To enhance the long stability of sulfur cathode for a high energy lithium-sulfur battery system, a sulfur-carbon sphere composite was prepared by encapsulating sulfur into micropores of carbon spheres by thermal treatment of a mixture of sublimed sulfur and carbon spheres. The elemental sulfur exists as a highly dispersed state inside the micropores of carbon spheres with a large surface area and a narrow pore distribution, based on the analyses of the X-ray powder diffraction (XRD), transmission electron microscopy (TEM), Brunauer-Emmett-Teller (BET), thermogravimetry (TG) and local element line-scanning. It is demonstrated from galvanostatic discharge-charge process, cyclic voltammetry (CV) and electrochemical impedance spectra (EIS) that the sulfur-carbon sphere composite has a large reversible capacity and an excellent high rate discharge capability as cathode materials. In particular, the sulfur-carbon sphere composite with 42 wt% sulfur presents a long electrochemical stability up to 500 cycles, based on the constrained electrochemical reaction inside the narrow micropores of carbon spheres due to strong adsorption. Therefore, the electrochemical reaction constrained inside the micropores proposed here would be the dominant factor for the enhanced long stability of the sulfur cathode. The knowledge acquired in this study is important not only for the design of efficient new electrode materials, but also for understanding the effect of the micropores on the electrochemical cycle stability.

Sulfur/highly porous carbon (HPC) composites were synthesized by thermally treating a mixture of sublimed sulfur and HPC. The microstructure of the HPC and the composite was characterized by transmission electron microscopy (TEM), scanning electron microscopy (SEM), X-ray diffraction (XRD), and Brunauer-Emmett-Teller (BET) surface area. The specific surface area of HPC reaches up to 1472.9 m 2 /g, which is sharply reduced to 24.4 m 2 /g in the sulfur/HPC composite with 57 wt % sulfur. The electrochemical performance of the composites as cathode materials in organic electrolytes was studied by the galvanostatic method and cyclic voltammetry. The sulfur/HPC composite with 57 wt % sulfur delivers the initial high specific capacity up to 1155 mAh/g and a stable capacity of 745 mAh/g after 84 cycles at the current density of 40 mA/g. In addition, it is demonstrated that the excellent cycling stability of the sulfur/HPC composite can be obtained at different current densities. On the basis of the analysis of the microstructure and electrochemical performance, it is confirmed that HPC can effectively prevent the shuttle behavior of the lithium/sulfur battery.

It has become increasingly clear that microRNAs (miRNAs) play important roles in tumorigenesis and metastasis. Recently, miR-203 was reported as a suppressor microRNA often silenced in different malignancies including hepatocellular carcinoma, prostate cancer, oral cancer, and hematopoietic malignancy, but little is known about its potential role in breast carcinogenesis. In this study, we found that in breast cancer, miR-203 was upregulated in primary tumors and some nonmetastatic cell lines but was significantly downregulated in metastatic cell lines including BT549, Hs578T, and MDA-MB-231, as measured by regular and real-time PCR. Downregulation of miR-203 in metastatic breast cancer cells appeared to be caused by hypermethylation of its promoter. Functionally, ectopic expression of miR-203 in BT549 and MDA-MB-231 breast cancer cell lines caused cell cycle arrest and apoptosis and inhibited cell invasion and migration in vitro. Bioinformatic analysis predicted the snail homolog 2 (SNAI2 or SLUG), a transcription factor that promotes cell invasion and tumor metastasis, as a target of miR-203, and the prediction was validated by expression analysis and luciferase reporter assay of the 3' untranslated region of SNAI2 that contains the miR-203 target sequences. These results suggest that in malignant breast cancer cells, miR-203 is epigenetically silenced, and the silencing promotes tumor cell growth and invasion at least in part by upregulating the SNAI2 transcription factor.

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