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  • 1
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-03-25
    Description: Author: L. Bryan Ray
    Keywords: Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-09-03
    Description: Author: L. Bryan Ray
    Keywords: Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-05-20
    Description: Author: L. Bryan Ray
    Keywords: Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-04-29
    Description: Author: L. Bryan Ray
    Keywords: Signal Transduction
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2016-01-20
    Description: Massive open online courses (MOOCs) are often characterized as remedies to educational disparities related to social class. Using data from 68 MOOCs offered by Harvard and MIT between 2012 and 2014, we found that course participants from the United States tended to live in more-affluent and better-educated neighborhoods than the average U.S. resident. Among those who did register for courses, students with greater socioeconomic resources were more likely to earn a certificate. Furthermore, these differences in MOOC access and completion were larger for adolescents and young adults, the traditional ages where people find on-ramps into science, technology, engineering, and mathematics (STEM) coursework and careers. Our findings raise concerns that MOOCs and similar approaches to online learning can exacerbate rather than reduce disparities in educational outcomes related to socioeconomic status.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hansen, John D -- Reich, Justin -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1245-8. doi: 10.1126/science.aab3782. Epub 2015 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard Graduate School of Education, Harvard University, Cambridge, MA 02138, USA. john_hansen@mail.harvard.edu. ; Office of Digital Learning, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785488" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Career Choice ; Certification/*methods ; Education, Distance/*methods ; Engineering/education ; Humans ; Internet ; Learning ; Mathematics/education ; *Online Systems ; Science/education ; *Social Class ; Students ; Technology/education ; United States ; Young Adult
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  • 6
    Publication Date: 2016-02-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Claiborne, Anne B -- English, Rebecca A -- Kahn, Jeffrey P -- 10002265/PHS HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):668-70. doi: 10.1126/science.aaf3091. Epub 2016 Feb 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Medicine, U.S. National Academies of Sciences, Engineering, and Medicine, Washington, DC 20001, USA. aclaiborne@nas.edu. ; Institute of Medicine, U.S. National Academies of Sciences, Engineering, and Medicine, Washington, DC 20001, USA. ; Johns Hopkins Berman Institute of Bioethics, Johns Hopkins University, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26842937" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Nucleus/genetics ; DNA, Mitochondrial/genetics ; Ethics, Medical ; *Government Regulation ; Humans ; Mitochondrial Diseases/genetics/*prevention & control ; Mitochondrial Replacement Therapy/*ethics/*standards ; *Oocytes ; United States ; United States Food and Drug Administration ; *Zygote
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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):16-9. doi: 10.1126/science.351.6268.16.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721985" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomedical Research/*economics ; Communicable Disease Control/*economics ; Financial Management ; Humans ; National Institutes of Health (U.S.) ; United States ; Vaccines/*economics
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shanahan, Jesse -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):418. doi: 10.1126/science.351.6271.418.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jesse Shanahan is a master's student in astronomy at Wesleyan University in Middletown, Connecticut. Send your story to SciCareerEditor@aaas.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26798017" target="_blank"〉PubMed〈/a〉
    Keywords: Astronomy/*education ; *Career Mobility ; Disabled Persons/*psychology/statistics & numerical data ; Fear ; *Hostility ; Humans ; Male ; United States
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  • 9
