Reactive oxygen or nitrogen species (ROS/RNS) generated endogenously or in response to environmental stress have long been implicated in tissue injury in the context of a variety of disease states. ROS/RNS can cause cell death by nonphysiological (necrotic) or regulated pathways (apoptotic). The mechanisms by which ROS/RNS cause or regulate apoptosis typically include receptor activation, caspase activation, Bcl-2 family proteins, and mitochondrial dysfunction. Various protein kinase activities, including mitogen-activated protein kinases, protein kinases-B/C, inhibitor-of-I-kappaB kinases, and their corresponding phosphatases modulate the apoptotic program depending on cellular context. Recently, lipid-derived mediators have emerged as potential intermediates in the apoptosis pathway triggered by oxidants. Cell death mechanisms have been studied across a broad spectrum of models of oxidative stress, including H2O2, nitric oxide and derivatives, endotoxin-induced inflammation, photodynamic therapy, ultraviolet-A and ionizing radiations, and cigarette smoke. Additionally ROS generated in the lung and other organs as the result of high oxygen therapy or ischemia/reperfusion can stimulate cell death pathways associated with tissue damage. Cells have evolved numerous survival pathways to counter proapoptotic stimuli, which include activation of stress-related protein responses. Among these, the heme oxygenase-1/carbon monoxide system has emerged as a major intracellular antiapoptotic mechanism.

Solution processing, including printing technology, is a promising technique for oxide thin-film transistor (TFTs) fabrication because it tends to be a costeffective process with high composition controllability and high throughput. However, solution-processed oxide TFTs are limited by low-performance and stability issues, which require high-temperature annealing. This high thermal budget in the fabrication process inhibits oxide TFTs from being applied to flexible electronics. There have been numerous attempts to promote the desired electrical characteristics of solution-processed oxide TFTs at lower fabrication temperatures. Recent techniques for achieving low-temperature (<350 °C) solution-processed and printed oxide TFTs, in terms of the materials, processes, and structural engineering methods currently in use are reviewed. Moreover, the core techniques for both n-type and p-type oxidebased channel layers, gate dielectric layers, and electrode layers in oxide TFTs are addressed. Finally, various multifunctional and emerging applications based on low-temperature solution-processed oxide TFTs are introduced and future outlooks for this highly promising research are suggested.

Previously, we have reported tissue- and stage-specific expression of miR-372 in human embryonic stem cells and so far, not many reports speculate the function of this microRNA (miRNA). In this study, we screened various human cancer cell lines including gastric cancer cell lines and found first time that miR-372 is expressed only in AGS human gastric adenocarcinoma cell line. Inhibition of miR-372 using antisense miR-372 oligonucleotide (AS-miR-372) suppressed proliferation, arrested the cell cycle at G2/M phase, and increased apoptosis of AGS cells. Furthermore, AS-miR-372 treatment increased expression of LATS2, while over-expression of miR-372 decreased luciferase reporter activity driven by the 3' untranslated region (3' UTR) of LATS2 mRNA. Over-expression of LATS2 induced changes in AGS cells similar to those in AGS cells treated with AS-miR-372. Taken together, these findings demonstrate an oncogenic role for miR-372 in controlling cell growth, cell cycle, and apoptosis through down-regulation of a tumor suppressor gene, LATS2.

Tristetraprolin (TTP) is an AU‐rich element‐binding protein that regulates mRNA stability. Here, we report that TTP suppress the growth of human colon cancer cells both in vivo and in vitro by regulating of the expression of vascular endothelial growth factor (VEGF). TTP protein expression in human colonic tissues was markedly decreased in colonic adenocarcinoma compared with in normal mucosa and adenoma. VEGF expression was higher in colonic adenocarcinoma than in normal mucosa and adenoma. Specific inhibition of TTP expression by RNA‐interference increased the expression of VEGF in cultured human colon cancer cells, and TTP overexpression markedly decreased it. In addition, elevated expression of TTP decreased the expression level of luciferase linked to a 3′ terminal AU‐rich element (ARE) of VEGF mRNA. Colo320/TTP cells overexpressing TTP grew slowly in vitro and became tumors small in size when xenografted s.c into nude mice. These findings demonstrate that TTP acts as a negative regulator of VEGF gene expression in colon cancer cells, suggesting that it can be used as novel therapeutic agent to treat colon cancer.

