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To obtain efficient organic light-emitting diodes (OLEDs), the degradation in the surface properties of the indium tin oxide (ITO) electrode during the device fabrication should be prevented. In this study, we investigated the effect of the waiting time of ITO in the entry chamber before the transfer to the deposition chamber on the device performances of OLEDs. The current density and luminance of the OLED significantly decreased owing to the reduced hole injection with the increase in the waiting time. The origin of the reduced hole injection was estimated to be (1) the formation of trap sites at the interface between ITO and hole-transport layer and (2) decreased work function of ITO by an interface dipole. These phenomena could be attributed to the contamination of the ITO surface by the waiting under a relatively low vacuum and room light illumination.

Loss of PTEN, the major negative regulator of the PI3K/AKT pathway induces a cellular senescence as a failsafe mechanism to defend against tumorigenesis, which is called PTEN-loss-induced cellular senescence (PICS). Although many studies have indicated that the mTOR pathway plays a critical role in cellular senescence, the exact functions of mTORC1 and mTORC2 in PICS are not well understood. In this study, we show that mTOR acts as a critical relay molecule downstream of PI3K/AKT and upstream of p53 in PICS. We found that PTEN depletion induces cellular senescence via p53-p21 signaling without triggering DNA damage response. mTOR kinase, a major component of mTORC1 and mTORC2, directly binds p53 and phosphorylates it at serine 15. mTORC1 and mTORC2 compete with MDM2 and increase the stability of p53 to induce cellular senescence via accumulation of the cell cycle inhibitor, p21. In embryonic fibroblasts of PTEN-knockout mice, PTEN deficiency also induces mTORC1 and mTORC2 to bind to p53 instead of MDM2, leading to cellular senescence. These results collectively demonstrate for the first time that mTOR plays a critical role in switching cells from proliferation signaling to senescence signaling via a direct link between the growth-promoting activity of AKT and the growth-suppressing activity of p53.

High-throughput sequencing analyses have revealed that transposable elements (TEs) comprise approximately half of the human genome and frequently involved in genomic rearrangements and instability by various mechanisms. Interestingly, many noncoding RNAs (ncRNAs) contain TEs and the TE-containing ncRNAs that have been implicated in cellular processes and various diseases in mammals. In this study, we retrieved 94 human long noncoding RNAs (lncRNAs; >200 nucleotides in length) from lncRNAdb and analyzed TEs which are embedded within the lncRNAs, focusing on their chromosomal distribution. The result showed that TEs occupy ~27 % of the lncRNA transcripts in mass and lncRNA containing TEs are enriched in human chromosome 11. We further analyzed subfamily of the TEs and found that most of the TEs belong to AluSx and L1 which are the most successful TE subfamilies in the human genome. Numerous lncRNAs have been reported to be expressed in a cell-type specific manner. Thus, using reverse transcription PCR with specific primers for the lncRNAs, we examined their expression pattern in human normal tissues and cancer cells. Most of the lncRNAs were universally amplified from 20 different types of normal human tissues but some of them displayed tissue-specific expression. Especially, 11 lncRNAs were expressed only in human cancer cells, implying the possibility of their involvement in carcinogenesis.