The liver is the second most commonly injured organ following blunt abdominal trauma. The stable patient with minimal physical findings with a history of blunt abdominal trauma presents a challenge for diagnosis of liver injury. This study was conducted to determine the usefulness of hepatic transaminases in predicting the presence of liver injury and its severity following blunt abdominal trauma. In this retrospective study, we included all patients who had sustained blunt abdominal injury and were treated at our institution between January 2008 and December 2010. The grading of the liver injury was verified using CT scans or surgical findings. One hundred and eighty-two patients with blunt abdominal trauma underwent the required blood tests and were included in the study. Using receiver operating characteristic (ROC) curve assessment, optimum alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and γ-glutamyl transpeptidase (GGT) thresholds were determined to be >57 U/l, 113 U/l, 595 U/l and 50 U/l. ALT >57 U/l (OR, 66.1; P113 U/l (OR, 30.6; P595 U/l (OR, 3.8; P50 U/l (OR, 3.0; P57 U/l and AST >113 U/l are strongly associated with liver injury and require further imaging studies and close management.

Laparoscopic common bile duct exploration (LCBDE) for stone can be carried out by either laparoscopic transcystic stone extraction (LTSE) or laparoscopic choledochotomy (LC). It remains unknown as to which approach is optimal for management of gallbladder stone with common bile duct stones (CBDS) in Chinese patients. From May 2000 to February 2009, we prospective treated 346 consecutive patients with gallbladder stones and CBDS with laparoscopic cholecystectomy and LCBDE. Intraoperative findings, postoperative complications, postoperative hospital stay and costs were analyzed. Because of LCBDE failure,16 cases (4.6%) required open surgery. Of 330 successful LCBDE-treated patients, 237 underwent LTSE and 93 required LC. No mortality occurred in either group. The bile duct stone clearance rate was similar in both groups. Patients in the LTSE group were significantly younger and had fewer complications with smaller, fewer stones, shorter operative time and postoperative hospital stays, and lower costs, compared to those in the LC group. Compared with patients with T-tube insertion, patients in the LC group with primary closure had shorter operative time, shorter postoperative hospital stay, and lower costs. In cases requiring LCBDE, LTSE should be the first choice, whereas LC may be restricted to large, multiple stones. LC with primary closure without external drainage of the CBDS is as effective and safe as the T-tube insertion approach.

The current study elucidated the role of a long non‐coding RNA (lncRNA), FOXD2‐AS1, in the pathogenesis of hepatocellular carcinoma (HCC) and the regulatory mechanism underlying FOXD2‐AS1/miR‐150‐5p/transmembrane protein 9 (TMEM9) signalling in HCC. Microarray analysis was used for preliminary screening of candidate lncRNAs in HCC tissues. qRT‐PCR and Western blot analyses were used to detect the expression of FOXD2‐AS1. Cell proliferation assays, luciferase assay and RNA immunoprecipitation were performed to examine the mechanism by which FOXD2‐AS1 mediates sorafenib resistance in HCC cells. FOXD2‐AS1 and TMEM9 were significantly decreased and miR‐150‐5p was increased in SR‐HepG2 and SR‐HUH7 cells compared with control parental cells. Overexpression of FOXD2‐AS1 increased TMEM9 expression and overcame the resistance of SR‐HepG2 and SR‐HUH7 cells. Conversely, knockdown of FOXD2‐AS1 decreased TMEM9 expression and increased the sensitivity of HepG2 and Huh7 cells to sorafenib. Our data also demonstrated that FOXD2‐AS1 functioned as a sponge for miR‐150‐5p to modulate TMEM9 expression. Taken together, our findings revealed that FOXD2‐AS1 is an important regulator of TMEM9 and contributed to sorafenib resistance. Thus, FOXD2‐AS1 may serve as a therapeutic target against sorafenib resistance in HCC.