Highly-efficient and sequential recovery of rare earth elements, alumina and silica from coal fly ash via a novel recyclable ZnO sinter method.

A novel sinter method using ZnO as the activator instead of the conventional Na2CO3/CaCO3, (NH4)2SO4, and K2S2O7 was developed to achieve efficient sequential extraction of rare earth elements (REEs), alumina (Al), and silica (Si) from coal fly ash (CFA). Up to 93.3% Si, 87.1% REEs (70.7% Ce, 82.5% La, 83.2% Gd, 87.1% Nd, 62.3% Dy, and 81.7% Y), and 92.9% Al were extracted from CFA, respectively. Moreover, 93.1% of the ZnO activator was efficiently recycled, and the yield of red mud was only 14.9%. X-ray diffraction (XRD) and X-ray absorption near edge structure (XANES) results showed that the speciation transformation of Al/Si during CFA/ZnO roasting was as follows: mullite, quartz, amorphous Al2O3, and SiO2 → Zn0.75Al1.5Si1.5O6, kyanite and willemite → gahnite and quartz/cristobalite solid solutions. The change in the REEs occurrence mode hinted at the migration of most REEs in aluminosilicates forms with Si during roasting, and disassociation with Si into the acid-soluble form after alkali leaching. These results indicate that the coupling of Al-Si-REE in CF was broken by this ZnO sinter method, promoting the sequential and efficient extraction of REEs, Al, and Si from CFA. This study provides a green and efficient strategy for element recovery from CFA, substantially reducing residues and favoring REEs concentration.

The differential inhibitive effects and fates of As(III) and As(V) mediated by Sulfobacillus thermosulfidooxidans grown on S0, Fe2+ and FeS2.

Arsenic often coexists with metal sulfide minerals and occurs in different speciation and different toxicity in responding to Fe/S biooxidation. The differential inhibitive effects and fates of As(III) and As(V) during biooxidations of elemental sulfur (S0), ferrous ions (Fe2+) and pyrite (FeS2) by Sulfobacillus thermosulfidooxidans were studied. The results revealed that the arsenic species hardly changed for the biooxidation of S0, but dramatically changed for the biooxidation of Fe2+ and FeS2. Different transformation degree between As(III) and As(V) occurred for biooxidation of FeS2 in the presence of arsenic, where about 72% of As(III) was transformed to As(V) for the group with As(III) added, and 16% of As(V) was transformed to As(III) for that with As(V) added. Both formation and dissolution of amorphous ferric arsenate occurred during biooxidation of FeS2 with the addition of As(III) or As(V) and for the group grown on Fe2+ with added As(V), which were controlled by the changes of Fe/As molar ratio and pH value in the solution. Jarosite was detected for the group grown on Fe2+ and could adsorb As(III) and As(V). The inhibitive effects of As(V) were higher than As(III) when the strain grew on FeS2, which was contrary to those when the strain grew on S0 and Fe2+. The above results signify that the fates and inhibitive effects of arsenic are much related to each other, and such a relationship is significantly affected by the utilization of Fe/S energy substrates by the sulfur- and ferrous-oxidizing microorganisms.

Humic acid promotes arsenopyrite bio-oxidation and arsenic immobilization.

The bio-oxidative dissolution of arsenopyrite, the most severe arsenic contamination source, can be mediated by organic substances, but pertinent studies on this subject are scarce. In this study, the bio-oxidative dissolution of arsenopyrite by Sulfobacillus thermosulfidooxidans and arsenic immobilization were evaluated in the presence of humic acid (HA). The mineral dissolution was monitored through analyses of the parameters in solution, phase and element speciation transformations on the mineral surface, and arsenic immobilization on the surfaces of cells and jarosites-HA. The results show that the presence of HA enhances the dissolution of arsenopyrite, e.g., 7.1% of arsenopyrite was in the residue after 12 d of bio-oxidation compared to 19.3% in the absence of HA. Meanwhile, the presence of HA led to changes of the fates of As and Fe and no accumulation of elemental sulfur (S0) or ferric arsenate on the mineral surface. Moreover, a flocculent porous structure was formed on the surfaces of both microbial cells and jarosites, on which a large amount of arsenic was adsorbed. These results clearly indicate that HA can simultaneously promote the dissolution of arsenopyrite and arsenic immobilization, which may be significant for bioleaching of arsenopyrite-bearing contaminated sites.

Epigenetic silencing of ITGA2 by MiR-373 promotes cell migration in breast cancer.

The loss of ITGA2 plays an important role in cancer metastasis in several solid cancers. However, the molecular mechanism of ITGA2 loss in primary cancers remains unclear. In this study, we found that a lower ITGA2 protein level was observed in breast cancers compared to adjacent non-cancerous breast tissues. Interestingly, the reduction degree of ITGA2 at the protein level was far more than that at the mRNA level. We further showed that the translation of ITGA2 mRNA was directly inhibited by miR-373 through binding to ITGA2-3'UTR. Silencing of ITGA2 detached cell-cell interactions, induced the deploymerization of stress fiber F-actin and stimulated cancer cell migration, similar to the effect of miR-373 over-expression. The co-expression of ITGA2, not ITGA2-3'UTR, could abrogate miR-373-induced cancer cell migration because that the expression of ITGA2-3'UTR was inhibited by co-transfected miR-373. ITGA2 protein level was inversely associated with miR-373 level in breast cancers (r = -0.663, P<0.001). 73.33% of breast cancer patients with high miR-373 and low ITGA2 expression exhibited the lymph node-positive metastases. Together, our results show that epigenetic silencing of ITGA2 by miR-373 stimulates breast cancer migration, and miR-373high/ITGA2low may be as a prognosis biomarker for breast cancer patients.