    Publication Date: 2016-04-02
    Description: Global climate change is a major threat to biodiversity. Large-scale analyses have generally focused on the impacts of climate change on the geographic ranges of species and on phenology, the timing of ecological phenomena. We used long-term monitoring of the abundance of breeding birds across Europe and the United States to produce, for both regions, composite population indices for two groups of species: those for which climate suitability has been either improving or declining since 1980. The ratio of these composite indices, the climate impact indicator (CII), reflects the divergent fates of species favored or disadvantaged by climate change. The trend in CII is positive and similar in the two regions. On both continents, interspecific and spatial variation in population abundance trends are well predicted by climate suitability trends.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stephens, Philip A -- Mason, Lucy R -- Green, Rhys E -- Gregory, Richard D -- Sauer, John R -- Alison, Jamie -- Aunins, Ainars -- Brotons, Lluis -- Butchart, Stuart H M -- Campedelli, Tommaso -- Chodkiewicz, Tomasz -- Chylarecki, Przemyslaw -- Crowe, Olivia -- Elts, Jaanus -- Escandell, Virginia -- Foppen, Ruud P B -- Heldbjerg, Henning -- Herrando, Sergi -- Husby, Magne -- Jiguet, Frederic -- Lehikoinen, Aleksi -- Lindstrom, Ake -- Noble, David G -- Paquet, Jean-Yves -- Reif, Jiri -- Sattler, Thomas -- Szep, Tibor -- Teufelbauer, Norbert -- Trautmann, Sven -- van Strien, Arco J -- van Turnhout, Chris A M -- Vorisek, Petr -- Willis, Stephen G -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):84-7. doi: 10.1126/science.aac4858.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Conservation Ecology Group, School of Biological and Biomedical Sciences, Durham University, South Road, Durham DH1 3LE, UK. ; Royal Society for the Protection of Birds, Centre for Conservation Science, The Lodge, Sandy, Bedfordshire SG19 2DL, UK. ; Royal Society for the Protection of Birds, Centre for Conservation Science, The Lodge, Sandy, Bedfordshire SG19 2DL, UK. Conservation Science Group, Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, UK. ; United States Geological Survey, Patuxent Wildlife Research Center, 12100 Beech Forest Road, Laurel, MD 20708, USA. ; Institute of Integrative Biology, University of Liverpool, Crown Street, Liverpool L69 3BX, UK. ; Faculty of Biology, University of Latvia, Jelgavas iela 1, Riga, LV-1004, Latvia. ; Center for Mediterranean Forest Research, Centre Tecnologic Forestal de Catalunya, InForest JRU, Solsona 25280, Spain. REAF, Cerdanyola del Valles 08193, Catalonia, Spain. CSIC, Cerdanyola del Valles 08193, Catalonia, Spain. ; Conservation Science Group, Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, UK. BirdLife International, The David Attenborough Building, Pembroke Street, Cambridge CB2 3QZ, UK. ; MITO2000 National Committee; c/o Dream Italia, Via Garibaldi 3, 52015, Pratovecchio-Stia, Arezzo, Italy. ; Ogolnopolskie Towarzystwo Ochrony Ptakow, Odrowaza 24,05-270 Marki, Poland. ; Museum and Institute of Zoology, Polish Academy of Sciences, Wilcza 64, 00-679 Warszawa, Poland. ; BirdWatch Ireland, Unit 20 Block D Bullford Business Campus, Kilcoole, County Wicklow, Ireland. ; Institute of Ecology and Earth Sciences, University of Tartu, Vanemuise Street 46, 51014 Tartu, Estonia. Estonian Ornithological Society, Veski 4, 51005 Tartu, Estonia. ; Sociedad Espanola de Ornitologia/BirdLife Melquiades Biencinto, 34, 28053 Madrid. Spain. ; European Bird Census Council, Post Office Box 6521, 6503 GA Nijmegen, Netherlands. Sovon Dutch Centre for Field Ornithology, Post Office Box 6521, 6503 GA Nijmegen, Netherlands. Department of Animal Ecology and Ecophysiology, Institute for Water and Wetland Research, Radboud University, Post Office Box 9010, 6500 GL Nijmegen, Netherlands. ; Dansk Ornitologisk Forening-BirdLife Denmark and University of Aarhus, Vesterbrogade 140, 1620 Kobenhavn V, Denmark. ; European Bird Census Council-Catalan Ornithological Institute, Natural History Museum of Barcelona, Placa Leonardo da Vinci 4-5, 08019 Barcelona, Catalonia, Spain. ; Section for Science, Nord University, 7600 Levanger, Norway. ; UMR7204 Sorbonne Universites-MNHN-CNRS-UPMC, CESCO, CRBPO, CP 135, 43 Rue Buffon, 75005 Paris, France. ; The Helsinki Lab of Ornithology, Finnish Museum of Natural History, Post