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  • 1
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    Rapid cycling of reactive nitrogen in the marine boundary layer (2016)
    Nature Publishing Group (NPG)
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    Publikationsdatum: 2016-04-12
    Beschreibung: Nitrogen oxides are essential for the formation of secondary atmospheric aerosols and of atmospheric oxidants such as ozone and the hydroxyl radical, which controls the self-cleansing capacity of the atmosphere. Nitric acid, a major oxidation product of nitrogen oxides, has traditionally been considered to be a permanent sink of nitrogen oxides. However, model studies predict higher ratios of nitric acid to nitrogen oxides in the troposphere than are observed. A 'renoxification' process that recycles nitric acid into nitrogen oxides has been proposed to reconcile observations with model studies, but the mechanisms responsible for this process remain uncertain. Here we present data from an aircraft measurement campaign over the North Atlantic Ocean and find evidence for rapid recycling of nitric acid to nitrous acid and nitrogen oxides in the clean marine boundary layer via particulate nitrate photolysis. Laboratory experiments further demonstrate the photolysis of particulate nitrate collected on filters at a rate more than two orders of magnitude greater than that of gaseous nitric acid, with nitrous acid as the main product. Box model calculations based on the Master Chemical Mechanism suggest that particulate nitrate photolysis mainly sustains the observed levels of nitrous acid and nitrogen oxides at midday under typical marine boundary layer conditions. Given that oceans account for more than 70 per cent of Earth's surface, we propose that particulate nitrate photolysis could be a substantial tropospheric nitrogen oxide source. Recycling of nitrogen oxides in remote oceanic regions with minimal direct nitrogen oxide emissions could increase the formation of tropospheric oxidants and secondary atmospheric aerosols on a global scale.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ye, Chunxiang -- Zhou, Xianliang -- Pu, Dennis -- Stutz, Jochen -- Festa, James -- Spolaor, Max -- Tsai, Catalina -- Cantrell, Christopher -- Mauldin, Roy L 3rd -- Campos, Teresa -- Weinheimer, Andrew -- Hornbrook, Rebecca S -- Apel, Eric C -- Guenther, Alex -- Kaser, Lisa -- Yuan, Bin -- Karl, Thomas -- Haggerty, Julie -- Hall, Samuel -- Ullmann, Kirk -- Smith, James N -- Ortega, John -- Knote, Christoph -- England -- Nature. 2016 Apr 28;532(7600):489-91. doi: 10.1038/nature17195. Epub 2016 Apr 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wadsworth Center, New York State Department of Health, Albany, New York, USA. ; Department of Environmental Health Sciences, State University of New York, Albany, New York, USA. ; Department of Atmospheric and Oceanic Sciences, University of California, Los Angeles (UCLA), California, USA. ; Department of Atmospheric and Oceanic Sciences, University of Colorado at Boulder, Boulder, Colorado, USA. ; Department of Physics, University of Helsinki, Helsinki, Finland. ; National Center for Atmospheric Research, Boulder, Colorado, USA. ; Pacific Northwest National Laboratory, Richland, Washington, USA. ; NOAA, Earth System Research Laboratory, Chemical Sciences Division, Boulder, Colorado, USA. ; Cooperative Institute for Research in Environmental Sciences, University of Colorado at Boulder, Boulder, Colorado, USA. ; Institute for Meteorology and Geophysics, University of Innsbruck, Innsbruck, Austria. ; University of Eastern Finland, Kuopio, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27064904" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aerosols/chemistry ; Atlantic Ocean ; Atmosphere/*chemistry ; Nitrates/analysis/chemistry ; Nitric Acid/chemistry ; Nitrogen/*analysis/*chemistry ; Nitrogen Oxides/*analysis/*chemistry ; Nitrous Acid/analysis/chemistry ; North Carolina ; Oxidants/chemistry ; Photolysis ; Seawater/*chemistry ; South Carolina
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 2
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    Activation of the A2A adenosine G-protein-coupled receptor by conformational selection (2016)
    Nature Publishing Group (NPG)
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    Publikationsdatum: 2016-05-05
