S doped NiCo2O4 nanosheet arrays by Ar plasma: An efficient and bifunctional electrode for overall water splitting.

Transition metal oxides show great potential as electrocatalysts, owing to the low cost and rich chemical states. However, the limited surface areas, low intrinsic activity and poor hydrogen evolution reaction (HER) activity greatly restrict the application for overall water splitting. Herein, we have constructed S doped NiCo2O4 nanosheet arrays by Ar plasma (Ar-NiCo2O4|S) to enhance active sites and boost catalytic kinetics. Consequently, the Ar-NiCo2O4|S shows the improved performances for HER and oxygen evolution reaction (OER). Further, as bifunctional electrocatalysts, Ar-NiCo2O4|S exhibit a voltage of 1.63 V at 10 mA cm-2, as well as good stability.

Hypoxia responsive miR-210 promotes cell survival and autophagy of endometriotic cells in hypoxia.

OBJECTIVE: Hypoxia may play a role in the survival of ectopic endometrial cells. This study aimed to explore how hypoxia responsive miR-210 is involved in cell survival and autophagic response of endometriotic cells. MATERIALS AND METHODS: The expression of hypoxia-inducible factor 1-alpha (HIF-1α) and miR-210 in eutopic and ectopic endometrial tissues were measured. The expression changes of HIF-1α and miR-210 in ovarian endometriotic cell line CRL-7566 after hypoxic culture were further explored. The influence of miR-210 on cell viability and apoptosis was quantified using CCK-8 assay and flow cytometry analysis. The effect of miR-210 on Bcl-2 expression and the effect of miR-210/Bcl-2 axis on autophagy in the cells were measured by Western blot analysis. RESULTS: Ectopic lesion had stronger HIF-1α positive signals, as well as more HIF-1α positive cells per visual field than the eutopic endometrium. MiR-210 expression was also elevated in the ectopic lesions. In in-vitro models, CRL-7566 cells had significantly higher expression of HIF-1α and miR-210 after hypoxic treatment. MiR-210 overexpression partly preserved cell viability in hypoxia, while miR-210 knockdown facilitated the loss of cell viability. In addition, miR-210 significantly attenuated hypoxia-induced apoptosis in CRL-7566 cells. Enforced miR-210 overexpression significantly promoted autophagy in hypoxia. Knockdown of endogenous Bcl-2 significantly enhanced autophagy, the effect of which was similar to that of miR-210. CONCLUSIONS: The hypoxia-induced higher miR-210 expression may contribute to pathological development of endometriosis at least through enhancing cell survival and promoting autophagy via Bcl2/Beclin-1 axis.