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Pulmonary Emphysema (pulmonary + emphysema)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Cellular and molecular mechanisms in chronic obstructive pulmonary disease: an overview

CLINICAL & EXPERIMENTAL ALLERGY, Issue 8 2004
A. Di Stefano
Summary In the last decade, the analysis of bronchial biopsies and lung parenchyma obtained from chronic obstructive pulmonary disease (COPD) patients compared with those from smokers with normal lung function and non-smokers has provided new insights on the role of the different inflammatory and structural cells, their signalling pathways and mediators, contributing to a better knowledge of the pathogenesis of COPD. This review summarizes and discusses the lung pathology of COPD patients with emphasis on inflammatory cell phenotypes that predominate in different clinical conditions. In bronchial biopsies, a cascade of events takes place during progression from mild-to-severe disease. T lymphocytes, particularly CD8+ cells and macrophages are the prevalent inflammatory cells in the lung of healthy smokers and patients with mild COPD, while total and activated neutrophils predominate in severe COPD. The number of CD4+, CD8+ cells and macrophages expressing nuclear factor-kappa B (NF-,B), STAT-4 and IFN-, proteins as well as endothelial adhesion molecule-1 in endothelium is increased in mild/moderate disease. In contrast, activated neutrophils (MPO+ cells) and increased nitrotyrosine immunoreactivity develops in severe COPD. In bronchial biopsies obtained during COPD exacerbations, some studies have shown an increased T cell and granulocyte infiltration. Regular treatment with high doses of inhaled glucocorticoids does not significantly change the number of inflammatory cells in bronchial biopsies from patients with moderate COPD. The profile in lung parenchyma is similar to bronchial biopsies. ,Healthy' smokers and mild/moderate diseased patients show increased T lymphocyte infiltration in the peripheral airways. Pulmonary emphysema is associated with a general increase of inflammatory cells in the alveolar septa. The molecular mechanisms driving the lymphocyte and neutrophilic prevalence in mild and severe disease, respectively, needs to be extensively studied. Up-regulation of pro-inflammatory transcription factors NF-,B and STAT-4 in mild, activated epithelial and endothelial cells in the more severe disease may contribute to this differential prevalence of infiltrating cells. [source]

Dynamic oxygen-enhanced MRI reflects diffusing capacity of the lung

MAGNETIC RESONANCE IN MEDICINE, Issue 6 2002
Yoshiharu Ohno
Abstract The purpose of this study was to demonstrate the feasibility of dynamic oxygen-enhanced MRI in a clinical setting. We hypothesized that dynamic oxygen enhancement can reflect the regional diffusing capacity of the lung. Ten patients with pulmonary emphysema and seven healthy volunteers were examined with a respiratory-synchronized inversion recovery single-shot turbo spin-echo sequence (TR = 3200,5000 ms, TE = 16 ms, TI = 720 ms, ETS = 4 ms) following 100% oxygen inhalation, using a 1.5 T whole-body scanner. Maximum mean relative enhancement ratios calculated by averaging six defined regions of interest (ROIs) in both lungs were statistically compared between healthy volunteers and patients, and were correlated with diffusing lung capacity (%DLCO). In patients with pulmonary emphysema, maximum mean relative enhancement ratios were significantly decreased compared to those in healthy volunteers (P = 0.0008). Maximum mean relative enhancement ratio had excellent correlation with % DLC0 (r2 = 0.83). Dynamic oxygen-enhanced MRI may reflect the diffusing capacity of the lung; therefore, imaging of oxygen enhancement with MRI may provide maps of the diffusing capacity. Magn Reson Med 47:1139,1144, 2002. © 2002 Wiley-Liss, Inc. [source]

Bullous lung disease due to marijuana

RESPIROLOGY, Issue 1 2008
Su W. HII
Background and objective: In contrast to the well-described effects of tobacco smoking upon pulmonary emphysema, with ,15% of smokers being affected at the age of 65 years, the effects of marijuana smoking are rarely reported and poorly understood. Methods: We report a series of 10 patients (mean age 41 ± 9 years, eight male, two female), who presented over a period of 12 months to our respiratory unit with new respiratory symptoms, and who admitted to regular chronic marijuana smoking (>1 year continuously). Symptoms on presentation were dyspnoea (n = 4), pneumothorax (n = 4) and chest infection (n = 2). Results: High-resolution CT revealed asymmetrical, variably sized, emphysematous bullae in the upper and mid zones. However, the CXR was normal in four patients and lung function was normal in five. Conclusions: Marijuana smoking leads to asymmetrical bullous disease, often in the setting of normal CXR and lung function. In subjects who smoke marijuana, these pathological changes occur at a younger age (approximately 20 years earlier) than in tobacco smokers. [source]

Age of SERPINA1 Gene PI Z Mutation: Swedish and Latvian Population Analysis

ANNALS OF HUMAN GENETICS, Issue 3 2008
B. Lace
Summary Alpha 1-antitrypsin (A1AT) deficiency, one of the most common inborn errors of metabolism in Caucasians, is characterized by a low serum concentration of A1AT and a high risk of pulmonary emphysema and liver disease. The allelic frequency for the most common protease inhibitor (PI) Z mutation in the SERPINA1 gene is 2,5% in Caucasians of European descent. The objective of our study was to estimate the PI Z mutation age using molecular analysis in Latvian and Swedish populations, which have the highest frequency of PI Z mutation. DNA samples of heterozygous and homozygous PI Z allele carriers from Latvia (n = 21) and Sweden (n = 65) were analysed; 113 unrelated healthy donors from Latvia were used as a control group. MALDI-TOF analysis was performed on all samples. Pairwise Fst was computed to compare the PI Z mutation ages between the two populations and controls. A p value less than 0.05 was considered significant. Analysis of non-recombinant SNPs revealed that the PI Z mutation age was 2902 years in Latvia (SD 1983) and 2362 years in Sweden (SD 1614) which correlates with previous studies based on microsatellite analysis. [source]