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  • 1
    Publication Date: 2018-03-16
    Description: Purpose: A major challenge in platinum-based cancer therapy is the clinical management of chemoresistant tumors, which have a largely unknown pathogenesis at the level of epigenetic regulation. Experimental Design: We evaluated the potential of using global loss of 5-hydroxymethylcytosine (5-hmC) levels as a novel diagnostic and prognostic epigenetic marker to better assess platinum-based chemotherapy response and clinical outcome in high-grade serous tumors (HGSOC), the most common and deadliest subtype of ovarian cancer. Furthermore, we identified a targetable pathway to reverse these epigenetic changes, both genetically and pharmacologically. Results: This study shows that decreased 5-hmC levels are an epigenetic hallmark for malignancy and tumor progression in HGSOC. In addition, global 5-hmC loss is associated with a decreased response to platinum-based chemotherapy, shorter time to relapse, and poor overall survival in patients newly diagnosed with HGSOC. Interestingly, the rescue of 5-hmC loss restores sensitivity to platinum chemotherapy in vitro and in vivo , decreases the percentage of tumor cells with cancer stem cell markers, and increases overall survival in an aggressive animal model of platinum-resistant disease. Conclusions: Consequently, a global analysis of patient 5-hmC levels should be included in future clinical trials, which use pretreatment with epigenetic adjuvants to elevate 5-hmC levels and improve the efficacy of current chemotherapies. Identifying prognostic epigenetic markers and altering chemotherapeutic regimens to incorporate DNMTi pretreatment in tumors with low 5-hmC levels could have important clinical implications for newly diagnosed HGSOC disease. Clin Cancer Res; 24(6); 1389–401. ©2017 AACR .
    Print ISSN: 1078-0432
    Electronic ISSN: 1557-3265
    Topics: Medicine
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  • 2
    Publication Date: 2011-11-01
    Description: A full description of the human proteome relies on the challenging task of detecting mature and changing forms of protein molecules in the body. Large-scale proteome analysis has routinely involved digesting intact proteins followed by inferred protein identification using mass spectrometry. This 'bottom-up' process affords a high number of identifications (not always unique to a single gene). However, complications arise from incomplete or ambiguous characterization of alternative splice forms, diverse modifications (for example, acetylation and methylation) and endogenous protein cleavages, especially when combinations of these create complex patterns of intact protein isoforms and species. 'Top-down' interrogation of whole proteins can overcome these problems for individual proteins, but has not been achieved on a proteome scale owing to the lack of intact protein fractionation methods that are well integrated with tandem mass spectrometry. Here we show, using a new four-dimensional separation system, identification of 1,043 gene products from human cells that are dispersed into more than 3,000 protein species created by post-translational modification (PTM), RNA splicing and proteolysis. The overall system produced greater than 20-fold increases in both separation power and proteome coverage, enabling the identification of proteins up to 105 kDa and those with up to 11 transmembrane helices. Many previously undetected isoforms of endogenous human proteins were mapped, including changes in multiply modified species in response to accelerated cellular ageing (senescence) induced by DNA damage. Integrated with the latest version of the Swiss-Prot database, the data provide precise correlations to individual genes and proof-of-concept for large-scale interrogation of whole protein molecules. The technology promises to improve the link between proteomics data and complex phenotypes in basic biology and disease research.