The reversed halo sign, although seen only in one fifth of patients with the disease, appears relatively specific to make a diagnosis of cryptogenic organizing pneumonia on CT.

Although cigarette smoking is implicated in the pathogenesis of emphysema, the precise mechanisms of chronic progressive alveolar septal destruction are not well understood. We show, in a novel animal model, that immunocompetent, but not athymic, nude rats injected intraperitoneally with xenogeneic endothelial cells (ECs) produce antibodies against ECs and develop emphysema. Immunization with ECs also leads to alveolar septal cell apoptosis and activation of matrix metalloproteases MMP-9 and MMP-2. Anti-EC antibodies cause EC apoptosis in vitro and emphysema in passively immunized mice. Moreover, immunization also causes accumulation of CD4+ T cells in the lung. Adoptive transfer of pathogenic, spleen-derived CD4+ cells into naive immunocompetent animal also results in emphysema. This study shows for the first time that humoral- and CD4+ cell-dependent mechanisms are sufficient to trigger the development of emphysema, suggesting that alveolar septal cell destruction might result from immune mechanisms.

-Severe pulmonary hypertension (SPH) is characterized by precapillary arteriolar lumen obliteration, dramatic right ventricular hypertrophy, and pericardial effusion. Our recently published rat model of SPH recapitulates major components of the human disease. We used this model to develop new treatment strategies for SPH. SPH in rats was induced using VEGF receptor blockade in combination with chronic hypoxia. A large variety of drugs used in this study, including anticancer drugs (cyclophosphamide and paclitaxel), the angiotensin-converting enzyme inhibitor lisinopril, the antiangiogenic agent thalidomide, and the peroxisome proliferator-actived receptor-␥ agonist PGJ2, failed to decrease mean pulmonary artery pressure (PAP) or right ventricular hypertrophy. In contrast, treatment of rats with established SPH with simvastatin markedly reduced mean PAP and right ventricular hypertrophy, and this reduction was associated with caspase-3 activation and pulmonary microvascular endothelial cell apoptosis. Simvastatin partially restored caveolin-1, caveolin-2, and phospho-caveolin expression in vessel walls. In rat primary pulmonary microvascular endothelial cells, simvastatin induced caspase 3 activation and Rac 1 expression while suppressing Rho A and attenuated levels of Akt and ERK phosphorylation. We conclude that simvastatin is effective in inducing apoptosis in hyperproliferative pulmonary vascular lesions and could be considered as a potential drug for treatment of human SPH. statins HUMAN SEVERE PULMONARY HYPERTENSION (SPH), including pulmonary hypertension secondary to congenital cardiac abnormalities, collagen vascular disorders, human immunodeficiency virus and human herpes virus-8 infection (7,8,32,38,41,51), anorexigen drug intake, and so-called idiopathic pulmonary hypertension, are unfortunately diagnosed when the pulmonary vascular bed already has been extensively remodeled and is not usually responsive to vasodilators (42). Although continuous infusion of prostacyclin has prolonged the survival of many patients with SPH and improved their ability to exercise and function (15,39,44), prostacyclin does not cure the disease. Vascular lesions are frequently localized at sites distal to arteriolar bifurcations (9) and contain phenotypically altered endothelial and smooth muscle cells (25,52,53) that have lost the expression of p27, caveolin-1, and -2 protein and of prostacyclin synthase and peroxisome proliferator-activated receptor (PPAR)-␥ genes and proteins (1, 51). These endothelial cells also do not obey the "law of the monolayer" and instead form cell clusters or tumorlets (52, 53).Our rat model of SPH (48, 50) resembles the human disease because it demonstrates endothelial cell proliferation and the occlusion of small precapillary arterioles. In this model, chronic VEGF receptor blockade in combination with chronic hypoxia causes the initial apoptosis of lung endothelial cells, which is followed by the selection of phenotypically altered apoptosis-resistant endothelial cells. Endothelial cell proli...

CT fluoroscopy-guided NAB of pulmonary lesions provides high diagnostic accuracy and can be performed with significantly fewer complications. However, radiation exposure to both patient and doctor were significantly higher than conventional CT-guided NAB.