American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Jan 2012
Prostaglandin E2 as an inhibitory modulator of fibrogenesis in human lung allografts.
Donor mesenchymal stromal/stem cell (MSC) expansion and fibrotic differentiation is associated with development of bronchiolitis obliterans syndrome (BOS) in human lung allografts. However, the regulators of fibrotic differentiation of these resident mesenchymal cells are not well understood. ⋯ These data identify the PGE2 axis as an important autocrine-paracrine brake on fibrotic differentiation of LR-MSCs, a failure of which is associated with BOS.
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Am. J. Respir. Crit. Care Med. · Jan 2012
Doubling times and CT screen–detected lung cancers in the Pittsburgh Lung Screening Study.
As computed tomography (CT) screening for lung cancer becomes more widespread, volumetric analyses, including doubling times, of CT-screen detected lung nodules and lung cancers may provide useful information in the follow-up and management of CT-detected lung nodules and cancers. ⋯ Volumetric analysis of CT-detected lung cancers is particularly useful in AC/BAC. Prevalent cancers have a significantly slower DT than nonprevalent cancers and a higher percentage of adenocarcinoma/bronchioloalveolar carcinoma. These results should affect the management of indeterminant lung nodules detected on screening CT scans.
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Am. J. Respir. Crit. Care Med. · Jan 2012
The implications of long-term acute care hospital transfer practices for measures of in-hospital mortality and length of stay.
The National Quality Forum recently endorsed in-hospital mortality and intensive care unit length of stay (LOS) as quality indicators for patients in the intensive care unit. These measures may be affected by transferring patients to long-term acute care hospitals (LTACs). ⋯ LTAC hospital transfer rate has a significant impact on reported mortality and LOS indices for patients requiring prolonged acute mechanical ventilation. This is an example of factors unrelated to quality of medical care or illness severity that must be considered when interpreting mortality and LOS as quality indicators.
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Am. J. Respir. Crit. Care Med. · Jan 2012
Late intervention with a myeloperoxidase inhibitor stops progression of experimental chronic obstructive pulmonary disease.
Inflammation and oxidative stress are linked to the deleterious effects of cigarette smoke in producing chronic obstructive pulmonary disease (COPD). Myeloperoxidase (MPO), a neutrophil and macrophage product, is important in bacterial killing, but also drives inflammatory reactions and tissue oxidation. ⋯ We conclude that an MPO inhibitor is able to stop progression of emphysema and small airway remodeling and to partially protect against pulmonary hypertension, even when treatment starts relatively late in the course of long-term smoke exposure, suggesting that inhibition of MPO may be a novel and useful therapeutic treatment for COPD. Protection appears to relate to inhibition of oxidative damage and down-regulation of the smoke-induced inflammatory response.