18 research outputs found

    Geologic mapping of the AV-8 Marcia Quadrangle of Asteroid 4 Vesta

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    NASA’s Dawn spacecraft entered orbit of the inner main belt asteroid 4 Vesta on July 16, 2011, and is spending one year in orbit to characterize the geology, chemical and mineralogical composition, topography, shape, and internal structure of Vesta before departing to asteroid 1 Ceres in late 2012. As part of the Dawn data analysis the Science Team is conducting geological mapping of the surface, in the form of 15 quadrangle maps. This abstract reports results from the mapping of quadrangle Av-8, named Marcia. Data: The base for mapping this quadrangle is a monochrome Framing Camera (FC) mosaic produced from the High Altitude Mapping Orbit (HAMO) data with a spatial resolution of ~70 m/pixel. This base is supplemented by a Digital Terrain Model (DTM) derived from Survey orbit stereo image data with a lateral spacing of 450 m/pixel (10 pixels per degree) and a vertical accuracy of ~30 meters. Also used to support the mapping are FC color ratio images from the Survey orbit with a spatial resolution of ~250 m/pixel, slope and contour maps derived from the DTM, and Visible and InfraRed (VIR) hyperspectral images from the Survey and HAMO orbits with spatial resolutions of 700 and 200 m/pixel, respectively

    Glucose Uptake by GLUT1 in Photoreceptors is Essential for Outer Segment Renewal and rod Photoreceptor Survival

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    Photoreceptors consume glucose supplied by the choriocapillaris to support phototransduction and outer segment (OS) renewal. Reduced glucose supply underlies photoreceptor cell death in inherited retinal degeneration and age-related retinal disease. We have previously shown that restricting glucose transport into the outer retina by conditional deletion of Slc2a1 encoding GLUT1 resulted in photoreceptor loss and impaired OS renewal. However, retinal neurons, glia, and the retinal pigment epithelium play specialized, synergistic roles in metabolite supply and exchange, and the cell-specific map of glucose uptake and utilization in the retina is incomplete. In these studies, we conditionally deleted Slc2a1 in a pan-retinal or rod-specific manner to better understand how glucose is utilized in the retina. Using non-invasive ocular imaging, electroretinography, and histochemical and biochemical analyses we show that genetic deletion of Slc2a1 from retinal neurons and Müller glia results in reduced OS growth and progressive rod but not cone photoreceptor cell death. Rhodopsin levels were severely decreased even at postnatal day 20 when OS length was relatively normal. Arrestin levels were not changed suggesting that glucose uptake is required to synthesize membrane glycoproteins. Rod-specific deletion of Slc2a1 resulted in similar changes in OS length and rod photoreceptor cell death. These studies demonstrate that glucose is an essential carbon source for rod photoreceptor cell OS maintenance and viability

    Mitochondrial Cu,Zn-Superoxide Dismutase Mediates Pulmonary Fibrosis by Augmenting H2O2 Generation*

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    The release of H2O2 from alveolar macrophages has been linked to the development of pulmonary fibrosis, but little is known about its source or mechanism of production. We found that alveolar macrophages from asbestosis patients spontaneously produce high levels of H2O2 and have high expression of Cu,Zn-superoxide dismutase (SOD). Because Cu,Zn-SOD is found in the mitochondrial intermembrane space (IMS), we hypothesized that mitochondrial Cu,Zn-SOD-mediated H2O2 generation contributed to pulmonary fibrosis. Asbestos-induced translocation of Cu,Zn-SOD to the IMS was unique to macrophages and dependent on functional mitochondrial respiration and the presence of at least one of the conserved cysteines required for disulfide bond formation. These conserved cysteine residues were also necessary for enzyme activation and H2O2 generation. Cu,Zn-SOD-mediated H2O2 generation was inhibited by knockdown of the iron-sulfur protein, Rieske, in complex III. The role of Cu,Zn-SOD was biologically relevant in that Cu,Zn-SOD−/− mice generated significantly less H2O2 and had less oxidant stress in bronchoalveolar lavage fluid and lung parenchyma. Furthermore, Cu,Zn-SOD−/− mice did not develop pulmonary fibrosis, and knockdown of Cu,Zn-SOD in monocytes attenuated collagen I deposition by lung fibroblasts. Our findings demonstrate a novel mechanism for the pathogenesis of pulmonary fibrosis where the antioxidant enzyme Cu,Zn-SOD translocates to the mitochondrial IMS to increase H2O2 generation in alveolar macrophages
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