Proton conducting electrochemical cells, especially protonic ceramic fuel cells (PCFCs), are expected to be a breakthrough technology in next-generation energy conversion systems, primarily because of their high proton conductivity and...

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.

Cation segregation, particularly Sr segregation, toward a perovskite surface has a significant effect on the performance degradation of a solid oxide cell (solid oxide electrolysis/fuel cell). Among the number of key reasons generating the instability of perovskite oxide, surface-accumulated positively charged defects (oxygen vacancy, Vo ··) have been considered as the most crucial drivers in strongly attracting negatively charged defects (SrA – site ′) toward the surface. Herein, we demonstrate the effects of a heterointerface on the redistribution of both positively and negatively charged defects for a reduction of Vo ·· at a perovskite surface. We took Sm0.5Sr0.5CoO3−δ (SSC) as a model perovskite film and coated Gd0.1Ce0.9O2−δ (GDC) additionally onto the SSC film to create a heterointerface (GDC/SSC), resulting in an ∼11-fold reduction in a degradation rate of ∼8% at 650 °C and ∼10-fold higher surface exchange (k q) than a bare SSC film after 150 h at 650 °C. Using X-ray photoelectron spectroscopy and electron energy loss spectroscopy, we revealed a decrease in positively charged defects of Vo ·· and transferred electrons in an SSC film at the GDC/SSC heterointerface, resulting in a suppression of negatively charged Sr (SrSm ′) segregation. Finally, the energetic behavior, including the charge transfer phenomenon, O p-band center, and oxygen vacancy formation energy calculated using the density functional theory, verified the effects of the heterointerface on the redistribution of the charged defects, resulting in a remarkable impact on the stability of perovskite oxide at elevated temperatures.

Abstract. 3,3'-Diindolylmethane (DIM), an active metabolite of indole-3-carbinol, is thought to have antitumor effects in experimental animals and induce apoptosis in various cancer cells. However, the biological functions of DIM in human esophageal cancer cells are unknown. Thus, the purpose of this study was to investigate the cytotoxic effects of DIM in human esophageal squamous cell carcinoma (ESCC) cells to elucidate the molecular mechanism of cell death. Three human ESCC cell lines (TT, TE-8 and TE-12) were used to test the response to DIM. MTT, cell cycle and western blot analyses were conducted. DIM significantly inhibited the proliferation of ESCC cells in a dose-and time-dependent manner. The percentage of G1 phase cells increased 48 h after being treated with DIM. DIM also reduced cyclin D1, cyclin E2, cyclin-dependent kinase (CDK) 4 and CDK 6 activities, and increased p15 and p27 levels. Additionally, DIM diminished pro-caspase-9 protein expression levels and induced increased cleaved poly (ADP-ribose) polymerase levels. These results indicate that DIM leads to G1 phase cell cycle arrest and induces apoptosis by activating caspase-9 in ESCC cells.

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