    Beschreibung: Conformational selection and induced fit are two prevailing mechanisms to explain the molecular basis for ligand-based activation of receptors. G-protein-coupled receptors are the largest class of cell surface receptors and are important drug targets. A molecular understanding of their activation mechanism is critical for drug discovery and design. However, direct evidence that addresses how agonist binding leads to the formation of an active receptor state is scarce. Here we use (19)F nuclear magnetic resonance to quantify the conformational landscape occupied by the adenosine A2A receptor (A2AR), a prototypical class A G-protein-coupled receptor. We find an ensemble of four states in equilibrium: (1) two inactive states in millisecond exchange, consistent with a formed (state S1) and a broken (state S2) salt bridge (known as 'ionic lock') between transmembrane helices 3 and 6; and (2) two active states, S3 and S3', as identified by binding of a G-protein-derived peptide. In contrast to a recent study of the beta2-adrenergic receptor, the present approach allowed identification of a second active state for A2AR. Addition of inverse agonist (ZM241385) increases the population of the inactive states, while full agonists (UK432097 or NECA) stabilize the active state, S3', in a manner consistent with conformational selection. In contrast, partial agonist (LUF5834) and an allosteric modulator (HMA) exclusively increase the population of the S3 state. Thus, partial agonism is achieved here by conformational selection of a distinct active state which we predict will have compromised coupling to the G protein. Direct observation of the conformational equilibria of ligand-dependent G-protein-coupled receptor and deduction of the underlying mechanisms of receptor activation will have wide-reaching implications for our understanding of the function of G-protein-coupled receptor in health and disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ye, Libin -- Van Eps, Ned -- Zimmer, Marco -- Ernst, Oliver P -- Prosser, R Scott -- England -- Nature. 2016 May 4;533(7602):265-8. doi: 10.1038/nature17668.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Toronto, UTM, 3359 Mississauga Road North, Mississauga, Ontario L5L 1C6, Canada. ; Department of Biochemistry, University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada. ; Department of Technical Biochemistry, University of Stuttgart, 31 Allmandring, Stuttgart, Baden-Wurttemberg, D-70569, Germany. ; Department of Molecular Genetics, University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27144352" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 3
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    A pressure-amplifying framework material with negative gas adsorption transitions (2016)
    Nature Publishing Group (NPG)
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    Publikationsdatum: 2016-04-07
    Beschreibung: Adsorption-based phenomena are important in gas separations, such as the treatment of greenhouse-gas and toxic-gas pollutants, and in water-adsorption-based heat pumps for solar cooling systems. The ability to tune the pore size, shape and functionality of crystalline porous coordination polymers--or metal-organic frameworks (MOFs)--has made them attractive materials for such adsorption-based applications. The flexibility and guest-molecule-dependent response of MOFs give rise to unexpected and often desirable adsorption phenomena. Common to all isothermal gas adsorption phenomena, however, is increased gas uptake with increased pressure. Here we report adsorption transitions in the isotherms of a MOF (DUT-49) that exhibits a negative gas adsorption; that is, spontaneous desorption of gas (methane and n-butane) occurs during pressure increase in a defined temperature and pressure range. A combination of in situ powder X-ray diffraction, gas adsorption experiments and simulations shows that this adsorption behaviour is controlled by a sudden hysteretic structural deformation and pore contraction of the MOF, which releases guest molecules. These findings may enable technologies using frameworks capable of negative gas adsorption for pressure amplification in micro- and macroscopic system engineering. Negative gas adsorption extends the series of counterintuitive phenomena such as negative thermal expansion and negative refractive indices and may be interpreted as an adsorptive analogue of force-amplifying negative compressibility transitions proposed for metamaterials.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krause, Simon -- Bon, Volodymyr -- Senkovska, Irena -- Stoeck, Ulrich -- Wallacher, Dirk -- Tobbens, Daniel M -- Zander, Stefan -- Pillai, Renjith S -- Maurin, Guillaume -- Coudert, Francois-Xavier -- Kaskel, Stefan -- England -- Nature. 2016 Apr 21;532(7599):348-52. doi: 10.1038/nature17430. Epub 2016 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Inorganic Chemistry, Technische Universitat Dresden, Bergstrasse 66, 01062 Dresden, Germany. ; Department Sample Environments, Helmholtz-Zentrum Berlin fur Materialien und Energie, Hahn-Meitner-Platz 1, 14109 Berlin, Germany. ; Department Structure and Dynamics of Energy Materials, Helmholtz-Zentrum Berlin fur Materialien und Energie, Hahn-Meitner-Platz 1, 14109 Berlin, Germany. ; Institut Charles Gerhardt Montpellier UMR 5253 CNRS UM ENSCM, Universite Montpellier, Place E. Bataillon, 34095 Montpellier cedex 05, France. ; Chimie ParisTech, PSL Research University, CNRS, Institut de Recherche de Chimie Paris, 75005 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27049950" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 4
