Boosting the Electrochemical Storage Properties of Co3O4 Nanowires by the Mn Doping Strategy with Appropriate Mn Doping Concentrations.

High specific capacitance, high energy density, and high power density have always been important directions for the improvement of electrode materials for supercapacitors. In this paper, Co3O4 nanowire arrays with various Mn doping concentrations (Mn:Co molar ratio = 1:11, 1:5, 1:2) directly grown on nickel foam (NF) were prepared by a simple hydrothermal method and annealing process. The influence of Mn doping on the morphology, structure, and electrochemical behaviors of Co3O4 was investigated. The results show that partial substitution of Co ions with Mn ions in the spinel structure does not change the nanowire morphology of pure Co3O4 but increases the lattice parameter and decreases the crystallinity of cobalt oxide. Electrochemical measurements showed that Mn doping in Co3O4 could effectively enhance the redox activity, especially Co3O4 with a Mn doping ratio of 1:5, which exhibits the most excellent electrochemical performance, with the maximum specific capacitance of 1210.8 F·g-1 at 1 A·g-1 and a rate capability of 33.0% at 30 A·g-1. The asymmetric supercapacitor (ASC) device assembled with the optimal Mn-Co3O4 (1:5) and activated carbon (AC) electrode performs a high specific capacitance of 105.8 F·g-1, a high energy density of 33 Wh·kg-1 at a power density of 748.1 W·kg-1, and a capacitance retention of 60.2% after 5000 cycles. This work indicates that an appropriate Mn doping concentration in the Co3O4 lattice structure will have great potential in rationalizing the design of spinel oxides for efficient electrochemical performance.

CDGSH Iron Sulfur Domain 2 Deficiency Inhibits Cell Proliferation and Induces Cell Differentiation of Neuroblastoma.

CDGSH iron sulfur domain 2 (CISD2) is reported to be highly expressed in several cancers, but the role of it in neuroblastoma has not been identified yet. Here, for the first time, we show that CISD2 is involved in neuroblastoma tumorigenesis and regulates neuroblastoma cell proliferation and differentiation. We found that high CISD2 expression correlated significantly with poor outcome of neuroblastoma patients, as well as advanced neuroblastoma tumor stages. Knockdown of CISD2 greatly repressed neuroblastoma cell proliferation and tumorigenesis both in vitro and in vivo. Further investigation showed that CISD2 deficiency resulted in cell cycle arrest in G1 phase and induced cell differentiation of neuroblastoma. Several Cyclins and Cyclin-Dependent Kinases (CDKs) were down-regulated by CISD2 knockdown, indicating that CISD2 probably regulates cell cycle through those genes. Together, we provide evidence that CISD2 is an indicator for neuroblastoma patients prognosis and is indispensable for neuroblastoma cell proliferation and tumorigenesis; CISD2 deficiency can induce neuroblastoma cell cycle arrest and differentiation. These findings suggest that CISD2 could work as a novel and potential therapeutic target for neuroblastoma treatment.