[Evaluation of 90 kV Beam with 0.15 mm Cu Filter in Chest Radiography Using CsI-flat Panel Detector].

PURPOSE: To compare the visibility of anatomic structure in chest radiography acquired with different beam quality (120 kV beam and 90 kV beam with 0.15 mmCu) using CsI-flat panel detector. METHOD: Pair image obtained by different beam quality of 100 person's chest radiographies which were taken periodical health examination were compared with the visibility of normal structures (pulmonary vessels) and abnormal opacities by two pulmonologists and four radiological technologists. Moreover, the spectrum of the two beam quality were calculated using Monte Carlo simulation. RESULT: Dominant observers gave high score significantly (p<0.01) to the 90 kV beam's image in spite of 20% less dose. Monte Carlo simulation showed that 90 kV beam with 0.15 mmCu were much absorbed primary photon than 120 kV beam to CsI detector, and less absorbed secondary photon. CONCLUSION: The visibility of anatomic structure and abnormal opacities in FPD chest radiography was improved by using the 90 kV beam with 0.15 mmCu than traditional 120 kV beam's chest radiography.

Senescence-associated secretory phenotype in a mouse model of bleomycin-induced lung injury.

Bleomycin produces DNA damage, apoptosis and senescence, all of which play crucial roles in the development of pulmonary fibrosis. Recently, close attention has been paid to a DNA damage-induced phenotypic change (senescence-associated secretory phenotype; SASP) as a trigger for the secretion of various mediators which modify the processes of tissue injury, inflammation, repair and fibrosis. We characterized the SASP in a murine model of bleomycin-induced lung injury. Mice were intratracheally administered bleomycin or control saline, and the lungs were obtained on days 7, 14 and 21. The occurrence of DNA damage and the SASP in the lungs was examined by immunostaining. γH2AX immunostaining of the bleomycin-treated lungs revealed double-strand breaks (DSBs), largely within E-cadherin-positive, ß4-integirn-positive alveolar epithelial cells. The DSBs were associated with phosphorylation of ATM/ATR, a central signal transducer mediating the DNA damage response, and upregulation of the cyclin-dependent kinase inhibitor p21(CIP1). The DSBs persisted for at least 21 days after the bleomycin exposure, although it began to wane after 7 days. A subpopulation of the γH2AX-positive, DNA-damaged cells exhibited the SASP, characterized by overexpression of IL-6, TNFα, MMP-2 and MMP-9, in association with the phosphorylation of IKKα/ß and p38 MAPK. Persistent DNA damage and the SASP are induced in the process of bleomycin-induced lung injury and repair, suggesting that these events play an important role in the regulation of inflammation and tissue remodeling in bleomycin-induced pneumopathy.

Air exposure causes oxidative stress in cultured bovine tracheal epithelial cells and produces a change in cellular glutathione systems.

An air-liquid interface culture system accelerates cell differentiation and growth in airway epithelial cells. In this study, the authors investigated whether glutathione (GSH) affects cell growth in an air-liquid interface culture. Various components of the cellular GSH system were measured and the number of cells was counted after conversion from an immersed feeding to an air-liquid interface. The effect of medium supplementation with cystine, a precursor of GSH, on cell growth was also examined. After conversion to an air-liquid interface, the cellular GSH level increased by 4 to 5-fold. The increase in GSH preceded the rise in cell number. The glutathione disulfide (GSSG)/total GSH ratio (an indicator of oxidative stress) increased initially and reached a plateau (time 0: 0.379%+/-0.054%; day 2: 0.824%+/-0.063%; day 6: 0.806%+/-0.093%). The level of glutathione reductase activity in the cells increased in a time-dependent manner, whereas the glutathione peroxidase activity level declined. When the amount of cystine in the medium was varied after conversion, the cellular GSH level was closely correlated with the rate of cell growth. In conclusion, air exposure causes oxidative stress in cultured cells and produces a change in the cellular glutathione system, resulting in the promotion of cell growth.

[Acute form of eexogenous lipoid pneumonia caused by inhalation of liquid paraffin in a fire-eater].

We report a case of acute exogenous lipoid pneumonia in a 34-year-old-fire-eater. Six hours after inhalation of liquid paraffin, dyspnea, cough, fever, hemoptysis, and chest pain developed in this patient. Chest computed tomography showed nodular infiltrations with ground glass opacities (GGO) in the right middle lobes, GGO alone in the right lower lobes, and consolidations with GGO in the left lower lobes. Lipid-laden alveolar macrophages in bronchoalveolar lavage fluid were detected by lipid staining (Sudan III stain, oil-red-O stain) and transmission electron microscopy. The symptoms and lung infiltrations were improved by treatment with predonisolone, together with antibiotics and urinastatin.