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    Corrigendum: CEACAM1 regulates TIM-3-mediated tolerance and exhaustion (2016)
    Nature Publishing Group (NPG)
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    Publikationsdatum: 2016-03-17
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Yu-Hwa -- Zhu, Chen -- Kondo, Yasuyuki -- Anderson, Ana C -- Gandhi, Amit -- Russell, Andrew -- Dougan, Stephanie K -- Petersen, Britt-Sabina -- Melum, Espen -- Pertel, Thomas -- Clayton, Kiera L -- Raab, Monika -- Chen, Qiang -- Beauchemin, Nicole -- Yazaki, Paul J -- Pyzik, Michal -- Ostrowski, Mario A -- Glickman, Jonathan N -- Rudd, Christopher E -- Ploegh, Hidde L -- Franke, Andre -- Petsko, Gregory A -- Kuchroo, Vijay K -- Blumberg, Richard S -- Nature. 2016 Mar 16. doi: 10.1038/nature17421.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982724" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 5
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    Cullin-RING ubiquitin E3 ligase regulation by the COP9 signalosome (2016)
    Nature Publishing Group (NPG)
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    Publikationsdatum: 2016-04-01
    Beschreibung: The cullin-RING ubiquitin E3 ligase (CRL) family comprises over 200 members in humans. The COP9 signalosome complex (CSN) regulates CRLs by removing their ubiquitin-like activator NEDD8. The CUL4A-RBX1-DDB1-DDB2 complex (CRL4A(DDB2)) monitors the genome for ultraviolet-light-induced DNA damage. CRL4A(DBB2) is inactive in the absence of damaged DNA and requires CSN to regulate the repair process. The structural basis of CSN binding to CRL4A(DDB2) and the principles of CSN activation are poorly understood. Here we present cryo-electron microscopy structures for CSN in complex with neddylated CRL4A ligases to 6.4 A resolution. The CSN conformers defined by cryo-electron microscopy and a novel apo-CSN crystal structure indicate an induced-fit mechanism that drives CSN activation by neddylated CRLs. We find that CSN and a substrate cannot bind simultaneously to CRL4A, favouring a deneddylated, inactive state for substrate-free CRL4 complexes. These architectural and regulatory principles appear conserved across CRL families, allowing global regulation by CSN.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cavadini, Simone -- Fischer, Eric S -- Bunker, Richard D -- Potenza, Alessandro -- Lingaraju, Gondichatnahalli M -- Goldie, Kenneth N -- Mohamed, Weaam I -- Faty, Mahamadou -- Petzold, Georg -- Beckwith, Rohan E J -- Tichkule, Ritesh B -- Hassiepen, Ulrich -- Abdulrahman, Wassim -- Pantelic, Radosav S -- Matsumoto, Syota -- Sugasawa, Kaoru -- Stahlberg, Henning -- Thoma, Nicolas H -- England -- Nature. 2016 Mar 31;531(7596):598-603. doi: 10.1038/nature17416.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, 4058 Basel, Switzerland. ; University of Basel, Petersplatz 10, 4003 Basel, Switzerland. ; Department of Cancer Biology, Dana-Farber Cancer Institute, LC-4312, 360 Longwood Avenue, Boston, Massachusetts 02215, USA. ; Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02215, USA. ; Center for Cellular Imaging and NanoAnalytics, Biozentrum, University of Basel, 4058 Basel, Switzerland. ; Novartis Institutes for Biomedical Research, 250 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA. ; Novartis Pharma AG, Institutes for Biomedical Research, Novartis Campus, 4056 Basel, Switzerland. ; Gatan R&D, 5974 W. Las Positas Boulevard, Pleasanton, California 94588, USA. ; Biosignal Research Center, Organization of Advanced Science and Technology, Kobe University, Kobe 657-8501, Japan. ; Graduate School of Science, Kobe University, Kobe, 657-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27029275" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Allosteric Regulation ; Apoproteins/chemistry/metabolism/ultrastructure ; Binding Sites ; *Biocatalysis ; Carrier Proteins/chemistry/metabolism/ultrastructure ; Cryoelectron Microscopy ; Crystallography, X-Ray ; Cullin Proteins/chemistry/metabolism/ultrastructure ; DNA Damage ; DNA-Binding Proteins/chemistry/metabolism/ultrastructure ; Humans ; Kinetics ; Models, Molecular ; Multiprotein Complexes/chemistry/*metabolism/*ultrastructure ; Peptide Hydrolases/chemistry/*metabolism/*ultrastructure ; Protein Binding ; Ubiquitination ; Ubiquitins/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 6
