Objective To observe the manifestations of MSCT and CT virtual endoscopy (CTVE) images of pleural windows in spontaneous pneumothorax.Methods MSCT data of 73 patients of spontaneous pneumothorax were analyzed.Taking pneumatized sac as the center,thin cross sectional planer (1 mm thickness) MPR and CTVE were reconstructed.Then the size and location of pleural windows,form of pleural surface defect or niche and the relationship with the chest were observed.Results In all 73 patients of spontaneous pneumothorax,27 pleural windows were detected in 15 patients with MSCT thin cross-sectional planer reconstruction image.Pleural windows were observed on the left side in 11 patients,while on the right side in 4 patients.Most of pleural windows located at apex (15/27,55.56％),followed by anterior chest wall (7/27,25.93％) and mediastinum (5/27,18.52％).The connection of pleura window with thorax was shown in 23 (23/27,85.19％).Small defection on parietal pleural with pneumatized sac bulging was seen in all pleural windows,with circular,elliptic,short columnar or hockey shapes.On the front view of CTVE,pleural windows showed niche on parietal pleural surface with round or oval form,and the bottom of the pneumatized sac could be straightly seen in 19 pleural windows.The walls were flat,tunnel shaped in 6 pleural windows,while cavernous shaped in other pleural windows.Conclusion Pleural windows often displayed as small diverticulum like shadows on parietal pleural surfaces,and the pathogenesis might be associated with negative pressure increased in local pleural cavity and pleural damages.

Objective To investigate the effect of ERH gene knockdown on the proliferation and apoptosis of human bladder cancer T24 cells. Methods T24 cells infected by lentivirus with interference on ERH gene sequence were cloned to establish stable T24 cells clone in ERH gene suppression. The expression of ERH mRNA gene in bladder cancer was detected by using quantitative real time polymerase chain reaction (qPCR). The effects of ERH knockout on the cell proliferation and apoptosis were examined by using methylthiazolyl tetrazolium (MTT) assay, colony formation assay and flow cytometry. The effect of ERH knockout on the tumorigenic effect of T24 cells in vivo was verified by subcutaneous tumor formation in nude mice. Results After lentiviral transfection, qPCR results showed that the knockdown effect of ERH mRNA in ERH normal group (untreated T24 cells) was better than that in ERH gene knockdown group, and the difference was statistically significant [(1.006±0.126) vs. (0.079±0.007); t=12.72, P=0.0002]. After knocking out ERH gene, MTT assay showed that the proliferation ability of T24 cells in ERH gene knockdown group was weakened compared with ERH normal group, and the difference was statistically significant [A490 value: (0.13±0.00) vs. (0.66±0.01);t=104.61, P<0.0001]. Colony formation assay indicated that the ability of clone in ERH normal group was weakened compared with ERH gene knockdown group [(10.5 ±1.2) vs. (196.4 ±4.0); t= 73.63, P< 0.0001]. Flow cytometry showed that the cell apoptosis rate in ERH gene knockdown group was higher than that in ERH normal group [(11.0 ±0.5) ％ vs. (4.2 ±0.5) ％; t= 16.06, P<0.0001]. Imaging results of subcutaneous tumor formation in nude mice showed that the total fluorescence intensity of the tumor area in ERH gene knockdown group was (4.67 ±0.59) × 1010 μW/cm2, and the corresponding part in ERH normal group was (9.54±4.20) × 1010μW/cm2 (t=3.64, P=0.0051);tumor weight in ERH gene knockdown group was (0.80±0.62) g, and in ERH normal group was (1.79±0.71) g (t=3.33, P=0.0037). Conclusion ERH gene knockout can inhibit the proliferation of human bladder cancer T24 cells, and promote the cell apoptosis.