386 research outputs found

    Conditions for the Long-Term Preservation of a Deep Brine Reservoir in Ceres

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    We propose a new internal evolution model for the dwarf planet Ceres matching the constraints on Ceres' present internal state from the Dawn mission observations. We assume an interior differentiated into a volatile-dominated crust and rocky mantle, and with remnant brines in the mantle, all consistent with inferences from the Dawn geophysical observations. Simulations indicate Ceres should preserve a warm crust until present if the crust is rich in clathrate hydrates. The temperature computed at the base of the crust exceeds 220 K for a broad range of conditions, allowing for the preservation of a small amount of brines at the base of the crust. However, a temperature ≄250 K, for which at least 1 wt.% sodium carbonate gets in solution requires a crustal abundance of clathrate hydrates greater than 55 vol.%, a situation possible for a narrow set of evolutionary scenarios

    Extensive water ice within Ceres’ aqueously altered regolith: Evidence from nuclear spectroscopy

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    The surface elemental composition of dwarf planet Ceres constrains its regolith ice content, aqueous alteration processes, and interior evolution. Using nuclear spectroscopy data acquired by NASA’s Dawn mission, we determined the concentrations of H, Fe, and K on Ceres. The data show that surface materials were processed by the action of water within the interior. The non-icy portion of Ceres’ C-bearing regolith contains similar amounts of H to aqueously altered carbonaceous chondrites, but less Fe. This allows for the possibility that Ceres experienced modest ice-rock fractionation, resulting in differences between surface and bulk composition. At mid-to-high latitudes, the regolith contains high concentrations of H, consistent with broad expanses of water ice, confirming theoretical predictions that ice can survive for billions of years just beneath the surface

    Pharmacological inhibition of Ras-transformed epithelial cell growth is linked to down-regulation of epidermal growth factor–related peptides

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    AbstractBackground & Aims: Posttranslational farnesylation is required for Ras activation. Farnesyl transferase inhibitors (FTIs) selectively block protein farnesylation and reduce the growth of many Ras-transformed cells in vitro and in vivo. Activated Ras transforms rat intestinal epithelial (RIE-1) cells by a mechanism distinct from NIH 3T3 fibroblasts in that an epidermal growth factor receptor (EGFR) autocrine loop contributes significantly to the Ras-transformed RIE-1 phenotype. Methods: The ability of FTIs to block growth of Ras-transformed RIE-1 cells was evaluated, and these results were correlated with decreased EGFR ligand production. Results: FTI L744,832 caused a selective, dose-dependent, reversible blockade in proliferation of H-Ras–transformed RIE-1 cells, whereas control cell lines, K-Ras–transformed cells, and activated raf-transfected RIE cells were unaffected. The growth-inhibitory effects of L744,832 correlated with loss of farnesylated H-Ras protein and a marked reduction in transforming growth factor (TGF)-α and amphiregulin expression. Inhibition of proliferation of H-Ras RIE-1 cells by L744,832 was overcome by exogenous TGF-α, and enhanced growth inhibition was achieved by EGFR blockade in combination with L744,832. Conclusions: These data suggest that one mechanism by which FTIs inhibit growth of H-Ras–transformed epithelial cells is by reducing Ras-induced EGFR ligand production.GASTROENTEROLOGY 1999;117:567-57

    A Science-Based Policy for Managing Free-Roaming Cats

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    Free-roaming domestic cats (i.e., cats that are owned or unowned and are considered ‘at large’) are globally distributed non-native species that have marked impacts on biodiversity and human health. Despite clear scientific evidence of these impacts, free-roaming cats are either unmanaged or managed using scientifically unsupported and ineffective approaches (e.g., trap-neuter-release [TNR]) in many jurisdictions around the world. A critical first initiative for effective, science-driven management of cats must be broader political and legislative recognition of free-roaming cats as a non-native, invasive species. Designating cats as invasive is important for developing and implementing science-based management plans, which should include efforts to prevent cats from becoming free-roaming, policies focused on responsible pet ownership and banning outdoor cat feeding, and better enforcement of existing laws. Using a science-based approach is necessary for responding effectively to the politically charged and increasingly urgent issue of managing free-roaming cat populations

    Participation of the PI-3K/Akt-NF-ÎșB signaling pathways in hypoxia-induced mitogenic factor-stimulated Flk-1 expression in endothelial cells

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    BACKGROUND: Hypoxia-induced mitogenic factor (HIMF), a lung-specific growth factor, promotes vascular tubule formation in a matrigel plug model. We initially found that HIMF enhances vascular endothelial growth factor (VEGF) expression in lung epithelial cells. In present work, we tested whether HIMF modulates expression of fetal liver kinase-1 (Flk-1) in endothelial cells, and dissected the possible signaling pathways that link HIMF to Flk-1 upregulation. METHODS: Recombinant HIMF protein was intratracheally instilled into adult mouse lungs, Flk-1 expression was examined by immunohistochemistry and Western blot. The promoter-luciferase reporter assay and real-time RT-PCR were performed to examine the effects of HIMF on Flk-1 expression in mouse endothelial cell line SVEC 4–10. The activation of NF-kappa B (NF-ÎșB) and phosphorylation of Akt, IKK, and IÎșBα were examined by luciferase assay and Western blot, respectively. RESULTS: Intratracheal instillation of HIMF protein resulted in a significant increase of Flk-1 production in lung tissues. Stimulation of SVEC 4–10 cells by HIMF resulted in increased phosphorylation of IKK and IÎșBα, leading to activation of NF-ÎșB. Blocking NF-ÎșB signaling pathway by dominant-negative mutants of IKK and IÎșBα suppressed HIMF-induced Flk-1 upregulation. Mutation or deletion of NF-ÎșB binding site within Flk-1 promoter also abolished HIMF-induced Flk-1 expression in SVEC 4–10 cells. Furthermore, HIMF strongly induced phosphorylation of Akt. A dominant-negative mutant of PI-3K, Δp85, as well as PI-3K inhibitor LY294002, blocked HIMF-induced NF-ÎșB activation and attenuated Flk-1 production. CONCLUSION: These results suggest that HIMF upregulates Flk-1 expression in endothelial cells in a PI-3K/Akt-NF-ÎșB signaling pathway-dependent manner, and may play critical roles in pulmonary angiogenesis
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