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    sFRP2 in the aged microenvironment drives melanoma metastasis and therapy resistance (2016)
    Nature Publishing Group (NPG)
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    Publikationsdatum: 2016-04-05
    Beschreibung: Cancer is a disease of ageing. Clinically, aged cancer patients tend to have a poorer prognosis than young. This may be due to accumulated cellular damage, decreases in adaptive immunity, and chronic inflammation. However, the effects of the aged microenvironment on tumour progression have been largely unexplored. Since dermal fibroblasts can have profound impacts on melanoma progression, we examined whether age-related changes in dermal fibroblasts could drive melanoma metastasis and response to targeted therapy. Here we find that aged fibroblasts secrete a Wnt antagonist, sFRP2, which activates a multi-step signalling cascade in melanoma cells that results in a decrease in beta-catenin and microphthalmia-associated transcription factor (MITF), and ultimately the loss of a key redox effector, APE1. Loss of APE1 attenuates the response of melanoma cells to DNA damage induced by reactive oxygen species, rendering the cells more resistant to targeted therapy (vemurafenib). Age-related increases in sFRP2 also augment both angiogenesis and metastasis of melanoma cells. These data provide an integrated view of how fibroblasts in the aged microenvironment contribute to tumour progression, offering new possibilities for the design of therapy for the elderly.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4833579/" 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/PMC4833579/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaur, Amanpreet -- Webster, Marie R -- Marchbank, Katie -- Behera, Reeti -- Ndoye, Abibatou -- Kugel, Curtis H 3rd -- Dang, Vanessa M -- Appleton, Jessica -- O'Connell, Michael P -- Cheng, Phil -- Valiga, Alexander A -- Morissette, Rachel -- McDonnell, Nazli B -- Ferrucci, Luigi -- Kossenkov, Andrew V -- Meeth, Katrina -- Tang, Hsin-Yao -- Yin, Xiangfan -- Wood, William H 3rd -- Lehrmann, Elin -- Becker, Kevin G -- Flaherty, Keith T -- Frederick, Dennie T -- Wargo, Jennifer A -- Cooper, Zachary A -- Tetzlaff, Michael T -- Hudgens, Courtney -- Aird, Katherine M -- Zhang, Rugang -- Xu, Xiaowei -- Liu, Qin -- Bartlett, Edmund -- Karakousis, Giorgos -- Eroglu, Zeynep -- Lo, Roger S -- Chan, Matthew -- Menzies, Alexander M -- Long, Georgina V -- Johnson, Douglas B -- Sosman, Jeffrey -- Schilling, Bastian -- Schadendorf, Dirk -- Speicher, David W -- Bosenberg, Marcus -- Ribas, Antoni -- Weeraratna, Ashani T -- P01 CA 114046-06/CA/NCI NIH HHS/ -- P01 CA114046/CA/NCI NIH HHS/ -- P30 CA010815/CA/NCI NIH HHS/ -- P50 CA093372/CA/NCI NIH HHS/ -- R01 CA174746/CA/NCI NIH HHS/ -- R01 CA174746-01/CA/NCI NIH HHS/ -- T32 CA009171/CA/NCI NIH HHS/ -- T32 CA9171-36/CA/NCI NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2016 Apr 14;532(7598):250-4. doi: 10.1038/nature17392. Epub 2016 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Wistar Institute, Philadelphia, Pennsylvania 19104, USA. ; University of the Sciences, Philadelphia, Pennsylvania 19104, USA. ; Department of Dermatology, University of Zurich, Zurich CH-8006, Switzerland. ; The National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA. ; Department of Dermatology and Pathology, Yale University, New Haven, Connecticut 06511, USA. ; Massachusetts General Hospital Cancer Center, Developmental Therapeutics, Boston 02114, Massachusetts, USA. ; Department of Surgical Oncology, MD Anderson Cancer Center, Houston, Texas 77030, USA. ; Departments of Surgery and Pathology, Abramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Department of Medical Oncology, City of Hope Medical Center, Duarte, California 91010, USA. ; Department of Medicine, Division of Hematology-Oncology, University of California Los Angeles, Los Angeles, California 90095, USA. ; Crown Princess Mary Cancer Centre, Westmead Hospital, Westmead 2145, Australia. ; Melanoma Institute Australia and The University of Sydney, Sydney 2000, Australia. ; Department of Medicine, Vanderbilt University Medical Center, Nashville Tennessee 37232, USA. ; Department of Dermatology, University Hospital, West German Cancer Center, University Duesburg-Essen, Essen, Germany. ; German Cancer Consortium (DKTK), Heidelberg 45127, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27042933" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Aging/*metabolism ; Animals ; Cell Line, Tumor ; Culture Media, Conditioned/pharmacology ; DNA Damage ; DNA-(Apurinic or Apyrimidinic Site) Lyase/metabolism ; Disease Progression ; *Drug Resistance, Neoplasm ; Fibroblasts/secretion ; Humans ; Indoles/pharmacology/therapeutic use ; Male ; Melanoma/blood supply/*drug therapy/genetics/*pathology ; Membrane Proteins/*metabolism/secretion ; Mice ; Microphthalmia-Associated Transcription Factor/metabolism ; Middle Aged ; Molecular Targeted Therapy ; *Neoplasm Metastasis ; Neovascularization, Pathologic ; Oxidative Stress ; Phenotype ; Reactive Oxygen Species/metabolism ; Sulfonamides/pharmacology/therapeutic use ; *Tumor Microenvironment ; Wnt Signaling Pathway ; Wnt1 Protein/antagonists & inhibitors ; beta Catenin/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 7
