One hundred forty-three patients with bronchogenic carcinoma were studied prospectively with computed tomography (CT) to determine the accuracy of CT in the evaluation of mediastinal nodal metastases. Mediastinal lymph nodes were localized according to the lymph node mapping scheme of the American Thoracic Society and were considered abnormal if they exceeded 1 cm in short-axis diameter. All patients underwent surgical staging, which consisted of either mediastinoscopy alone or mediastinoscopy and thoracotomy. At the time of surgical staging, all accessible nodes were either removed or sampled. The sensitivity of CT for mediastinal nodes on a per-patient basis was 64%, with a specificity of 62%. The sensitivity of CT for individual nodal stations involved with tumor was only 44%. The presence of obstructive pneumonitis did not appreciably alter the sensitivity of CT, but the specificity was lower (43%). The likelihood of metastases increased with lymph node size; however, seven of 19 (37%) lymph nodes that measured 2-4 cm in short-axis diameter were hyperplastic and did not contain metastases. The relative insensitivity of CT makes formal nodal sampling at the time of mediastinoscopy or thoracotomy essential to detect lymph node metastases.

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The author examined computed tomographic (CT) scans of the chest from 40 patients with cultures positive for atypical mycobacteria. Common manifestations included bronchiectasis, air-space disease, nodules, and scarring and/or volume loss. Less commonly observed signs were cavities, lymphadenopathy, and pleural disease. Serial scans were obtained in 10 patients and showed new areas of bronchiectasis and progression of existing bronchiectasis, suggesting that the bronchiectasis was not a preexisting condition but resulted from infection. The anatomic distribution of the above findings was diffuse, not strongly favoring any lung zone. The identification of multifocal coexistent bronchiectasis, air-space disease, and nodules at CT should raise the possibility of atypical mycobacterial lung disease, even in an otherwise healthy patient.

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The effects of low-density lipoprotein (LDL) and chylomicron remnants on lipid accumulation in human monocyte-derived macrophages (HMDMs) and in macrophages derived from the human monocyte cell line THP-1 were compared. The HMDMs or THP-1 macrophages were incubated with LDL, oxidized LDL (oxLDL), chylomicron remnant-like particles (CMR-LPs), or oxidized CMR-LPs (oxCMR-LPs), and the amount and type of lipid accumulated were determined. As expected, the lipid content of both cell types was increased markedly by oxLDL but not LDL, and this was due to a rise in cholesterol, cholesteryl ester (CE), and triacylglycerol (TG) levels. In contrast, both CMR-LPs and oxCMR-LPs caused a considerable increase in cellular lipid in HMDMs and THP-1 macrophages, but in this case there was a greater rise in the TG than in the cholesterol or CE content. Lipid accumulation in response to oxLDL, CMR-LPs, and oxCMR-LPs was prevented by the ACAT inhibitor CI976 in HMDMs but not in THP-1 macrophages, where TG levels remained markedly elevated. The rate of incorporation of [(3)H]oleate into CE and TG in THP-1 macrophages was increased by oxLDL, CMR-LPs, and oxCMR-LPs, but incorporation into TG was increased to a greater extent with CMR-LPs and oxCMR-LPs compared with oxLDL. These results demonstrate that both CMR-LPs and oxCMR-LPs cause lipid accumulation in human macrophages comparable to that seen with oxLDL and that oxidation of the remnant particles does not enhance this effect. They also demonstrate that a greater proportion of the lipid accumulated in response to CMR-LPs compared with oxLDL is TG rather than cholesterol or CE and that this is associated with a higher rate of TG synthesis. This study, therefore, provides further evidence to suggest that chylomicron remnants have a role in foam cell formation that is distinct from that of oxLDL.