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A commercial activated carbon was functionally modified by silylation with 3-aminopropyltriethoxysilane (APTES). The silylation led to the fixation of weakly basic functional groups, -NH 2 , on the surface as indicated by pH titration, Boehm titration, N 2 − BET analysis and X-ray photoelectron spectroscopic (XPS) analysis. Despite reducing the specific BET area and the pore volume, silylation improved the H 2 S removal capacity so that APTES modified activated carbon (APTES-AC) was 3.55 times more effective than the original activated carbon. XPS results indicate that H 2 S removal may be associated with the amino (-NH 2 ) group and the presence of sulfur in the four oxidation states S 2− , S 0 , S 4+ and S 6+ . The effects of moisture, oxygen content and temperature on the performance of APTES-AC for H 2 S removal were investigated. The presence of moisture in the gas stream was found to have an adverse effect on the H 2 S removal, whilst the presence of oxygen favored the removal of H 2 S by APTES-AC. The higher removal capacity of APTES-AC relative to the original activated carbon indicates that APTES-AC is a potential candidate for the removal of H 2 S from gas streams. The H 2 S removal efficiency of APTES-AC was proved be superior to that of Na 2 CO 3 -impregnated AC by the pilot-scale test of purification H 2 S containing industrial waste gas, yellow phosphorus off-gas.

Background Activation of autocrine VEGF-VEGFR2 signalling in tumour cells activates cell proliferation, survival, and angiogenesis, all of which are crucial for tumour progression. Ovarian cancer-associated antigen 66 (OVA66) is now known to be overexpressed in multiple tumours and plays a role in tumour development, but the underlying mechanisms has not been fully investigated. Methods We employed ovarian and cervical cancer cells and mouse models to detect the role of OVA66 in angiogenesis, growth, and metastasis of cancer cells. Immunofluorescence and western blot were used to determine the function of OVA66 in regulating autocrine VEGF-VEGFR2 signalling. Immunohistochemistry and bioinformatics analysis were used to detect the correlation of OVA66 and VEGF expression. Findings OVA66 overexpression in the cancer cell lines promoted VEGF secretion, tumour growth and angiogenesis in vitro and in vivo. Conversely, shRNA-mediated OVA66 knockdown had the opposite effects. Mechanistically, OVA66 overexpression was found to boost an autocrine VEGF–VEGFR2 positive-feedback signalling loop in the tumour cells, leading to amplified effect of VEGF on tumour angiogenesis and proliferation and increased migration in vitro and in vivo , respectively. Finally, we identified a significant positive correlation between the expression levels of OVA66 and VEGF in ovarian and cervical cancer specimens, and found that OVA66 was significantly associated with advanced ovarian cancer. Interpretation We identify a novel function for OVA66 in regulating an autocrine VEGF–VEGFR2 feed-forward signalling loop that promotes tumour progression and angiogenesis. Fund This work was supported by the National Natural Science Foundation of China (81602262); and Excellent Youth Scholar Program of Tongji University (2015KJ062).