Influence of Fe3+ Ions on Nitrate Removal by Autotrophic Denitrification Using Thiobacillus denitrificans

The sulphur-based autotrophic denitrification process utilizing Thiobacillus denitrificans was studied experimentally as an alternative method of removing nitrates from industrial wastewater. The objective of the work was to examine the effect of ferric iron addition to the reaction mixture and determine optimal dosage for specific conditions. All experiments were carried out in anoxic batch bioreactor, and elemental sulphur was used as an electron donor. Compared to the control operation without ferric iron addition, significant increases in nitrates removal were demonstrated for the concentration of ferric iron equal to 0.1 mg L–1. However, under these conditions, increased nitrite content was detected in the reaction mixture which exceeds the limits for drinking water. This work is licensed under a Creative Commons Attribution 4.0 International License

Integrated analysis of multiple receptor tyrosine kinases identifies Axl as a therapeutic target and mediator of resistance to sorafenib in hepatocellular carcinoma.

Background: Aberrant activation of Axl is implicated in the progression of HCC. We explored biologic significance and preclinical efficacy of Axl inhibition as a therapeutic strategy in sorafenib-naïve and resistant HCC. Methods: We evaluated Axl expression in sorafenib-naïve and resistant (SR) clones of epithelial (HuH7) and mesenchymal origin (SKHep-1) using antibody arrays and confirmed tissue expression. We tested the effect of Axl inhibition with RNA-interference and pharmacologically with R428 on a number of phenotypic assays. Results: Axl mRNA overexpression in cell lines (n=28) and RNA-seq tissue datasets (n=373) correlated with epithelial-to-mesenchymal transition (EMT). Axl was overexpressed in HCC compared to cirrhosis and normal liver. We confirmed sorafenib-resistance to be associated with EMT and enhanced motility in both HuH7-SR and SKHep-1-SR cells documenting a 4-fold increase in Axl phosphorylation as an adaptive feature of chronic sorafenib treatment in SKHep-1-SR cells. Axl inhibition reduced motility and enhanced sensitivity to sorafenib in SKHep-1SR cells. In patients treated with sorafenib (n=40) circulating Axl levels correlated with shorter survival. Conclusions: Suppression of Axl-dependent signaling influences the transformed phenotype in HCC cells and contributes to adaptive resistance to sorafenib, providing a pre-clinical rationale for the development of Axl inhibitors as a measure to overcome sorafenib resistance