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    Schizophrenia: From genetics to physiology at last (2016)
    Nature Publishing Group (NPG)
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    Publikationsdatum: 2016-01-28
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dhindsa, Ryan S -- Goldstein, David B -- England -- Nature. 2016 Feb 11;530(7589):162-3. doi: 10.1038/nature16874. Epub 2016 Jan 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomic Medicine, Columbia University Medical Center, New York, New York 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26814972" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 8
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    Lunar true polar wander inferred from polar hydrogen (2016)
    Nature Publishing Group (NPG)
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    Publikationsdatum: 2016-03-25
    Beschreibung: The earliest dynamic and thermal history of the Moon is not well understood. The hydrogen content of deposits near the lunar poles may yield insight into this history, because these deposits (which are probably composed of water ice) survive only if they remain in permanent shadow. If the orientation of the Moon has changed, then the locations of the shadowed regions will also have changed. The polar hydrogen deposits have been mapped by orbiting neutron spectrometers, and their observed spatial distribution does not match the expected distribution of water ice inferred from present-day lunar temperatures. This finding is in contrast to the distribution of volatiles observed in similar thermal environments at Mercury's poles. Here we show that polar hydrogen preserves evidence that the spin axis of the Moon has shifted: the hydrogen deposits are antipodal and displaced equally from each pole along opposite longitudes. From the direction and magnitude of the inferred reorientation, and from analysis of the moments of inertia of the Moon, we hypothesize that this change in the spin axis, known as true polar wander, was caused by a low-density thermal anomaly beneath the Procellarum region. Radiogenic heating within this region resulted in the bulk of lunar mare volcanism and altered the density structure of the Moon, changing its moments of inertia. This resulted in true polar wander consistent with the observed remnant polar hydrogen. This thermal anomaly still exists and, in part, controls the current orientation of the Moon. The Procellarum region was most geologically active early in lunar history, which implies that polar wander initiated billions of years ago and that a large portion of the measured polar hydrogen is ancient, recording early delivery of water to the inner Solar System. Our hypothesis provides an explanation for the antipodal distribution of lunar polar hydrogen, and connects polar volatiles to the geologic and geophysical evolution of the Moon and the bombardment history of the early Solar System.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Siegler, M A -- Miller, R S -- Keane, J T -- Laneuville, M -- Paige, D A -- Matsuyama, I -- Lawrence, D J -- Crotts, A -- Poston, M J -- England -- Nature. 2016 Mar 24;531(7595):480-4. doi: 10.1038/nature17166.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Planetary Science Institute, Tucson, Arizona 85719, USA. ; Southern Methodist University, Dallas, Texas 75275, USA. ; University of Alabama in Huntsville, Huntsville, Alabama 35899, USA. ; Lunar and Planetary Laboratory, University of Arizona, Tucson, Arizona 85721, USA. ; Earth Life Sciences Institute, Tokyo Institute of Technology, Meguro, Tokyo 152-8551, Japan. ; University of California, Los Angeles, California 90095, USA. ; The Johns Hopkins University Applied Physics Laboratory, Laurel, Maryland 20723, USA. ; Columbia University, New York, New York 10027, USA. ; California Institute of Technology, Pasadena, California 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27008966" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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