) and with 3 mg of trestatin (7.2 +/- 2.0 mg/dl) when compared to placebo (19.5 +/- 5.1 mg/dl) (P less than 0.01 in both cases). The mean elevation of plasma insulin was decreased with both 10 mg (mean +/- s.e.m.: 1 +/- 1 microU/ml) and 3 mg of trestatin (6 +/- 2 microU/ml) when compared to placebo (20 +/- 4 microU/ml) (P less than 0.01 in both cases). Suprabasal glucose oxidation, measured by indirect calorimetry, was markedly decreased by trestatin (mean +/- s.e.m.: 2.5 +/- 1.1 g/4 h with 10 mg of trestatin versus 12.0 +/- 2.0 g/4 h with placebo, P less than 0.001). To examine whether trestatin had any action on alpha-1-4 glycosidase activity, an oral load of 100 g sucrose together with either 50 mg trestatin or with a placebo was administered to four healthy human subjects. Trestatin was observed to have only few effects on plasma glucose and insulin levels following sucrose ingestion. This suggests that its main site of action is at the alpha-amylase level. Breath hydrogen was shown to increase after ingestion of starch plus trestatin at the two doses studied. It is concluded that trestatin is a powerful inhibitor of pancreatic alpha-amylase which could be of great help in the dietary management of diabetic patients.

Adult↗