Destruction of 4-chlorophenol by the hydrogen-accelerated catalytic Fenton system enhanced by Pd/NH2-MIL-101(Cr).

4-chlorophenol (4-CP) could be rapidly mineralized by using Fenton reaction. However, massive iron sludge will be generated because of the excessive consumption of iron salt and poor recycling of FeIII back to FeII. In this paper, by introducing hydrogen gas and solid catalyst Pd/NH2-MIL-101(Cr) to classic Fenton reactor, the novel system named MHACF-NH2-MIL-101(Cr) was constructed. Much less FeII was needed in this system because the hydrogen could significantly accelerate the regeneration of FeII. The catalyst improved the utilization of H2. The degradation reaction of 4-CP could be driven by using only trace amount of FeII. It could be rapidly degraded by the hydroxyl radical detected by the 4-Hydroxy-benzoicacid which is the oxidative product of benzoic acid and hydroxyl radical. The effects of dosage of ferrous salt, H2O2 and catalyst, H2 flow, Pd content, and initial pH of and concentration of 4-CP aqueous solution were investigated. The robustness and morphology changes of this catalytic material were also systematically analysed. By clarifying the role of this solid MOFs material in this hydrogen-mediated Fenton reaction system, it will provide a new direction for the research and development of advanced oxidation processes with high efficiency and low sludge generation in future.

HOXB4 promotes the malignant progression of ovarian cancer via DHDDS.

BACKGROUND: Homeobox B4 (HOXB4) is correlated with poor prognosis of various cancer types. However, how HOXB4 promotes ovarian cancer (OV) progression remains unclear. METHODS: The Cancer Genome Atlas (TCGA) database indicated that a high level of HOXB4 in OV was correlated with poor prognosis. The biological functions of HOXB4 were confirmed by colony formation, migration, and invasion assays. The effect of HOXB4 on the expression of EMT cell markers was determined. The transcriptional target of HOXB4 was DHDDS, which was detected by a ChIP assay. A xenograft tumor model was generated in nude mice to detect the role of HOXB4 in tumor proliferation and metastasis. RESULTS: The results showed that HOXB4 protein levels were higher in OV tissues than in normal tissues and correlated with poor prognosis of OV. HOXB4 reduction inhibited the proliferation and invasion ability of OV cells in vitro. Conversely, these effects were enhanced by the upregulation of HOXB4 in OV cells. The binding of HOXB4 to two DNA motifs regulated DHDDS expression and contributed to the malignant progression of OV. The role of HOXB4 in contributing to tumor development in vivo was verified in mice. Further results indicated that HOXB4 induced Snail and Zeb1 expression. CONCLUSION: Overall, HOXB4 overexpression was remarkably correlated with poor prognosis of OV. Mechanistically, HOXB4 enhances the proliferation and invasion of tumor cells by activating DHDDS, thereby promoting the malignant progression of OV.