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3237778/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3237778/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tran, John C -- Zamdborg, Leonid -- Ahlf, Dorothy R -- Lee, Ji Eun -- Catherman, Adam D -- Durbin, Kenneth R -- Tipton, Jeremiah D -- Vellaichamy, Adaikkalam -- Kellie, John F -- Li, Mingxi -- Wu, Cong -- Sweet, Steve M M -- Early, Bryan P -- Siuti, Nertila -- LeDuc, Richard D -- Compton, Philip D -- Thomas, Paul M -- Kelleher, Neil L -- F30 DA026672/DA/NIDA NIH HHS/ -- F30 DA026672-03/DA/NIDA NIH HHS/ -- GM 067193-08/GM/NIGMS NIH HHS/ -- P30 DA018310/DA/NIDA NIH HHS/ -- P30 DA018310-06/DA/NIDA NIH HHS/ -- P30DA 018310/DA/NIDA NIH HHS/ -- R01 GM067193/GM/NIGMS NIH HHS/ -- R01 GM067193-08/GM/NIGMS NIH HHS/ -- England -- Nature. 2011 Oct 30;480(7376):254-8. doi: 10.1038/nature10575.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, and the Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22037311" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Cell Aging/genetics ; Cell Line ; DNA Damage ; Databases, Protein ; HMGA1a Protein/analysis ; HMGA1b Protein/analysis ; HeLa Cells ; Humans ; Phenotype ; Protein Isoforms/*analysis/*chemistry ; Protein Processing, Post-Translational ; Proteolysis ; Proteome/*analysis/*chemistry ; Proteomics/instrumentation/*methods
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2014-08-01
    Description: Self-renewal is the hallmark feature both of normal stem cells and cancer stem cells. Since the regenerative capacity of normal haematopoietic stem cells is limited by the accumulation of reactive oxygen species and DNA double-strand breaks, we speculated that DNA damage might also constrain leukaemic self-renewal and malignant haematopoiesis. Here we show that the histone methyl-transferase MLL4, a suppressor of B-cell lymphoma, is required for stem-cell activity and an aggressive form of acute myeloid leukaemia harbouring the MLL-AF9 oncogene. Deletion of MLL4 enhances myelopoiesis and myeloid differentiation of leukaemic blasts, which protects mice from death related to acute myeloid leukaemia. MLL4 exerts its function by regulating transcriptional programs associated with the antioxidant response. Addition of reactive oxygen species scavengers or ectopic expression of FOXO3 protects MLL4(-/-) MLL-AF9 cells from DNA damage and inhibits myeloid maturation. Similar to MLL4 deficiency, loss of ATM or BRCA1 sensitizes transformed cells to differentiation, suggesting that myeloid differentiation is promoted by loss of genome integrity. Indeed, we show that restriction-enzyme-induced double-strand breaks are sufficient to induce differentiation of MLL-AF9 blasts, which requires cyclin-dependent kinase inhibitor p21(Cip1) (Cdkn1a) activity. In summary, we have uncovered an unexpected tumour-promoting role of genome guardians in enforcing the oncogene-induced differentiation blockade in acute myeloid leukaemia.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4410707/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4410707/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santos, Margarida A -- Faryabi, Robert B -- Ergen, Aysegul V -- Day, Amanda M -- Malhowski, Amy -- Canela, Andres -- Onozawa, Masahiro -- Lee, Ji-Eun -- Callen, Elsa -- Gutierrez-Martinez, Paula -- Chen, Hua-Tang -- Wong, Nancy -- Finkel, Nadia -- Deshpande, Aniruddha -- Sharrow, Susan -- Rossi, Derrick J -- Ito, Keisuke -- Ge, Kai -- Aplan, Peter D -- Armstrong, Scott A -- Nussenzweig, Andre -- CA140575/CA/NCI NIH HHS/ -- CA66996/CA/NCI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R00 CA139009/CA/NCI NIH HHS/ -- R01 DK098263/DK/NIDDK NIH HHS/ -- R01 DK100689/DK/NIDDK NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2014 Oct 2;514(7520):107-11. doi: 10.1038/nature13483. Epub 2014 Jul 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genome Integrity, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; 1] Laboratory of Genome Integrity, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA [2]. ; The Genetics Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. ; 1] Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, Massachusetts 02115, USA [2] Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, Massachusetts 02138, USA. ; Human Oncology and Pathogenesis Program and Department of Pediatrics, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA. ; Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Departments of Cell Biology and Medicine, Albert Einstein Cancer Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25079327" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins/metabolism ; BRCA1 Protein/genetics/metabolism ; Cell Transformation, Neoplastic ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; DNA Breaks, Double-Stranded ; *DNA Damage ; DNA Repair ; Female ; Gene Expression Regulation, Neoplastic ; Genes, BRCA1 ; Hematopoietic Stem Cells/cytology/metabolism/pathology ; Histone-Lysine N-Methyltransferase/deficiency/genetics/metabolism ; Leukemia, Myeloid, Acute/*enzymology/*pathology ; Male ; Mice ; *Myelopoiesis ; Oncogene Proteins, Fusion/genetics/metabolism ; Reactive Oxygen Species/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2012-01-28
    Description: Neighboring genes are often coordinately expressed within cis-regulatory modules, but evidence that nonparalogous genes share functions in mammals is lacking. Here, we report that mutation of either TMEM138 or TMEM216 causes a phenotypically indistinguishable human ciliopathy, Joubert syndrome. Despite a lack of sequence homology, the genes are aligned in a head-to-tail configuration and joined by chromosomal rearrangement at the amphibian-to-reptile evolutionary transition. Expression of the two genes is mediated by a conserved regulatory element in the noncoding intergenic region. Coordinated expression is important for their interdependent cellular role in vesicular transport to primary cilia. Hence, during vertebrate evolution of genes involved in ciliogenesis, nonparalogous genes were arranged to a functional gene cluster with shared regulatory elements.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3671610/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3671610/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Jeong Ho -- Silhavy, Jennifer L -- Lee, Ji Eun -- Al-Gazali, Lihadh -- Thomas, Sophie -- Davis, Erica E -- Bielas, Stephanie L -- Hill, Kiley J -- Iannicelli, Miriam -- Brancati, Francesco -- Gabriel, Stacey B -- Russ, Carsten -- Logan, Clare V -- Sharif, Saghira Malik -- Bennett, Christopher P -- Abe, Masumi -- Hildebrandt, Friedhelm -- Diplas, Bill H -- Attie-Bitach, Tania -- Katsanis, Nicholas -- Rajab, Anna -- Koul, Roshan -- Sztriha, Laszlo -- Waters, Elizabeth R -- Ferro-Novick, Susan -- Woods, C Geoffrey -- Johnson, Colin A -- Valente, Enza Maria -- Zaki, Maha S -- Gleeson, Joseph G -- DK068306/DK/NIDDK NIH HHS/ -- DK072301/DK/NIDDK NIH HHS/ -- DK075972/DK/NIDDK NIH HHS/ -- DK090917/DK/NIDDK NIH HHS/ -- EY021872/EY/NEI NIH HHS/ -- G0700073/Medical Research Council/United Kingdom -- GGP08145/Telethon/Italy -- HD042601/HD/NICHD NIH HHS/ -- NS04843/NS/NINDS NIH HHS/ -- NS052455/NS/NINDS NIH HHS/ -- P30 CA023100/CA/NCI NIH HHS/ -- P30NS047101/NS/NINDS NIH HHS/ -- R01 DK068306/DK/NIDDK NIH HHS/ -- R01 DK072301/DK/NIDDK NIH HHS/ -- R01 DK075972/DK/NIDDK NIH HHS/ -- R01 EY021872/EY/NEI NIH HHS/ -- R01 HD042601/HD/NICHD NIH HHS/ -- R01 NS048453/NS/NINDS NIH HHS/ -- R01 NS052455/NS/NINDS NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Feb 24;335(6071):966-9. doi: 10.1126/science.1213506. Epub 2012 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurogenetics Laboratory, Howard Hughes Medical Institute (HHMI), Department of Neurosciences, University of California, San Diego, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22282472" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cerebellar Diseases/*genetics/metabolism/pathology ; Cilia/metabolism/*ultrastructure ; Conserved Sequence ; DNA, Intergenic ; *Evolution, Molecular ; Eye Abnormalities/*genetics/metabolism/pathology ; Gene Expression Profiling ; *Gene Expression Regulation ; Genetic Heterogeneity ; *Genetic Loci ; Humans ; Kidney Diseases, Cystic/*genetics/metabolism/pathology ; Membrane Proteins/chemistry/*genetics/metabolism ; Molecular Sequence Data ; Multigene Family ; Mutation ; Mutation, Missense ; Phenotype ; Protein Transport ; *Regulatory Sequences, Nucleic Acid ; Retina/abnormalities/metabolism/pathology ; Transport Vesicles/metabolism/ultrastructure
