Risk assessment of first upper gastrointestinal bleeding using computerized tomoscanning in esophageal varices patients with cirrhosis and portal hypertension.

To evaluate the risk of first upper gastrointestinal bleeding by computerized tomoscanning (CT) for esophageal varices patients with cirrhotic portal hypertension.One hundred thirty two esophageal varices patients with cirrhotic portal hypertension who are also complicated with gastrointestinal bleeding were recruited as bleeding group, while another 132 patients without bleeding as non-bleeding group. The diameter of esophageal varices, number of vascular sections, and total area of blood vessels were measured by CT scanning. The sensitivity and specificity of these indicators were calculated, and Youden index was adjusted with the critical point.The diameter of esophageal varices was 7.83 ±â€Š2.76 mm in bleeding group, and 6.57 ±â€Š3.42 mm in non-bleeding group. The Youden index was 0.32 with the critical point 5.55 mm. The area under the receiver operating characteristics (AUROC) was 0.72. The number of venous vessels was 4.5 ±â€Š2 in bleeding group, whereas being 4 ±â€Š2 in non-bleeding group. The Youden index was 0.35 with a critical point 4, and the area under the curve (AUC) was 0.68. The blood vessel area was 1.73 ±â€Š1.15 cm in bleeding group, and 1.12 ±â€Š0.89 cm in non-bleeding group. The Youden index was 0.48 with the critical point being 1.03 cm, and corresponding AUC was 0.82.Among all 3 indicators of the total area, diameter, and number of sections of the esophageal varices, the total area of esophageal varices showed more accuracy as a potential and novel indicator for bleeding prediction.

LncRNA DGCR5 represses the development of hepatocellular carcinoma by targeting the miR-346/KLF14 axis.

Long non-coding RNAs (lncRNAs) are a class of regulatory noncoding RNAs. Emerging evidence highlights the critical roles of lncRNAs in the progression of hepatocellular carcinoma (HCC). Although many lncRNAs have been identified in the development of HCC, the association between DiGeorge syndrome critical region gene 5 (DGCR5) and HCC remains unclear. In the current study, we focused on the biological role of DGCR5 in HCC. We observed that DGCR5 was decreased in HCC cells, including SMCC7721, Hep3B, HepG2, MHCC-97L, MHCC-97H, and SNU449 hepatocellular carcinoma cells, compared with the normal human liver cell line THLE-3 normal human liver cells. In addition, DGCR5 overexpression could repress HCC cell growth, migration, and invasion considerably. Increasing studies have indicated the interactions between lncRNAs and microRNAs. MicroRNAs are endogenous small noncoding RNAs and they can play important roles in tumorigenesis. MicroRNA 346 (miR-346) has been demonstrated in various human cancer types, including HCC. MiR-346 was found to be increased in HCC cells and DGCR5 can act as a sponge of miR-346 to modulate the progression of HCC. The binding correlation between DGCR5 and miR-346 was validated in our research. Subsequently, Krüppel-like factor 14 (KLF14) was predicted as a downstream target of miR-346 and miR-346 can induce the development of HCC by inhibiting KLF14. Finally, we proved that DGCR5 can rescue the inhibited levels of KLF14 repressed by miR-346 mimics in MHCC-97H and Hep3B cells. Taken together, it was indicated in our study that DGCR5 can restrain the progression of HCC through sponging miR-346 and modulating KLF14 in vitro.