The anionic sites on podocytes were decreased in number in the AHN rats; however, the distributions of anionic sites on the GBM were similar in density to those seen in the control animals. From these results, we consider that

the decrease in anionic charge density on podocytes might be attributable to protein leakage and that the charge barrier of the GBM is irrelevant to the protein leakage in AHN rats. (DOI: 10.1293/tox.26.11; J Toxicol Pathol 2013; 26: 11-17)”
“Objective: It is not known how airway structure is altered U0126 molecular weight during real-life acute asthma exacerbations. The aim of this study was to examine changes in airway structure during acute asthma exacerbations and at convalescence by using lung-volume controlled high resolution computerised tomography (HRCT). Methods: Eight subjects with acute asthma exacerbation admitted to hospital were recruited. HRCT was performed within 72 h of admission (n = 8) and repeated after 8 weeks of convalescence (n = 7). GSK3326595 solubility dmso Individual airways were carefully matched on acute and convalescent CT data sets for comparisons of airway parameters. A novel methodology was employed

for standardisation of lung volumes to permit valid comparisons of lung imaging. Measurements of bronchial cross sectional airway area (Aa) and bronchial luminal area (Ai) for each matched airway were find more obtained using a validated program. Results: The airway wall thickness was analysed as wall area (WA) calculated as a percentage: WA% = WA/Aa x 100. Wilcoxon signed-rank testing was used to compare acute and convalescent asthma and Spearman’s correlation to examine associations. Airway lumen (Ai) areas were similar in both acute and stable asthma phases (6.6 +/- 3.1 mm(2) versus 7.2 +/- 3.8 mm(2) p = 0.8). However, the airway wall was significantly thickened during acute asthma

exacerbations compared to convalescence (62 +/- 4% versus 55 perpendicular to 7%; p = 0.01). There was no correlation between airway structure dimensions and lung function measurements. Conclusions: This is the first study to demonstrate an increase in airway wall thickness during real-life acute asthma exacerbation. However, narrowing of the airway lumen area was variable and will require larger studies able to detect small differences. These results suggest that airway wall thickening linked to mucosal inflammation is likely to characterise acute asthma in vivo but that changes in the airway lumen accompanying bronchoconstriction may be more heterogeneous.