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2013-03-09
    Description: A molecule that treats multiple age-related diseases would have a major impact on global health and economics. The SIRT1 deacetylase has drawn attention in this regard as a target for drug design. Yet controversy exists around the mechanism of sirtuin-activating compounds (STACs). We found that specific hydrophobic motifs found in SIRT1 substrates such as PGC-1alpha and FOXO3a facilitate SIRT1 activation by STACs. A single amino acid in SIRT1, Glu(230), located in a structured N-terminal domain, was critical for activation by all previously reported STAC scaffolds and a new class of chemically distinct activators. In primary cells reconstituted with activation-defective SIRT1, the metabolic effects of STACs were blocked. Thus, SIRT1 can be directly activated through an allosteric mechanism common to chemically diverse STACs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3799917/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3799917/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hubbard, Basil P -- Gomes, Ana P -- Dai, Han -- Li, Jun -- Case, April W -- Considine, Thomas -- Riera, Thomas V -- Lee, Jessica E -- E, Sook Yen -- Lamming, Dudley W -- Pentelute, Bradley L -- Schuman, Eli R -- Stevens, Linda A -- Ling, Alvin J Y -- Armour, Sean M -- Michan, Shaday -- Zhao, Huizhen -- Jiang, Yong -- Sweitzer, Sharon M -- Blum, Charles A -- Disch, Jeremy S -- Ng, Pui Yee -- Howitz, Konrad T -- Rolo, Anabela P -- Hamuro, Yoshitomo -- Moss, Joel -- Perni, Robert B -- Ellis, James L -- Vlasuk, George P -- Sinclair, David A -- P01 AG027916/AG/NIA NIH HHS/ -- R01 AG019719/AG/NIA NIH HHS/ -- R01 AG028730/AG/NIA NIH HHS/ -- R37 AG028730/AG/NIA NIH HHS/ -- ZIA HL000659-20/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2013 Mar 8;339(6124):1216-9. doi: 10.1126/science.1231097.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23471411" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Amino Acid Motifs ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Cells, Cultured ; Enzyme Activation ; Forkhead Transcription Factors/chemistry/genetics ; Glutamic Acid/chemistry/genetics ; Heterocyclic Compounds with 4 or More Rings/chemistry/pharmacology ; Humans ; Hydrophobic and Hydrophilic Interactions ; Mice ; Molecular Sequence Data ; Myoblasts/drug effects/enzymology ; Protein Structure, Tertiary ; Sirtuin 1/*chemistry/genetics/*metabolism ; Stilbenes/chemistry/*pharmacology ; Substrate Specificity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2018-06-05
    Description: Recent evidence suggests early environmental factors are important for gut immune tolerance. Although the role of regulatory T (Treg) cells for gut immune homeostasis is well established, the development and tissue homing characteristics of Treg cells in children have not been studied in detail. In this article, we studied the development and homing characteristics of human peripheral blood Treg cell subsets and potential mechanisms inducing homing molecule expression in healthy children. We found contrasting patterns of circulating Treg cell gut and skin tropism, with abundant β7 integrin + Treg cells at birth and increasing cutaneous lymphocyte Ag (CLA + ) Treg cells later in life. β7 integrin + Treg cells were predominantly naive, suggesting acquisition of Treg cell gut tropism early in development. In vitro, IL-7 enhanced gut homing but reduced skin homing molecule expression in conventional T cells, whereas IL-2 induced a similar effect only in Treg cells. This effect was more pronounced in cord compared with adult blood. Our results suggest that early in life, naive Treg cells may be driven for gut tropism by their increased sensitivity to IL-2–induced β7 integrin upregulation, implicating a potential role of IL-2 in gut immune tolerance during this critical period of development.