Ge 2 Sb 2 Te 5 thin film is a promising candidate for recording material of phase-change optical disks, and nitrogen is doped into this film to increase overwrite characteristics. In this study, the crystal structure and the microstructure of nitrogen-doped Ge 2 Sb 2 Te 5 thin film were investigated. In the annealed nitrogen-doped thin film, the characteristic face-centered cubic peaks on the X-ray diffraction pattern were broadened and shifted to a smaller angle with the increase of nitrogen content. In addition, a remarkably reduced grain size and a highly strained structure are seen in the transmission electron microscopy image. Doped nitrogen in Ge 2 Sb 2 Te 5 thin film plays two roles. One is to distort the crystal lattice and induce a strain field in the film. The other is to refine the grain size of the film through precipitation. The crystal lattice is transformed from face-centered cubic to a hexagonal structure in nitrogen content above 20 at.%.

Despite its benefits, the clinical use of cyclosporine A (CsA) is limited by its nephrotoxic properties. Because paricalcitol (19-nor-1,25-hydroxyvitamin D(2)) has renoprotective effects, we tested whether it can blunt renal dysfunction and fibrosis in a rat model of CsA-induced nephropathy. Treatment with CsA decreased creatinine clearance, increased monocyte/macrophage infiltration, and increased the expression of inflammatory cytokines within the kidney. Paricalcitol reduced the decline in kidney function and pro-fibrotic changes and also blunted the increased transforming growth factor (TGF)-beta1 expression and Smad signaling. Using an in vitro model, we treated HK-2 cells with CsA and found that paricalcitol attenuated the CsA-induced increases in phosphorylated extracellular signal-regulated and c-Jun N-terminal kinases, and also prevented the activation of nuclear factor-kappaB. Paricalcitol effectively prevented TGF-beta1-induced epithelial-to-mesenchymal transitions and extracellular matrix accumulation as evidenced by attenuated collagen deposition and fibrosis in CsA-treated rats. In addition, paricalcitol decreased the number of TUNEL-positive nuclei and reduced the expression of pro-apoptotic markers in CsA-treated HK-2 cells. Thus, paricalcitol appears to attenuate CsA-induced nephropathy by suppression of inflammatory, pro-fibrotic, and apoptotic factors through inhibition of the nuclear factor-kappaB, Smad, and mitogen-activated protein kinase signaling pathways.

Obesity, a condition characterized by increased fat content and altered secretion of adipokines, is a risk factor for postmenopausal breast cancer. Visfatin has recently been established as a novel adipokine that is highly enriched in visceral fat. Here we report that visfatin regulated proliferation of MCF-7 human breast cancer cells. Exogenous administration of recombinant visfatin increased cell proliferation and DNA synthesis rate in MCF-7 cells. Furthermore, visfatin activated G1-S phase cell cycle progression by upregulation of cyclin D1 and cdk2 expression. Visfatin also increased the expression of matrix metalloproteinases 2, matrix metalloproteinases 9, and vascular endothelial growth factor genes, suggesting that it may function in metastasis and angiogenesis of breast cancer. Taken together, these findings suggest that visfatin plays an important role in breast cancer progression.

In this study, a structurally and materially designed thin-film encapsulation is proposed to guarantee the reliability of transparent, flexible displays by significantly improving their barrier properties, mechanical stability, and environmental reliability, all of which are essential for organic light-emitting diode (OLED) encapsulation. We fabricated a bioinspired, nacre-like ZnO/AlO/MgO laminate structure (ZAM) using atomic layer deposition for the microcrack toughening effect. The ZAM film was formed with intentional voids and defects through the formation of a quasi-perfect sublayer, rather than the simple fabrication of nanolaminate structures. The 240 nm thick ZAM-based multibarrier (ZAM-TFE) with a compressively strained organic layer demonstrated an optical transmittance of 91.35% in the visible range, an extremely low water vapor transmission rate of 2.06 × 10 g/m/day, a mechanical stability enduring a strain close to 1%, and a residual stress close to 0, showing significant improvement of key TFE properties in comparison to an AlO-based multibarrier. In addition, ZAM-TFE demonstrated superior environmental resistance without degradation of barrier properties in a severe environment of 85 °C and 90% relative humidity (RH). Thus, our structurally and materially designed ZAM film has been well optimized in terms of its applicability as a gas diffusion barrier as well as in terms of its mechanical and environmental reliability. Finally, we confirmed the feasibility of the ZAM-TFE through application in OLEDs. The low-temperature ZAM-TFE technology showed great potential to provide a highly robust and flexible TFE of TFOLEDs.