This study aimed to assess and compare sarcopenia with other prognostic factors for predicting long-term mortality in cirrhotic patients with ascites. Clinical data of 65 among 89 patients with measurement of all parameters were consecutively collected. Sarcopenia was evaluated as right psoas muscle thickness measurement divided by height (PMTH) (mm/m). During a mean follow-up of 20 (range: 1-49) months, 19 (29.2%) of 65 patients died. The values of the area under the receiver operating characteristics curve (AUROC) of Child-Pugh score, Model for End-Stage Liver Disease (MELD) score, MELD-Na, and PMTH for predicting 1-yr mortality were 0.777 (95% CI, 0.635-0.883), 0.769 (95% CI, 0.627-0.877), 0.800 (95% CI, 0.661-0.900), and 0.833 (95% CI, 0.699-0.924), whereas hepatic venous pressure gradient was not significant (AUROC, 0.695; 95% CI. 0.547-0.818, P=0.053). The differences between PMTH and other prognostic variables were not significant (all P>0.05). The best cut-off value of PMTH to predict long-term mortality was 14 mm/m. The mortality rates at 1-yr and 2-yr with PMTH>14 mm/m vs. PMTH≤14 mm/m were 2.6% and 15.2% vs. 41.6% and 66.8%, respectively (P<0.001). The mortality in cirrhotic patients with PMTH≤14 mm/m was higher than those with PMTH>14 mm/m (HR, 5.398; 95% CI, 2.111-13.800, P<0.001). In conclusion, sarcopenia, evaluated by PMTH, is an independent useful predictor for long-term mortality in cirrhotic patients with ascites.Graphical Abstract

In cirrhotic patients, LSM by SWE is highly correlated with HVPG value regardless of ascites. SWE is a new reliable non-invasive diagnostic tool to predict CSPH and SPH, even in cirrhotic patients with ascites.

We examined the anti-cancer effect of genistein, a soy-derived isoflavone, in human bladder transitional cell carcinoma T24 cells. According to our data, genistein induced G2/M phase arrest of the cell cycle and apoptosis. Genistein down-regulated the levels of cyclin A and cyclin B1, but up-regulated the levels of p21WAF1/CIP1, cyclin-dependent kinase (Cdk) inhibitor, that was complexed with Cdc2 and Cdk2. Furthermore, genistein induced the activation of caspases (caspase-3, -8 and -9), and cleavage of poly (ADP-ribose) polymerase cleavage. However, genistein-induced apoptosis was significantly inhibited by a pan-caspase inhibitor, indicating that the induction of apoptosis by genestein was caspase-dependent. In addition, genistein increased the cytosolic release of cytochrome c by increasing the Bax/Bcl-2 ratio and destroying mitochondria integrity. Moreover, genistein inactivated the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway, while LY294002, a PI3K/Akt inhibitor, increased the apoptosis-inducing effect of genistein. Genistein further increased the accumulation of reactive oxygen species (ROS), which was significantly suppressed by N-acetyl cysteine (NAC), a ROS scavenger, and in particular, NAC prevented genistein-mediated inactivation of PI3K/Akt signaling, G2/M arrest and apoptosis. Therefore, the present results indicated that genistein promoted apoptosis induction in human bladder cancer T24 cells, which was associated with G2/M phase cell cycle arrest via regulation of ROS-dependent PI3K/Akt signaling pathway.

Pancreatic lipase is the enzyme responsible for digestion and absorption of triglycerides, being its inhibition one of the widest studied methods used to determine the potential activity of natural products to inhibit dietary fat absorption. Decrease of energy intake from dietary fat through inhibition of this enzyme may be an excellent strategy to prevent and treat obesity. The inhibitory activity on pancreatic lipase enzyme of Diospyros kaki fruit and Citrus unshiu peel mixture extract (PCM) was evaluated in vitro and its antiobesity effects were studied based on the serum lipid parameters analysis from high-fat diet- (HFD-) fed mice in vivo. PCM was orally administered at a dose of 50 and 200 mg/kg body weight for 6 weeks. In addition, the activity of pancreatic lipase was assessed using orlistat (positive control). PCM exhibited inhibitory effect on lipase activity with IC50 value of 507.01 μg/mL. Moreover, serum triacylglycerol, total cholesterol levels, and visceral fat weight were significantly reduced compared to HFD control mice in PCM 200 mg/kg-treated mice (p < 0.05). These results suggest that PCM administration may be a novel potential antiobesity agent for reduction of fat absorption via inhibition of pancreatic lipase.

Licochalcone A (LCA) is a chalcone that is predominantly found in the root of Glycyrrhiza species, which is widely used as an herbal medicine. Although previous studies have reported that LCA has a wide range of pharmacological effects, evidence for the underlying molecular mechanism of its anti-cancer efficacy is still lacking. In this study, we investigated the anti-proliferative effect of LCA on human bladder cancer cells, and found that LCA induced cell cycle arrest at G2/M phase and apoptotic cell death. Our data showed that LCA inhibited the expression of cyclin A, cyclin B1, and Wee1, but increased the expression of cyclin-dependent kinase (Cdk) inhibitor p21WAF1/CIP1, and increased p21 was bound to Cdc2 and Cdk2. LCA activated caspase-8 and -9, which are involved in the initiation of extrinsic and intrinsic apoptosis pathways, respectively, and also increased caspase-3 activity, a typical effect caspase, subsequently leading to poly (ADP-ribose) polymerase cleavage. Additionally, LCA increased the Bax/Bcl-2 ratio, and reduced the integrity of mitochondria, which contributed to the discharge of cytochrome c from the mitochondria to the cytoplasm. Moreover, LCA enhanced the intracellular levels of reactive oxygen species (ROS); however, the interruption of ROS generation using ROS scavenger led to escape from LCA-mediated G2/M arrest and apoptosis. Collectively, the present data indicate that LCA can inhibit the proliferation of human bladder cancer cells by inducing ROS-dependent G2/M phase arrest and apoptosis.

Substantial liver fibrosis on SWE was observed in about 5% of MTX-treated patients with RA and was associated with only a high body mass index but not with the cumulative MTX dose, suggesting that other comorbidities might have a more important role in liver fibrosis.

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