Can maximum intensity projection images with multidetector-row computed tomography help to differentiate between the micronodular distribution of focal and diffuse infiltrative lung diseases?

OBJECTIVE: The objective of this study was to evaluate whether maximum intensity projection (MIP) images increased the ability of experienced and resident radiologists to differentiate between the micronodular distribution of focal and diffuse infiltrative lung diseases. METHODS: The cases used in the study were those of 26 patients with focal or diffuse micronodular lung diseases, including 7 cases of sarcoidosis, 6 of miliary tuberculosis, 3 of pulmonary tuberculosis, 3 of chronic bronchitis, 2 of human T-lymphotropic virus type 1-associated bronchoalveolar disorder, 2 of diffuse aspiration bronchiolitis, 1 of atypical mycobacterial infection, and 1 of lymphangitic carcinomatosis. Scans of the entire lung during a single breath hold at 1.25-2.5 mm thickness and a pitch of 6 were performed using a multidetector-row computed tomography (MDCT) apparatus with a 4-row detector. Additional MIP image slabs were produced from the initial axial images on all study patients on a workstation according to a protocol that incorporated a slab thickness of 10 mm, a reconstructed interval of 10 mm, and a window width of -1500 Hounsfield units. The ability of 10 radiologists (5 board-certified radiologists and 5 radiology residents) to interpret contiguous thin-section CT scans and additional MIP images was then studied in an observer performance study. The results of both sets of observer performances were compared using receiver operating characteristic analysis. RESULTS: In the resident observers, the mean area under the receiver operating characteristic curve (Az) value increased significantly from 0.654 without the MIP images to 0.753 with the MIP images (P < 0.01). In the board-certified radiologists, however, the mean Az values remained unchanged at 0.867 without the MIP images and 0.846 with the MIP images. CONCLUSIONS: This study showed that MIP images may help radiologists in training to differentiate between the micronodular distribution of focal and diffuse infiltrative lung diseases.

Argatroban, specific thrombin inhibitor, induced phenotype change of cultured rabbit vascular smooth muscle cells.

To investigate whether argatroban ((2R,4R)-4-methyl-1-[N(2)-((RS)-3-methyl-1,2,3,4-tetrahydro-8-quinolinesulfonyl)-L-arginyl]-2-piperidinecarboxylic acid hydrate, a selective thrombin inhibitor, exerts a direct action on phenotype conversion of vascular smooth muscle cells, cultured rabbit aortic vascular smooth muscle cells were employed. Myosin heavy chain isoforms (SM1, SM2, and SMemb) mRNA expressions were evaluated by in situ hybridization and reverse transcription-polymerase chain reaction (RT-PCR). After the cells were incubated in serum-free medium containing argatroban (10 and 50 microg/ml) and platelet-derived growth factor (PDGF)-BB (10 and 50 ng/ml) for 3 h, total RNA was extracted. In situ hybridization demonstrated that myosin heavy-chain isoform mRNAs were homogenously expressed in argatroban- and PDGF-BB-treated cells. RT-PCR revealed that SM1/SM2 mRNA expressions were not changed with argatroban, while SMemb mRNA expression was increased to 1.6-fold with a statistical significance (P<0.05). Treatment with argatroban (10 and 50 microg/ml) at 24 h did not change SM1/SM2 mRNA expressions. Although SMemb mRNA expression was slightly increased, there was no statistical significance. Other phenotype markers including plasminogen activator inhibitor-1 (PAI-1) and beta-actin mRNAs were also significantly increased by argatroban. In conclusion, argatroban can directly induce phenotype conversion of vascular smooth muscle cells with the resultant up-regulation of SMemb, PAI-1, and beta-actin mRNAs.