Review on the NO removal from flue gas by oxidation methods.

Due to the increasingly strict emission standards of NOx on various industries, many traditional flue gas treatment methods have been gradually improved. Except for selective catalytic reduction (SCR) and selective non-catalytic reduction (SNCR) methods to remove NOx from flue gas, theoxidation method is paying more attention to NOx removal now because of the potential to simultaneously remove multiple pollutants from flue gas. This paper summarizes the efficiency, reaction conditions, effect factors, and reaction mechanism of NO oxidation from the aspects of liquid-phase oxidation, gas-phase oxidation, plasma technology, and catalytic oxidation. The effects of free radicals and active components of catalysts on NO oxidation and the combination of various oxidation methods are discussed in detail. The advantages and disadvantages of different oxidation methods are summarized, and the suggestions for future research on NO oxidation are put forward at the end. The review on the NO removal by oxidation methods can provide new ideas for future studies on the NO removal from flue gas.

N-myc and STAT interactor correlates with severity and prognosis in acute-on-chronic liver failure of hepatitis B virus.

BACKGROUND AND AIM: Hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) is characterized by acute deterioration of chronic liver disease with excessive inflammation. N-myc and STAT interactor (NMI), an inflammation-mediated protein, involves in various inflammatory-related diseases, but the role of NMI in development and prognosis in HBV-ACLF remains to be elucidated. METHODS: Serum NMI from healthy controls (HCs, n = 20), chronic hepatitis B (CHB, n = 50) patients, and HBV-ACLF patients (n = 50) was determined using ELISA. NMI from peripheral blood mononuclear cells and liver was confirmed using quantitative real-time polymerase chain reaction, Western blot, and immunofluorescence. RESULTS: Serum NMI was increased 1.9-fold or 2.2-fold from HBV-ACLF patients compared with that from HCs (P < 0.01) or CHB patients (P < 0.01). Consistently, NMI from peripheral blood mononuclear cells was upregulated significantly from HBV-ACLF patients compared with that from HCs and CHB patients at mRNA and protein levels. Hepatic NMI from HBV-ACLF patients was 2.8-fold higher than that from HCs. Serum NMI was correlated with Model for End-stage Liver Disease, Chronic Liver Failure Consortium ACLF score, and ACLF grades. In contrast, serum NMI was significantly decreased in HBV-ACLF ameliorated patients during follow-up, whereas serum NMI was sustained at high levels in non-ameliorated patients. Elevated serum NMI (≥ 198.5 pg/mL) was correlated with poor survival rate of HBV-ACLF patients. Using receiver operating characteristics curves, it was suggested that serum NMI was a potential biomarker in predicting 3-month mortality of HBV-ACLF patients. CONCLUSIONS: Our study highlights the potential role of NMI in assessing the development and prognosis of HBV-ACLF.

Enhanced autophagy contributes to protective effects of IL-22 against acetaminophen-induced liver injury.

Acute or acute-on-chronic liver failure is a leading cause of death in liver diseases without effective treatment. Interleukin-22 (IL-22) is currently in clinical trials for the treatment of severe alcoholic hepatitis, but the underlying mechanisms remain to be explored. Autophagy plays a critical role in alleviating liver injury. The aim of the current study is to explore the role of autophagy in IL-22-mediated hepato-protective effect against acetaminophen (APAP)-induced liver injury. Methods: A model of acute liver injury induced by APAP was used in vivo. IL-22 was administrated to the APAP-treated mice. Hepatocytes were pre-incubated with IL-22, followed by exposure to APAP for in vitro analyses. Results: IL-22 administration significantly reduced serum ALT and AST, hepatic reactive oxygen species, and liver necrosis in APAP-challenged mice. APAP treatment increased hepatic autophagosomes, which was further intensified by IL-22 co-treatment. Hepatic LC3-II was moderately upregulated after APAP administration without obvious alteration of phosphorylation of AMP-activated kinase (p-AMPK). IL-22 pretreatment significantly upregulated hepatic LC3-II and p-AMPK in APAP-treated mice. IL-22 also alleviated APAP-induced cytotoxicity and upregulated LC3-II and p-AMPK expression in cultured hepatocytes treated with APAP in vitro. When p-AMPK was blocked with compound C (an AMPK inhibitor), IL-22-mediated LC3-II conversion and protection against APAP-induced cytotoxicity was weakened. Conclusions: Enhanced AMPK-dependent autophagy contributes to protective effects of IL-22 against APAP-induced liver injury.