At present, hepatic encephalopathy has a relatively high mortality and thus greatly affects patients’ quality of life. This article describes the changes of intestinal flora in patients with hepatic encephalopathy and analyzes the mechanism of action of intestinal flora in hepatic encephalopathy and related treatment methods. It is pointed out that the development of hepatic encephalopathy is closely associated with intestinal flora, and clinical treatment by regulating intestinal flora has achieved a marked effect in patients with hepatic encephalopathy. In the future, the research on intestinal flora in patients with hepatic encephalopathy can be deepened to provide better regimens for the treatment of hepatic encephalopathy.

As a novel form of programmed cell death different from cell necrosis, apoptosis, and autophagy discovered in recent years, pyroptosis is characterized by cell membrane rupture and release of cell contents and proinflammatory factors mediated by gasdermin, thus leading to cell death. Pyroptosis signaling pathways can be classified into classical pathways dependent on caspase-1 and non-classical pathways dependent on caspase-4/5/11; the activation of caspase-1 in classical pathways depends on the function of inflammasome, while the direct activation of caspase-4/5/11 is observed in non-classical pathways, which leads to the lysis of gasdermin D and induce the formation of membrane pores, the maturation and release of interleukin-1β and interleukin-18, and the rupture of cell membrane to cause pyroptosis. Latest research has shown that pyroptosis plays an important role in the development and progression of chronic liver diseases. This article introduces the mechanism of pyroptosis and summarizes the role of pyroptosis in the development and progression of nonalcoholic fatty liver disease, alcoholic liver disease, viral hepatitis, liver cirrhosis, and hepatocellular carcinoma, in order to provide new ideas and methods for the prevention and treatment of liver diseases in clinical practice.

Objective:To explore a method for detecting recombinant human Annexin A11 (ANXA11) in serum exosomes of pancreatic cancer patients, and then primarily evaluate the clinical value of ANXA11 in pancreatic cancer patients.Methods:A prospective study was conducted and serum specimens from 70 patients diagnosed with PC, 15 patients diagnosed with benign pancreatic mass and 70 patients diagnosed with pancreatitis from the Affiliated Hospital of Nantong University were collected from December 2016 to July 2019. 70 healthy subjects during the same period were selected as control group. The abundance of ANXA11 in serum and exosomes-free serum were detected through parallel reaction monitoring (PRM) basing on high-resolution, high-precision mass spectrometer. Dot immunoblotting created by ourselves for detecting ANXA11 in exosomes and then the methodological evaluation were carried out. Levels of ANXA11 in exosomes in all subjects were statistically analyzed. Moreover, the areas under the curve (AUC) of receiver operating characteristic (ROC) curves were adopted to evaluate the diagnostic efficacy of ANXA11, CA19-9, CEA on PC. The relationship between ANXA11 and clinicopathological parameters as well as prognosis of PC patients was analyzed in the next moment. For analysis, the Mann-Whitney U test was used for comparing between either two groups, and the kruskal-wallis test was used for comparison among four groups. Results:The detection of serum exosome ANXA11 has high sensitivity and repeatability by the method of self-established dot immunoblotting. ANXA11 increased most significantly in the PC group, and the difference was statistically significant ( Hc=58.079, P<0.01) compared with other three groups. ROC curve analysis showed that the diagnostic performance of ANXA11(area under the curve (AUC=0.836) was higher than CEA (AUC=0.656) and equal to CA19-9 (AUC=0.870). The combination of ANXA11 and CA19-9 could improve the sensitivity of diagnosing PC and maintain good specificity. The level of serum exosome ANXA11 before treatment in PC patients was not related to age, gender, tumor size, tumor growth site, lymph node metastasis, distant metastasis and TNM stage ( Z values are 0.052,-0.285,-0.402,0.324,0.888,0.658,1.734, P>0.05). Furthermore, during the 10th day after surgical treatment, the level of ANXA11 showed no statistical difference compared with that before surgery ( Z value is -1.569, P=0.12). The survival time of PC patients was related to the presence of lymph node metastasis, distant metastasis, TNM staging and treatment protocols (χ 2 values are 9.354,6.086,9.389,16.998, P<0.05), while had no correlation with levels of CEA, CA19-9 and ANXA11 (χ 2 values are 1.516, 0.011, 0.159, P>0.05). Conclusions:This study successfully established an original method for detecting ANXA11 levels in serum exosomes of human. Serum exosomes ANXA11 combined with CA19-9 could improve the diagnostic sensitivity of PC.

The development and progression of nonalcoholic fatty liver disease (NAFLD) have complex potential mechanisms. The traditional “two-hit” pathophysiological theory has been challenged, and in recent years, an increasing number of studies have been performed to investigate the interaction between insulin resistance, adipokines, and other unknown pathogenic factors in various organs. This article summarizes the factors of the liver, intestinal tract, hypothalamus, and extracellular cysts, as well as genetic factors, with an emphasis on the synergistic mechanism of action of the liver and extrahepatic organs in the pathogenesis of NAFLD, in order to provide a reference for obtaining new insights into NAFLD regulatory network and determining new targets for the prevention and treatment of NAFLD.