1,857 research outputs found

    Nano-mechanical behavior of ultra-stable amorphous metallic thin films

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    Metallic glass has amorphous structure that behave mechanically like solids but show catastrophic failure due to shear band propagation induced by short range order structure, and they are generally produced by quenching. Recently, it is observed that the slower cooling rate provides the larger time available for atoms to rearrange structure before freezing in glassy state, leading to glass transition temperature and thermal stability. These glasses with enhanced thermal stability synthesized by controlled cooling rate make it useful in various field such as mechanical or oxidation protection material. However, mechanical behavior for metallic glass with extraordinary thermodynamic and kinetic stability has not been studied. In this research, we developed a ultrastable metallic glass thin film by physical vapor deposition process at ambient temperature. Thermal stability is investigated using acceleration testing. Mechanical properties are measured using in-situ tensile testing and discuss thermal stability and fracture behavior dependent on compositio

    PPM1A Controls Diabetic Gene Programming through Directly Dephosphorylating PPAR?? at Ser273

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    Peroxisome proliferator-activated receptor gamma (PPAR gamma) is a master regulator of adipose tissue biology. In obesity, phosphorylation of PPAR gamma at Ser273 (pSer273) by cyclin-dependent kinase 5 (CDK5)/extracellular signal-regulated kinase (ERK) orchestrates diabetic gene reprogramming via dysregulation of specific gene expression. Although many recent studies have focused on the development of non-classical agonist drugs that inhibit the phosphorylation of PPAR gamma at Ser273, the molecular mechanism of PPAR gamma dephosphorylation at Ser273 is not well characterized. Here, we report that protein phosphatase Mg2+/Mn2+-dependent 1A (PPM1A) is a novel PPAR gamma phosphatase that directly dephosphorylates Ser273 and restores diabetic gene expression which is dysregulated by pSer273. The expression of PPM1A significantly decreases in two models of insulin resistance: diet-induced obese (DIO) mice and db/db mice, in which it negatively correlates with pSer273. Transcriptomic analysis using microarray and genotype-tissue expression (GTEx) data in humans shows positive correlations between PPM1A and most of the genes that are dysregulated by pSer273. These findings suggest that PPM1A dephosphorylates PPAR gamma at Ser273 and represents a potential target for the treatment of obesity-linked metabolic disorders

    Transcriptional Regulator TonEBP Mediates Oxidative Damages in Ischemic Kidney Injury

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    TonEBP (tonicity-responsive enhancer binding protein) is a transcriptional regulator whose expression is elevated in response to various forms of stress including hyperglycemia, inflammation, and hypoxia. Here we investigated the role of TonEBP in acute kidney injury (AKI) using a line of TonEBP haplo-deficient mice subjected to bilateral renal ischemia followed by reperfusion (I/R). In the TonEBP haplo-deficient animals, induction of TonEBP, oxidative stress, inflammation, cell death, and functional injury in the kidney in response to I/R were all reduced. Analyses of renal transcriptome revealed that genes in several cellular pathways including peroxisome and mitochondrial inner membrane were suppressed in response to I/R, and the suppression was relieved in the TonEBP deficiency. Production of reactive oxygen species (ROS) and the cellular injury was reproduced in a renal epithelial cell line in response to hypoxia, ATP depletion, or hydrogen peroxide. The knockdown of TonEBP reduced ROS production and cellular injury in correlation with increased expression of the suppressed genes. The cellular injury was also blocked by inhibitors of necrosis. These results demonstrate that ischemic insult suppresses many genes involved in cellular metabolism leading to local oxidative stress by way of TonEBP induction. Thus, TonEBP is a promising target to prevent AKI

    Ionized gas outflows in infrared-bright dust-obscured galaxies selected with WISE and SDSS

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    We present the ionized gas properties of infrared (IR)-bright dust-obscured galaxies (DOGs) that show an extreme optical/IR color, (i[22])AB>7.0(i - [22])_{\rm AB} > 7.0, selected with the Sloan Digital Sky Survey (SDSS) and Wide-field Infrared Survey Explorer (WISE). For 36 IR-bright DOGs that show [OIII]λ\lambda5007 emission in the SDSS spectra, we performed a detailed spectral analysis to investigate their ionized gas properties. In particular, we measured the velocity offset (the velocity with respect to the systemic velocity measured from the stellar absorption lines) and the velocity dispersion of the [OIII] line. We found that the derived velocity offset and dispersion of most IR-bright DOGs are larger than those of Seyfert 2 galaxies (Sy2s) at z<0.3z < 0.3, meaning that the IR-bright DOGs show relatively strong outflows compared to Sy2s. This can be explained by the difference of IR luminosity contributed from active galactic nucleus, LIRL_{\rm IR} (AGN), because we found that (i) LIRL_{\rm IR} (AGN) correlates with the velocity offset and dispersion of [OIII] and (ii) our IR-bright DOGs sample has larger LIRL_{\rm IR} (AGN) than Sy2s. Nevertheless, the fact that about 75% IR-bright DOGs have a large (>> 300 km s1^{-1}) velocity dispersion, which is a larger fraction compared to other AGN populations, suggests that IR-bright DOGs are good laboratories to investigate AGN feedback. The velocity offset and dispersion of [OIII] and [NeIII]λ\lambda3869 are larger than those of [OII]λ\lambda3727, which indicates that the highly ionized gas tends to show more stronger outflows.Comment: 19 pages, 16 figures, and 2 tables, accepted for publication in Ap
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