Developing electrode materials with high-energy densities is important for the development of lithium-ion batteries. Here, we demonstrate a mesoporous molybdenum dioxide material with abnormal lithium-storage sites, which exhibits a discharge capacity of 1,814 mAh g−1 for the first cycle, more than twice its theoretical value, and maintains its initial capacity after 50 cycles. Contrary to previous reports, we find that a mechanism for the high and reversible lithium-storage capacity of the mesoporous molybdenum dioxide electrode is not based on a conversion reaction. Insight into the electrochemical results, obtained by in situ X-ray absorption, scanning transmission electron microscopy analysis combined with electron energy loss spectroscopy and computational modelling indicates that the nanoscale pore engineering of this transition metal oxide enables an unexpected electrochemical mass storage reaction mechanism, and may provide a strategy for the design of cation storage materials for battery systems.

To monitor dynamic volume changes of electrode materials during electrochemical lithium storage and removal process is of utmost importance for developing high performance lithium storage materials. We herein report an in operando probing of mesoscopic structural changes in ordered mesoporous electrode materials during cycling with synchrotron-based small angel X-ray scattering (SAXS) technique. In operando SAXS studies combined with electrochemical and other physical characterizations straightforwardly show how porous electrode materials underwent volume changes during the whole process of charge and discharge, with respect to their own reaction mechanism with lithium. This comprehensive information on the pore dynamics as well as volume changes of the electrode materials will not only be critical in further understanding of lithium ion storage reaction mechanism of materials, but also enable the innovative design of high performance nanostructured materials for next generation batteries.

The enhancer of zeste homolog 2 (EZH2), a member of the polycomb group of proteins, plays an important role in cell proliferation and cell cycle regulation. EZH2 is overexpressed in aggressive forms of prostate, breast, bladder, and endometrial cancers. However, the role of EZH2 expression in gastric cancer has not been fully determined. This study was conducted to investigate the correlation between EZH2 and cell cycle-related molecules, and the clinical value of EZH2 expression in gastric cancer. We analyzed EZH2 expression using Western blotting in AGS, MKN-28, SNU-16, SNU-484, SNU-601, and SNU-638 gastric cancer cell lines. After transfection of EZH2 siRNA into MKN-28 cells, the change in cell cycle-related molecules was assessed by Western blot analysis. Expression of EZH2, Ki-67, and p53 was determined by immunohistochemical staining of tissue microarrays from specimens of 137 cases of resected gastric cancer. We found high expressions of EZH2 in all of the tested gastric cancer cell lines. RNA interference of EZH2 induced upregulation of p53 and HDAC1 and downregulation of cyclin D1 and cyclin E. High EZH2 expression was observed in 60.6% of gastric cancers and in 6.7% of non-neoplastic gastric tissues (p < 0.01); 40.1% were positive for p53 in gastric cancers. High EZH2 expression was correlated with Ki-67 and p53 expressions and was significantly associated with distant metastases and non-signet ring cells. Our results suggest that high EZH2 expression is associated with tumor cell proliferation and metastasis in gastric cancer.

Abstract. This study investigated whether advanced glycation end products (AGE) and RAGE (receptor for AGE) are involved in the proliferation of leukemia cells. AGE strongly induced the proliferation of primary acute myeloid leukemia (AML) cells and cell lines. MAP kinase, PI3K and JAK/STAT pathways were involved in cellular proliferation of HEL cells by AGE. RAGE antisense S-ODN effectively inhibited cell growth, induced apoptosis and reversed AGE-induced expression of targeting molecules in HEL cells. The study demonstrated for the first time that AGE directly induced human AML cell proliferation via the MAPK, PI3K and JAK/STAT pathways.

Mesoporous transition metal dichalcogenides with 2D layered crystallinity, synthesized through a melting-infiltration assisted nano-replication, exhibit excellent electrochemical performances for lithium-storage.

. Chloroquine enhances the chemotherapeutic activity of 5-fluorouracil in a colon cancer cell line via cell cycle alteration. APMIS 2012; 120: 597-604.Autophagy is a conserved catabolic process that degrades cytoplasmic proteins and organelles for recycling. The role of autophagy in tumorigenesis is controversial because autophagy can be either protective or damaging to tumor cells, and its effects may change during tumor progression. A number of cancer cell lines have been exposed to chloroquine, an anti-malarial drug, with the aim of inhibiting cell growth and inducing cell death. In addition, chloroquine inhibits a late phase of autophagy. This study was conducted to investigate the anti-cancer effect of autophagy inhibition, using chloroquine together with 5-fluorouracil (5-FU) in a colon cancer cell line. Human colon cancer DLD-1 cells were treated with 5-FU (10 lΜ) or chloroquine (100 lΜ), or a combination of both. Autophagy was evaluated by western blot analysis of microtubule-associated protein light chain3 (LC3). Proliferative activity, alterations of the cell cycle, and apoptosis were measured by MTT assays, flow cytometry, and western blotting. LC3-II protein increased after treatment with 5-FU, and chloroquine potentiated the cytotoxicity of 5-FU. MTT assays showed that 5-FU inhibited proliferation of the DLD-1 cells and that chloroquine enhanced this inhibitory effect of 5-FU. The combination of 5-FU and chloroquine induced G1 arrest, up-regulation of p27 and p53, and downregulation of CDK2 and cyclin D1. These results suggest that chloroquine may potentiate the anti-cancer effect of 5-FU via cell cycle inhibition. Chloroquine potentiates the anti-cancer effect of 5-FU in colon cancer cells. Supplementation of conventional chemotherapy with chloroquine may provide a new cancer therapy modality.

Lithiation–delithiation reactions in Li‐ion batteries do exhibit a huge electrochemically driven volume change of the anode material between the lithium‐free and lithiated‐host states, which results in a gradually fading capacity. Minimizing this volume change of the electrode during cycling is essential to achieve stable electrochemical behavior and thus for innovating design of electrode materials for Li storage. Here, ordered mesoporous CoSn intermetallic anode materials with various Co/Sn atomic ratios are developed. A dual‐buffer effect is discovered that accommodates the volume changes in the electrode material by not only repeatedly generating void nanospaces but also by incorporating electrochemically inactive elements. Novel insights into the nanostructural changes of electrode materials during the lithiation–delithiation process are obtained by in operando small angle X‐ray scattering. The degrees of volume change and nanoscopic order are found to be highly dependent on the Co contents in the mesoporous CoSn intermetallic anode materials, being possible to achieve a durable nanostructured electrode upon prolonged cycling.

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