Circulating activated Tfh and plasma cells may be associated with hypergammaglobulinaemia during the pathogenic process of AIH in humans.

This aim of this study was to assess the potential role of IL-33 in the pathogenic process of chronic hepatitis B (CHB). The levels of serum IL-33 and soluble ST2 (sST2) in CHB patients and healthy controls (HC) were determined using enzyme-linked-immunosorbent serologic assay, and the Th1 (IFN-γ, TNF-α, IL-2) and Th2 (IL-4, IL-6, IL-10) cytokines by cytometric bead array. It was found that the levels of serum IL-33 in CHB patients were significantly higher than that of HC at the base line, but decreased after treatment with adefovir dipivoxil for 12 weeks. The levels of serum sST2, as a decoy receptor of IL-33, were significantly higher in CHB patients than the HC. There was no correlation between the levels of serum sST2 and IL-33. The concentrations of serum Th1 (IFN-γ, IL-2) and Th2 (IL-6, IL-10) cytokines in CHB patients significantly increased after treatment compared to the baseline. These results suggest that IL-33 is involved in the pathogenesis of CHB and that adefovir dipivoxil therapy can attenuate the production of IL-33 in patients with CHB.

IL-37 is a new anti-inflammatory cytokine that plays an important role in protecting against tissue injury during infections via limiting immune and inflammatory reactions. This study aimed at determining serum IL-37 concentrations and HBeAg seroconversion in chronic hepatitis B virus (HBV) patients during Telbivudine (LDT) treatment. The serum levels of IL-37 were determined using enzyme-linked immunosorbent assay (ELISA) in 40 chronic hepatitis B virus infection (CHB) patients (HBeAg positive), 30 chronic hepatitis C virus infection (CHC) patients [25 with spontaneously resolved hepatitis C virus (SR-CHC)], and 30 healthy controls (HCs). Anti-inflammatory cytokines such as IL-2 and IL-10 were measured using cytometric bead array, and the concentrations of clinical parameters such as serum hepatitis B surface antigen (HBsAg), hepatitis B nucleocapsid antigen (HBeAg), alanine transaminase (ALT), aspartate transaminase (AST), HBV DNA, and hepatitis C virus (HCV) RNA loads were measured. It was found that the serum levels of IL-37 were higher in chronic HBV patients with high virus loads, but the association was not statistically significant. The serum levels of IL-37 were decreased in HBeAg seroconverted CHB patients after 48 weeks of LDT treatment. The serum levels of IL-37 had no significant difference in CHC patients compared with SR-HCV and HCs. The levels of anti-inflammatory cytokine, IL-2 and IL-10, were lower in CHB and CHC patients than the HC, but IL-2 levels increased after LDT treatment in CHB patients. The concentrations of serum IL-37 in CHB and CHC patients with abnormal levels of serum ALT ( > 50 U/L) or AST ( > 40 U/L) were significantly higher than CHB, CHC patients with normal levels of ALT ( < 50 U/L) or AST ( < 40 U/L). These results suggest that IL-37 may play a significant role in the immune response of CHB patients with HBeAg seroconversion. The serum levels of IL-37 are associated with liver damage in CHB patients.

With prevalence of 10–20% in adults in developed countries, gallstone disease (GSD) is one of the most prevalent and costly gastrointestinal tract disorders in the world. In addition to gallstone disease, chronic liver disease (CLD) is also an important global public health problem. The reported frequency of gallstone in chronic liver disease tends to be higher. The prevalence of gallstone disease might be related to age, gender, etiology, and severity of liver disease in patients with chronic liver disease. In this review, the aim was to identify the epidemiology, mechanisms, and treatment strategies of gallstone disease in chronic liver disease patients.

Apoptin is a chicken anemia virus-derived, p53-independent, bcl-2-insensitive apoptotic protein with the ability to specifically induce apoptosis in various human tumor cells, but not in normal cells. To explore the use of apoptin in tumor gene therapy, we assessed a recombinant adenovirus expressing the apoptin protein (Ad-hTERTp-E1a-Apoptin) in order to determine its lethal and growth-inhibitory effects on PC-3 and RM-1 cells in vitro and its antitumor effect on solid tumors in vivo. 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT), acridine orange (AO)/ethidium bromide (EB), 4'-6-diamidino-2-phenylindole (DAPI), and Annexin V assays showed that Ad-hTERTp-E1a-Apoptin inhibited the proliferation of PC-3 and RM-1 cells in vitro by inducing apoptosis of prostate cancer cells, and that this inhibitory effect was dose and time-dependent. In the animal models, Ad-hTERTp-E1a-Apoptin significantly inhibited tumor growth and extended the lifespan of animals. Experimental results indicate that Ad-hTERTp-E1a-Apoptin has a potential application in tumor gene therapy.

No abstract

Combination treatment with endostar, a novel modified endostatin, and cytotoxic chemotherapies showed a survival benefit in Chinese clinical trials. However, the exact mechanism for this synergism remains unclear. In this study, we report for the first time that the chemokine receptor CXCR4 and the hypoxia-inducible transcription factors (HIF)-1α and HIF-2α are involved in these synergistic antitumor effects in human colorectal cancer SW1116 cells in vitro when endostar treatment is combined with the cytotoxic drug oxaliplatin. Under normoxia, we demonstrate that endostar and oxaliplatin treatments synergize to inhibit SW1116 cell proliferation, Matrigel adhesion and invasion by reduction of CXCR4 expression. Consistently, these antitumor abilities of endostar and oxaliplatin were markedly reduced by silencing of CXCR4 in SW1116 cells. Under low oxygen conditions (hypoxia, 1% oxygen), enhanced proliferation of SW1116 cells exposed to oxaliplatin was observed due to the emergence of drug resistance. Strikingly, endostar overcame oxaliplatin-resistance, most likely as a consequence of reduced HIF-2α and CXCR4 levels. CXCR4, is only dependent on HIF-2α, which promotes more aggressive phenotype and more significant for oxaliplatin resistance in SW1116 cells. Our data not only provide clues to aid understanding of the mechanism of the synergism of endostar and chemotherapy under either normoxia or hypoxia, but also suggests a new strategy of combination endostar and chemotherapy treatments which might potentiate therapeutic efficacies and/or counteract chemotherapy resistance.

Background. The population of patients with acute pancreatitis treated by the staff at our department of gastroenterology includes those with mild and self-limited disease ranging to those with severe and fatal disease. Early diagnosis and accurate prediction of the severity and outcome of this disease, which is commonly seen by our department, is important for a successful outcome. Metabolic comorbidities (e.g., diabetes mellitus, fatty liver, obesity, and metabolic syndrome) are relevant to the severity and progression of many diseases. The objective of this review was to examine clinical relationships between metabolic comorbidities and occurrence, severity, and outcome of acute pancreatitis.