A bibliometric review of biochar for soil carbon sequestration and mitigation from 2001 to 2020.

To mitigate global warming and the greenhouse effect, biochar (BC) has been regarded as an important way of carbon sink. Therefore, this research explored the development trend of BC for soil carbon sequestration and mitigation from 2001 to 2020 based on bibliometric analysis. The results show that Yong Sik Ok and Johannes Lehmann are the top 2 high-impact authors. China, America, and Germany are the most widely collaborated countries, but China's research impact is lower than that of America. The Chinese Academy of Sciences has far more publications than any other institution, but Cornell University and Kangwon National University lead the way in terms of impact. Research hotspots can be divided into five clusters: (1) pyrolysis, nutrient, and microbial communities; (2) the immobilization of heavy metals; (3) crop yield and soil properties; (4) greenhouse gas, meta-analysis, and field experiment; (5) carbon fraction and sequestration. Reviews account for 60 % of the top 10 most highly cited papers, and eight of the top 10 focus on the early research period, setting the stage for the development of the BC field. Science of the Total Environment has the highest number of publications and total citations, and literature published in Soil Biology and Biochemistry is to some extent more likely to be cited. In the future, we need to carry out research in the following aspects: (1) Interaction mechanisms between BC, soil, and soil microbial communities. (2) Designing low-cost, high-yield, and high-effect optimization methods to improve the characteristics of BC. (3) Effect of BC on the environment and human health in long-term localization experiments. (4) Carbon sinks of BC need to be further evaluated on a global scale.

3-Acetyldeoxynivalenol induces apoptosis, barrier dysfunction and endoplasmic reticulum stress by inhibiting mTORC1-dependent autophagy in porcine enterocytes.

3-Acetyldeoxynivalenol (3-Ac-DON), an acetylated form of deoxynivalenol, is widely present in mycotoxin-contaminated food, feed as well as in other natural sources. Ingestion of 3-Ac-DON may result in intestinal dysfunction, leading to gut diseases in humans and animals. Nevertheless, the molecular mechanism of 3-Ac-DON in intestinal epithelial cytotoxicity remains unclear. In this study, intestinal porcine epithelial cell line 1 (IPEC-1) cells were treated with different concentrations of 3-Ac-DON for 12 h or 24 h, respectively. The results showed that 3-Ac-DON caused decreased cell viability, cell cycle arrest in G1 phase and depolarization of mitochondrial membrane potential. Western blotting analysis showed that 3-Ac-DON significantly decreased the expression of tight junction proteins, inhibited autophagy and activated endoplasmic reticulum (ER) stress in IPEC-1 cells (P < 0.05). Further investigation demonstrated that 3-Ac-DON caused apoptosis, ER stress and barrier dysfunction were reversed after co-treatment with the autophagy activator rapamycin (100 nM), indicating that autophagy plays a key role in the process of 3-Ac-DON-induced cell damage. In addition, we demonstrated that 3-Ac-DON inhibits the occurrence of autophagy mediated by mTORC1 protein. In conclusion, our research indicated that the mTORC1 protein and autophagy played a key role in the 3-Ac-DON-induced cytotoxic in IPEC-1 cells, which would provide new therapeutic targets and ideas for 3-Ac-DON-mediated intestinal injury.

4-Phenylbutyric acid alleviates 3-acetyldeoxynivalenol-induced immune cells response by inhibiting endoplasmic reticulum stress in mouse spleen.

3-Acetyldeoxynivalenol (3-Ac-DON), an acetylated derivative of deoxynivalenol (DON), is contaminated grains and grain-based products in general and been harmful to human and animal health. However, the damage effects and regulatory mechanisms to the host immune system have not been well explored. In the present study, our results revealed that 3-Ac-DON significantly decreased spleen index, elevated MPO activity, upregulated mRNA and protein levels of IL-1α, IL-1ß, IL-6, IL-17A, TNF-α, M-CSF, G-CSF, CCL2, IFN-ß, and IL-10 in the spleen and serum. Interestingly, 4-phenylbutyric acid (4-PBA), an inhibitor of endoplasmic reticulum (ER) stress, largely abolished the above adverse effects. Importantly, 3-Ac-DON enhanced the mRNA abundances of ER stress-related indicators, such as BIP, IRE1A, ATF6, XBP-1, EIF2A, ATF4, and CHOP, which were abolished by 4-PBA, indicating the inhibiting effects of ER stress by 4-PBA in the spleen. Furthermore, 3-Ac-DON reshaped the populations of innate immune cells (neutrophils, macrophages, dendritic cells, natural killer cells) and adaptive immune cells (T lymphocytes, helper T cells, suppressor T cells, and B lymphocytes) in the peripheral blood and spleen lymphocytes. In conclusion, our studies demonstrated that the adverse effects of 3-Ac-DON on immune cells response could be implemented by ER stress and the ameliorative effect of 4-PBA.