    Print ISSN: 0022-1767
    Electronic ISSN: 1550-6606
    Topics: Medicine
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  • 7
    Publication Date: 2013-11-23
    Description: The origin of the late preindustrial Holocene (LPIH) increase in atmospheric methane concentrations has been much debated. Hypotheses invoking changes in solely anthropogenic sources or solely natural sources have been proposed to explain the increase in concentrations. Here two high-resolution, high-precision ice core methane concentration records from Greenland and Antarctica are presented and are used to construct a high-resolution record of the methane inter-polar difference (IPD). The IPD record constrains the latitudinal distribution of emissions and shows that LPIH emissions increased primarily in the tropics, with secondary increases in the subtropical Northern Hemisphere. Anthropogenic and natural sources have different latitudinal characteristics, which are exploited to demonstrate that both anthropogenic and natural sources are needed to explain LPIH changes in methane concentration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mitchell, Logan -- Brook, Ed -- Lee, James E -- Buizert, Christo -- Sowers, Todd -- New York, N.Y. -- Science. 2013 Nov 22;342(6161):964-6. doi: 10.1126/science.1238920.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉College of Earth, Ocean, and Atmospheric Sciences, Oregon State University, Corvallis, OR 97331, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24264988" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Antarctic Regions ; Atmosphere/*chemistry ; Greenland ; Humans ; Ice Cover/*chemistry ; Industry/*trends ; Methane/*analysis ; Oryza
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2012-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chown, S L -- Lee, J E -- Hughes, K A -- Barnes, J -- Barrett, P J -- Bergstrom, D M -- Convey, P -- Cowan, D A -- Crosbie, K -- Dyer, G -- Frenot, Y -- Grant, S M -- Herr, D -- Kennicutt, M C 2nd -- Lamers, M -- Murray, A -- Possingham, H P -- Reid, K -- Riddle, M J -- Ryan, P G -- Sanson, L -- Shaw, J D -- Sparrow, M D -- Summerhayes, C -- Terauds, A -- Wall, D H -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):158-9. doi: 10.1126/science.1222821.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Invasion Biology, Stellenbosch University, Matieland, South Africa. steven.chown@monash.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22798586" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antarctic Regions ; Climate Change ; *Conservation of Natural Resources/trends ; *Ecosystem ; Forecasting ; Human Activities ; Humans ; Public Policy ; Travel
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2015-10-17
    Description: The Pluto system was recently explored by NASA's New Horizons spacecraft, making closest approach on 14 July 2015. Pluto's surface displays diverse landforms, terrain ages, albedos, colors, and composition gradients. Evidence is found for a water-ice crust, geologically young surface units, surface ice convection, wind streaks, volatile transport, and glacial flow. Pluto's atmosphere is highly extended, with trace hydrocarbons, a global haze layer, and a surface pressure near 10 microbars. Pluto's diverse surface geology and long-term activity raise fundamental questions about how small planets remain active many billions of years after formation. Pluto's large moon Charon displays tectonics and evidence for a heterogeneous crustal composition; its north pole displays puzzling dark terrain. Small satellites Hydra and Nix have higher albedos than expected.