Objective To explore the CT classification of lacerating lung injury in blunt thoracic trauma and its clinical significance. Methods A total of 63 patients with lung lacerating injury were classified using CT features as simple type injury (complete visceral pleura, with no pneumothorax or he-mopneumothorax) and complex type injury (accompanied by visceral pleura rupture, pneumothorax or he-mopneumothorax). A retrospective analysis was done on CT manifestations and clinical data. Results Of 63 patients, 35 patients (56%) had simple type of lacerating lung injury with complete visceral pleu-ra, most of which were focal pulmonary pseudocyst lesions present in the edge of lungs and could be dis-persed quickly after conservative therapy without complications. Mean hospital stay was 16 days. Of pa-tients with complex type of lacerating lung injury, 28 patients (44.4%) were accompanied by visceral pleura rupture with larger extent of pulmonary injury, 20 (71%) by lung eontnsion, 15 (54%) by ate-lectasis or pulmonary atelectasis and three (11%) by local pulmonary infection. Thoracic puncture or closed drainage was performed in 19 patients (69%) and thoracotomy in one (4%), with mean hospital stay of 58 days. Conclusions According to CT manifestations on whether there exists visceral pleura rupture or not, the lacerating lung injury is classified as simple type injury and complex type injury. CT classification of lacerating lung injury may be helpful in selecting clinical treatment protocols and predic-ting early prognosis.

OBJECTIVETo investigate the effects of microRNA-145 (miR-145) on epithelial-mesenchymal transition (EMT) of TGF-β1-induced human renal proximal tubular epithelial (HK-2) cells.

METHODSThe gene sequence of miR-145 was synthesized and cloned into pCMV-myc to construct recombinant plasmid pCMV-miR-145. HK-2 cells were divided into four groups: control (untreated), TGF-β1 (treated with TGF-β1), blank+TGF-β1 (treated with TGF-β1 after HK-2 cells transfected with blank plasmid) and miR-145+TGF-β1 (treated with TGF-β1 after HK-2 cells transfected with pCMV-miR-145 recombinant plasmid). Expression of miR-145 was detected by real-time PCR (RT-PCR). TGF-β1, Smad3, Smad2/3, p-Smad2/3, α-SMA, FN and type I collagen (Col I) protein levels were detected by Western blot. Concentrations of fibronectin (FN) and Col I in cell culture supernatants were measured using ELISA.

RESULTSpCMV-miR-145 recombinant plasmid was successfully transfected into HK-2 cells. Compared with the control group, the miR-145+TGF-β1 group showed a significant up-regulation in the expression level of miR-145 (P<0.01). However, the TGF-β1 and blank+TGF-β1 groups showed a significant down-regulation in the expression level of miR-145 compared with that in the control and miR-145+TGF-β1 groups (P<0.01). Compared with the TGF-β1 and blank+TGF-β1 groups, the miR-145+TGF-β1 group showed significantly reduced levels of the signal proteins TGF-β1, Smad3, Smad2/3 and p-Smad2/3 (P<0.05), as well as significantly reduced levels of the biomarkers α-SMA, FN and Col I (P<0.05). Meanwhile, concentrations of FN and Col I in cell culture supernatants also decreased (P<0.05).

CONCLUSIONSmiR-145 modulates the EMT of HK-2 cells treated with TGF-β1, possibly by inhibition of the activation of TGF-β-dependent Smad signaling pathway.

Cells, Cultured ; Epithelial Cells ; drug effects ; pathology ; Epithelial-Mesenchymal Transition ; Humans ; Kidney Tubules, Proximal ; drug effects ; pathology ; MicroRNAs ; physiology ; Transforming Growth Factor beta1 ; pharmacology