Emission of PAHs, NPAHs and OPAHs from residential honeycomb coal briquette combustion

Coal combustion is one of the most significant sources of air pollution in China. In this study, emission factors (EFs) of 15 polycyclic aromatic hydrocarbons (PAHs), 26 nitrated PAHs (NPAHs) and 6 oxygenated PAHs (OPAHs) were determined in five different coals with different geological maturity (vitrinite reflectance <i>R</i>_O = 0.77–1.88%) burned in the form of honeycomb briquettes. The total EFs ranged from 9.82 to 215 mg kg^–1 for PAHs, 0.14 to 1.88 mg kg^–1 for NPAHs and 4.47 to 20.8 mg kg^–1 for OPAHs. Measured EFs and gas-particle partitioning varied depending on the geological maturity. The lowest EFs were found in anthracite. The proportion of PAHs, NPAHs and OPAHs in gaseous phase increasing with increased geological maturity. The coal with higher geological maturity produced more 3-ring PAHs. On the basis of the statistical analysis for the residential sector of China in 2008, PAHs, NPAHs and OPAHs emitted from residential honeycomb coal briquettes were 4.36 Gg, 0.03 Gg and 0.47 Gg in 2007, respectively. By 2020, the emission would decrease to 2.18 Gg, 0.02 Gg and 0.24 Gg for PAHs, NPAHs and OPAHs due to the increasing usage of new energy resources. If only anthracite is used as the residential coal, 93% PAHs, 87% NPAHs and 71% OPAHs would be reduced in 2020

The role of Traditional Chinese medicine in anti-HBV: background, progress, and challenges

Abstract Chronic hepatitis B (CHB) remains a major world's most serious public health issues. Despite the remarkable effect of nucleos(t)ide analogues (NAs) in inhibiting hepatitis B virus (HBV) deoxyribonucleic acid (DNA) as the first-line drug, there are several limitations still, such as poor antigen inhibition, drug resistance, low-level viremia, restricting patients' functional cure. Due to the constraints of NAs, traditional medicines, such as traditional Chinese medicine (TCM), have become more prevalently used and researched in the clinical treatment of CHB as complementary alternative therapies. As a consequence, the review focuses on the background based on HBV’s life cycle as well as the NAs’ limitations, progress based on direct and indirect pathway of targeting HBV of TCM, and challenges of TCM. We found TCMs play an increasingly important role in anti-HBV. In a direct antiviral way, they regulate HBV infection, replication, assembly, and other aspects of the HBV life cycle. As for indirect way, TCMs can exert anti-HBV effects through targeting the host, including immune regulation, apoptosis, autophagy, oxidative stress, etc. Especially, TCMs have the advantages of strong antigenic inhibition compared to NAs. Specifically, we can combine the benefits of TCMs in strong HBV antigen inhibition with the benefits of NAs in targeted antiviral effects, in order to find a suitable combination of "TCM + NAs" to contribute to Chinese knowledge of the realisation of the “global elimination of HBV by 2030” goal of the World Health Organization

Tanshinone I specifically suppresses NLRP3 inflammasome activation by disrupting the association of NLRP3 and ASC

Abstract Background Abnormal activation of NLRP3 inflammasome is related to a series of inflammatory diseases, including type 2 diabetes, gouty arthritis, non-alcoholic steatohepatitis (NASH), and neurodegenerative disorders. Therefore, targeting NLRP3 inflammasome is regarded as a potential therapeutic strategy for many inflammatory diseases. A growing number of studies have identified tanshinone I (Tan I) as a potential anti-inflammatory agent because of its good anti-inflammatory activity. However, its specific anti-inflammatory mechanism and direct target are unclear and need further study. Methods IL-1β and caspase-1 were detected by immunoblotting and ELISA, and mtROS levels were measured by flow cytometry. Immunoprecipitation was used to explore the interaction between NLRP3, NEK7 and ASC. In a mouse model of LPS-induced septic shock, IL-1β levels in peritoneal lavage fluid and serum were measured by ELISA. Liver inflammation and fibrosis in the NASH model were analyzed by HE staining and immunohistochemistry. Results Tan I inhibited the activation of NLRP3 inflammasome in macrophages, but had no effect on the activation of AIM2 or NLRC4 inflammasome. Mechanistically, Tan I inhibited NLRP3 inflammasome assembly and activation by targeting NLRP3-ASC interaction. Furthermore, Tan I exhibited protective effects in mouse models of NLRP3 inflammasome-mediated diseases, including septic shock and NASH. Conclusions Tan I specifically suppresses NLRP3 inflammasome activation by disrupting the association of NLRP3 and ASC, and exhibits protective effects in mouse models of LPS-induced septic shock and NASH. These findings suggest that Tan I is a specific NLRP3 inhibitor and may be a promising candidate for treating NLRP3 inflammasome-related diseases. Graphical Abstrac