Progression of COPD is associated with the accumulation of inflammatory mucous exudates in the lumen and infiltration of the wall by innate and adaptive inflammatory immune cells that form lymphoid follicles. These changes are coupled to a repair or remodeling process that thickens the walls of these airways.

No abstract

This study examines the hypothesis that the cigarette smoke-induced inflammatory process is amplified in severe emphysema and explores the association of this response with latent adenoviral infection. Lung tissue from patients with similar smoking histories and either no (n = 7), mild (n = 7), or severe emphysema (n = 7) was obtained by lung resection. Numbers of polymorphonuclear cells (PMN), macrophages, B cells, CD4, CD8 lymphocytes, and eosinophils present in tissue and airspaces and of epithelial cells expressing adenoviral E1A protein were determined using quantitative techniques. Severe emphysema was associated with an absolute increase in the total number of inflammatory cells in the lung tissue and airspaces. The computed tomography (CT) determined extent of lung destruction was related to the number of cells/m(2) surface area by R(2) values that ranged from 0.858 (CD8 cells) to 0.483 (B cells) in the tissue and 0.630 (CD4 cells) to 0.198 (B cells) in the airspaces. These changes were associated with a 5- to 40-fold increase in the number of alveolar epithelial cells expressing adenoviral E1A protein in mild and severe disease, respectively. We conclude that cigarette smoke-induced lung inflammation is amplified in severe emphysema and that latent expression of the adenoviral E1A protein expressed by alveolar epithelial cells influenced this amplification process.

Quantitative analysis of computed tomography (CT) has been combined with a stereologically based histologic analysis of lung structure to assess regional lung inflation and the structural features of the lung parenchyma. In this study, CT measurements of lung inflation were compared with histologic estimates of surface area in order to develop prediction equations that allow lung surface to volume ratio and surface area to be predicted from an analysis of the CT scan. The results show that mild emphysema is associated with an increase in lung volume and a reduction in surface to volume ratio, whereas surface area and tissue weight were only decreased in severe disease. The CT predicted surface to volume ratio correlated with histology, and both predicted and measured surface areas correlated with the diffusing capacity. We conclude that this CT analysis can be used to monitor the progression of emphysematous lung destruction in individual patients, and to assess the impact of both surgical and medical treatments for emphysema.

ForewordWe are very happy to present the third edition of Applied Mathematics in Integrated Navigation Systems by Robert M. Rogers. The first two editions have been very well received, and we are certain that this comprehensive and in-depth treatment of such a timely and important topic in the aerospace field, as well as others, will be equally well received by the technical community. The book has sixteen chapters divided into two main parts and several appendices, including a bibliography, all in more than 400 pages. There is a detailed Preface and software for download.Robert Rogers is extremely well qualified to write this book, because of his broad and deep expertise in the area. His command of the material is excellent, and he is able to organize and present it in a very clear manner.The AIAA Education Book Series aims to cover a very broad range of topics in the general aerospace field, including basic theory, applications and design. Information about a complete list of titles can be found on the last page of this volume. The philosophy of the series is to develop textbooks that can be used in a university setting, instructional materials for continuing education and professional development courses, and also books that can serve as the basis for independent study. Suggestions for new topics or authors are always welcome. Joseph A. SchetzEditor-in-Chief AIAA Education Series Downloaded by Stanford University on September 28, 2012 | http://arc.aiaa.org |

Lung-reduction surgery can produce increases in the elastic recoil of the lung in patients with diffuse emphysema, leading to short-term improvement in dyspnea and exercise tolerance.

This study reviews the relationship between body weight, pulmonary function, and survival in the recent clinical trial of intermittent positive pressure breathing (IPPB). We related body weight, expressed as a percent of the ideal (%IBW), to the numerous other features of the disease recorded in this data set. Body weight was directly related to FEV1 (p = 0.0001), so that all subsequent analyses of body weight had to first consider FEV1. Mortality appeared to be influenced by body weight independent of FEV1. In patients with %FEV1 less than 35, mortality increased with decreasing body weight (p = 0.093), and this relationship was stronger in patients with %FEV1 35 to 47 (p = 0.048) and even stronger in patients with %FEV1 greater than 47 (p = 0.007). After adjusting for FEV1, body weight was a powerful positive correlate with exercise capacity (p = 0.0001). Body weight was also inversely related to %TLC (p = 0.0408) after adjusting for FEV1. Body weight was a powerful predictor of diffusing capacity (p = 0.0001) in patients with the same FEV1. These results support the hypothesis that factors related to nutritional status are an independent influence on the course of COPD.

The inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1-beta (IL-1 beta), have been associated with accelerated metabolism and protein turnover following exogenous administration in normal humans. We hypothesized that these inflammatory cytokines might contribute to the weight-losing process in patients with chronic obstructive pulmonary disease (COPD). COPD patients were identified prospectively as "weight losers" (WL; n = 10) if they reported > 5% weight loss during the preceding year or as "weight stable" (WS; n = 10) if their body weight fluctuated < or = 5%. Age-matched healthy volunteers were selected as the control group (C; n = 13). Monocytes were isolated from a peripheral blood sample, cultured, and exposed to lipopolysaccharide (LPS). The concentration of TNF-alpha and IL-1 beta in the monocyte supernatant was measured using a four layer enhanced ELISA. No significant difference in LPS-stimulated IL-1 beta production was found in the three study populations. However, LPS-stimulated TNF-alpha production (mean [range] ng/ml) by monocytes was significantly higher in the WL COPD patients (20.2 [6.3 to 44.8]), compared with WS patients (6.9 [1.5 to 16.6]), and C subjects (5.7 [0 to 61.8]). This difference was not maintained at 6 mo follow-up in the absence of ongoing weight loss. Definition of a causal relationship between TNF-alpha production and weight loss will require further understanding of the relationship between energy metabolism and TNF-alpha production in these patients.