BACKGROUNDIn China, hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) is the most common liver failure characterized by serious clinical syndromes of liver decompensation with a very high mortality. Bacterial and/or fungal infections are the most common complications that are associated with high short-term mortality. Bacterial translocation from the intestine, impaired hepatic clearance, and immune paralysis of circulating immune cells are thought to contribute to infectious complications in liver failure. The control of bacterial and fungal infections is the key to improving HBV-ACLF outcomes. Active prevention, early diagnosis, and timely treatment of bacterial and fungal infections are essential for treating HBV-ACLF.AIMTo investigate the frequency and role of bacterial and fungal infections in patients with HBV-ACLF.METHODSPatients with HBV-ACLF hospitalized at Taihe Hospital, Hubei University of Medicine from January 2014 to December 2017 were retrospectively enrolled. Patient-related information was retrieved from the hospital case database, including general information, blood biochemistry, complications, etc. According to the occurrence of secondary infection or not, the patients were divided into an infection group and a non-infection group. The sites, types, and incidences of bacterial and fungal infections and the influence of infections on the prognosis of HBV-ACLF were statistically analyzed. The risk factors for infections were assessed by unconditional logistic regression.RESULTSThere were 174 cases of HBV-ACLF that met the enrollment criteria, of which 114 (65.52%) were diagnosed with infectious complications. Infections occurred in the abdominal cavity (87 cases), respiratory tract (51 cases), urinary tract (18 cases), and biliary tract (10 cases). Patients with infectious complications had a significantly higher 28-d mortality (70.18%, 80/114) than those without (40.00%, 24/60) (70.18% vs 40.00%, P < 0.05). And patients with infectious complications had a much higher incidence of non-infectious complications (54.39%, 62/114) (54.39% vs 15.00%, P < 0.05), leading to an extremely high 28-d mortality of 88.71% (55/62) (P < 0.05). The grade of liver failure, period of hospital stay ≥ 30 d, age ≥ 45 years, and percentage of neutrophils > 70% were identified as risk factors for infectious complications.CONCLUSIONThe high incidence of infectious complications in patients with HBV-ACLF is associated with severity and deterioration of the disease and may contribute to the extremely high mortality of these patients.

Down-regulating Bmi-1 may inhibit the biological properties of CD133+ LCSC by blocking NF-κB signaling pathway, which lays a scientific foundation for the clinical treatment of liver cancer.

Overcoming resistance to alkylating agents has important clinical significance in glioma. Cyanidin-3-O-glucoside (C3G) has a tumor-suppressive effect on tumor cells. However, whether it plays a role in temozolomide resistance in glioma is still unclear. We constructed a TMZ-resistant LN-18/TR glioma cell line, observed the effect of C3G on TMZ resistance in this cell line, and explored the role of miR-214-5p in chemoresistance. Results showed that β-catenin and MGMT were significantly upregulated in LN-18/TR cells. C3G upregulated miR-214-5p and enhanced the cytotoxic effect of temozolomide on LN-18/TR cells. Contrarily, C3G downregulated β-catenin and MGMT. Moreover, the miR-214-5p mimic downregulated β-catenin and MGMT in LN-18/TR cells, whereas the miR-214-5p inhibitor had the opposite effect; the miR-214-5p inhibitor significantly blocked the C3G-induced downregulation of β-catenin and MGMT. C3G or the miR-214-5p mimic enhanced temozolomide-induced apoptosis in LN-18/TR cells, whereas the miR-214-5p inhibitor blocked this effect. Furthermore, C3G or miR-214-5p agomir combined with TMZ significantly inhibited the growth of LN-18/TR tumors. Collectively, our research discovered the potential signaling mechanism associated with C3G-mediated suppression of TMZ resistance in LN-18/TR cells through miR-214-5p, which can facilitate the treatment of MGMT-induced resistance in glioma cells.