The value of gadobenate dimeglumine-enhanced biliary imaging from the hepatobiliary phase for predicting post-hepatectomy liver failure in HCC patients.

Objectives: To determine the value of gadobenate dimeglumine-enhanced biliary imaging from the hepatobiliary phase for predicting post-hepatectomy liver failure (PHLF) in patients with hepatocellular carcinoma (HCC).

Methods: Patients with HCC who underwent gadobenate dimeglumine-enhanced hepatobiliary magnetic resonance imaging prior to hepatectomy were collected in two centers. The relative enhancement ratio of the biliary system (REB) and the liver to muscle ratio (LMR) were measured at the hepatobiliary phase.

CT-Based Radiomics Score Can Accurately Predict Esophageal Variceal Rebleeding in Cirrhotic Patients.

This study aimed to develop a radiomics score (Rad-score) extracted from liver and spleen CT images in cirrhotic patients to predict the probability of esophageal variceal rebleeding. In total, 173 cirrhotic patients were enrolled in this retrospective study. A total of 2,264 radiomics features of the liver and spleen were extracted from CT images.

Carvedilol attenuates carbon tetrachloride-induced liver fibrosis and hepatic sinusoidal capillarization in mice.

Aim: To investigate the effect of carvedilol on liver fibrosis and hepatic sinusoidal capillarization in mice with carbon tetrachloride (CCl)-induced fibrosis.

Methods: A liver fibrosis mouse model was induced by intraperitoneal CCl injection for 8 weeks. The mice were divided into five experimental groups: the normal group, the oil group, the CCl group, the CCl+carvedilol (5 mg/kg/d) group, and the CCl+carvedilol (10 mg/kg/d) group.

Carvedilol improves liver cirrhosis in rats by inhibiting hepatic stellate cell activation, proliferation, invasion and collagen synthesis.

Portal hypertension (PHT) is one of the most severe consequences of liver cirrhosis. Carvedilol is a first‑line pharmacological treatment of PHT. However, the antifibrogenic effects of carvedilol on liver cirrhosis and the intrinsic mechanisms underlying these effects have not been thoroughly investigated.

Balloon-Assisted Percutaneous Transhepatic Antegrade Embolization with 2-Octyl Cyanoacrylate for the Treatment of Isolated Gastric Varices with Large Gastrorenal Shunts.

Aims: To evaluate the safety and effectiveness of percutaneous transhepatic antegrade embolization (PTAE) with 2-octyl cyanoacrylate assisted with balloon occlusion of the left renal vein or gastrorenal shunts (GRSs) for the treatment of isolated gastric varices (IGVs) with large GRSs.

Methods: Thirty patients with IGVs associated with large GRSs who had underwent PTAE assisted with a balloon to block the opening of the GRS in the left renal vein were retrospectively evaluated and followed up. Clinical and laboratory data were collected to evaluate the technical success of the procedure, complications, changes in the liver function using Child-Pugh scores, worsening of the esophageal varices, the rebleeding rate, and survival.

Carvedilol Ameliorates Intrahepatic Angiogenesis, Sinusoidal Remodeling and Portal Pressure in Cirrhotic Rats.

BACKGROUND Carvedilol is the first-line drug for the primary prophylaxis of variceal bleeding due to portal hypertension (PHT) in liver cirrhosis. This study aimed to investigate the effects of carvedilol on intrahepatic angiogenesis and sinusoidal remodeling in cirrhotic rats and explore the underlying mechanisms of carvedilol in PHT. MATERIAL AND METHODS For in vivo experiments, carbon tetrachloride was used to induce liver cirrhosis in rats, and carvedilol was simultaneously administered by gavage.

Carvedilol attenuates liver fibrosis by suppressing autophagy and promoting apoptosis in hepatic stellate cells.

Carvedilol has been identified as a promising agent for the treatment of liver fibrosis. Meanwhile, autophagy and apoptosis have been reported to play key roles in the activation of hepatic stellate cells (HSCs), which can contribute to the progression of liver fibrosis. However, the effects of carvedilol on autophagy and apoptosis in HSCs remain unclear.

Metformin attenuates motility, contraction, and fibrogenic response of hepatic stellate cells and by activating AMP-activated protein kinase.

Aim: To investigate the effect of metformin on activated hepatic stellate cells (HSCs) and the possible signaling pathways involved.

Methods: A fibrotic mouse model was generated by intraperitoneal injection of carbon tetrachloride (CCl) and subsequent treatment with or without metformin. The level of fibrosis was detected by hematoxylin-eosin staining, Sirius Red staining, and immunohistochemistry.