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stern, S A -- Bagenal, F -- Ennico, K -- Gladstone, G R -- Grundy, W M -- McKinnon, W B -- Moore, J M -- Olkin, C B -- Spencer, J R -- Weaver, H A -- Young, L A -- Andert, T -- Andrews, J -- Banks, M -- Bauer, B -- Bauman, J -- Barnouin, O S -- Bedini, P -- Beisser, K -- Beyer, R A -- Bhaskaran, S -- Binzel, R P -- Birath, E -- Bird, M -- Bogan, D J -- Bowman, A -- Bray, V J -- Brozovic, M -- Bryan, C -- Buckley, M R -- Buie, M W -- Buratti, B J -- Bushman, S S -- Calloway, A -- Carcich, B -- Cheng, A F -- Conard, S -- Conrad, C A -- Cook, J C -- Cruikshank, D P -- Custodio, O S -- Dalle Ore, C M -- Deboy, C -- Dischner, Z J B -- Dumont, P -- Earle, A M -- Elliott, H A -- Ercol, J -- Ernst, C M -- Finley, T -- Flanigan, S H -- Fountain, G -- Freeze, M J -- Greathouse, T -- Green, J L -- Guo, Y -- Hahn, M -- Hamilton, D P -- Hamilton, S A -- Hanley, J -- Harch, A -- Hart, H M -- Hersman, C B -- Hill, A -- Hill, M E -- Hinson, D P -- Holdridge, M E -- Horanyi, M -- Howard, A D -- Howett, C J A -- Jackman, C -- Jacobson, R A -- Jennings, D E -- Kammer, J A -- Kang, H K -- Kaufmann, D E -- Kollmann, P -- Krimigis, S M -- Kusnierkiewicz, D -- Lauer, T R -- Lee, J E -- Lindstrom, K L -- Linscott, I R -- Lisse, C M -- Lunsford, A W -- Mallder, V A -- Martin, N -- McComas, D J -- McNutt, R L Jr -- Mehoke, D -- Mehoke, T -- Melin, E D -- Mutchler, M -- Nelson, D -- Nimmo, F -- Nunez, J I -- Ocampo, A -- Owen, W M -- Paetzold, M -- Page, B -- Parker, A H -- Parker, J W -- Pelletier, F -- Peterson, J -- Pinkine, N -- Piquette, M -- Porter, S B -- Protopapa, S -- Redfern, J -- Reitsema, H J -- Reuter, D C -- Roberts, J H -- Robbins, S J -- Rogers, G -- Rose, D -- Runyon, K -- Retherford, K D -- Ryschkewitsch, M G -- Schenk, P -- Schindhelm, E -- Sepan, B -- Showalter, M R -- Singer, K N -- Soluri, M -- Stanbridge, D -- Steffl, A J -- Strobel, D F -- Stryk, T -- Summers, M E -- Szalay, J R -- Tapley, M -- Taylor, A -- Taylor, H -- Throop, H B -- Tsang, C C C -- Tyler, G L -- Umurhan, O M -- Verbiscer, A J -- Versteeg, M H -- Vincent, M -- Webbert, R -- Weidner, S -- Weigle, G E 2nd -- White, O L -- Whittenburg, K -- Williams, B G -- Williams, K -- Williams, S -- Woods, W W -- Zangari, A M -- Zirnstein, E -- New York, N.Y. -- Science. 2015 Oct 16;350(6258):aad1815. doi: 10.1126/science.aad1815.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Southwest Research Institute, Boulder, CO 80302, USA. astern@boulder.swri.edu. ; Laboratory for Atmospheric and Space Physics, University of Colorado, Boulder, CO 80303, USA. ; National Aeronautics and Space Administration (NASA) Ames Research Center, Space Science Division, Moffett Field, CA 94035, USA. ; Southwest Research Institute, San Antonio, TX 28510, USA. ; Lowell Observatory, Flagstaff, AZ 86001, USA. ; Department of Earth and Planetary Sciences, Washington University, St. Louis, MO 63130, USA. ; Southwest Research Institute, Boulder, CO 80302, USA. ; Johns Hopkins University Applied Physics Laboratory, Laurel, MD 20723, USA. ; Universitat der Bundeswehr Munchen, Neubiberg 85577, Germany. ; Planetary Science Institute, Tucson, AZ 85719, USA. ; KinetX Aerospace, Tempe, AZ 85284, USA. ; NASA Jet Propulsion Laboratory, La Canada Flintridge, CA 91011, USA. ; Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; University of Bonn, Bonn D-53113, Germany. ; NASA Headquarters (retired), Washington, DC 20546, USA. ; University of Arizona, Tucson, AZ 85721, USA. ; Cornell University, Ithaca, NY 14853, USA. ; NASA Headquarters, Washington, DC 20546, USA. ; Rheinisches Institut fur Umweltforschung an der Universitat zu Koln, Cologne 50931, Germany. ; Department of Astronomy, University of Maryland, College Park, MD 20742, USA. ; Search for Extraterrestrial Intelligence Institute, Mountain View, CA 94043, USA. ; Department of Environmental Sciences, University of Virginia, Charlottesville, VA 22904, USA. ; NASA Goddard Space Flight Center, Greenbelt, MD 20771, USA. ; National Optical Astronomy Observatory, Tucson, AZ 26732, USA. ; NASA Marshall Space Flight Center, Huntsville, AL 35812, USA. ; Stanford University, Stanford, CA 94305, USA. ; Space Telescope Science Institute, Baltimore, MD 21218, USA. ; University of California, Santa Cruz, CA 95064, USA. ; Lunar and Planetary Institute, Houston, TX 77058, USA. ; Michael Soluri Photography, New York, NY 10014, USA. ; Johns Hopkins University, Baltimore, MD 21218, USA. ; Roane State Community College, Jamestown, TN 38556, USA. ; George Mason University, Fairfax, VA 22030, USA. ; Department of Astronomy, University of Virginia, Charlottesville, VA 22904, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26472913" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    ISSN: 0888-7543
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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