Office Box 17, 00014 University of Helsinki, Finland. ; Biodiversity Unit, Department of Biology, Lund University, Ecology Building, S-223 62 Lund, Sweden. ; The British Trust for Ornithology, The Nunnery, Thetford, Norfolk IP24 2PU, UK. ; Natagora, Departement Etudes, Rue Nanon 98, B-5000 Namur, Belgium. ; Institute for Environmental Studies, Faculty of Science, Charles University in Prague, Czech Republic. Department of Zoology and Laboratory of Ornithology, Faculty of Science, Palacky University Olomouc, 17 Listopadu 50, 771 43 Olomouc, Czech Republic. ; Swiss Ornithological Institute, Seerose 1, 6204 Sempach, Switzerland. ; Institute of Environmental Sciences, University of Nyiregyhaza, Sostoi ut 31/b, 4400 Nyiregyhaza, Hungary. ; BirdLife Austria, Museumsplatz 1/10/8, A-1070 Vienna, Austria. ; Dachverband Deutscher Avifaunisten e.V. (Federation of German Avifaunists), An den Speichern 6, D-48157 Munster, Germany. ; Statistics Netherlands, Post Office Box 24500, 2490 HA The Hague, Netherlands. ; Sovon Dutch Centre for Field Ornithology, Post Office Box 6521, 6503 GA Nijmegen, Netherlands. Department of Animal Ecology and Ecophysiology, Institute for Water and Wetland Research, Radboud University, Post Office Box 9010, 6500 GL Nijmegen, Netherlands. ; Department of Zoology and Laboratory of Ornithology, Faculty of Science, Palacky University Olomouc, 17 Listopadu 50, 771 43 Olomouc, Czech Republic. Pan-European Common Bird Monitoring Scheme, Czech Society for Ornithology, Na Belidle 252/34, CZ-15000 Prague 5, Czech Republic.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034371" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Migration ; Animals ; Biodiversity ; *Birds ; Breeding ; *Climate Change ; Ecological Parameter Monitoring ; Europe ; Population Dynamics ; United States
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, Richard -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1138-40. doi: 10.1126/science.351.6278.1138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965605" target="_blank"〉PubMed〈/a〉
    Keywords: Computer Simulation ; *Explosions ; *Forensic Sciences ; Humans ; *Nuclear Weapons ; United States
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  • 11
    Publication Date: 2016-04-09
    Description: Activation of various cell surface receptors triggers the reorganization of downstream signaling molecules into micrometer- or submicrometer-sized clusters. However, the functional consequences of such clustering have been unclear. We biochemically reconstituted a 12-component signaling pathway on model membranes, beginning with T cell receptor (TCR) activation and ending with actin assembly. When TCR phosphorylation was triggered, downstream signaling proteins spontaneously separated into liquid-like clusters that promoted signaling outputs both in vitro and in human Jurkat T cells. Reconstituted clusters were enriched in kinases but excluded phosphatases and enhanced actin filament assembly by recruiting and organizing actin regulators. These results demonstrate that protein phase separation can create a distinct physical and biochemical compartment that facilitates signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, Xiaolei -- Ditlev, Jonathon A -- Hui, Enfu -- Xing, Wenmin -- Banjade, Sudeep -- Okrut, Julia -- King, David S -- Taunton, Jack -- Rosen, Michael K -- Vale, Ronald D -- 5-F32-DK101188/DK/NIDDK NIH HHS/ -- F32 DK101188/DK/NIDDK NIH HHS/ -- R01 GM056322/GM/NIGMS NIH HHS/ -- R01-GM56322/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):595-9. doi: 10.1126/science.aad9964. Epub 2016 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute (HHMI) Summer Institute, Marine Biological Laboratory, Woods Hole, MA 02543, USA. Department of Cellular and Molecular Pharmacology and Howard Hughes Medical Institute, University of California, San Francisco, CA 94158, USA. ; Howard Hughes Medical Institute (HHMI) Summer Institute, Marine Biological Laboratory, Woods Hole, MA 02543, USA. Department of Biophysics and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; HHMI Mass Spectrometry Laboratory and Department of Molecular and Cellular Biology, University of California, Berkeley, CA 94720, USA. ; Howard Hughes Medical Institute (HHMI) Summer Institute, Marine Biological Laboratory, Woods Hole, MA 02543, USA. Department of Biophysics and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ron.vale@ucsf.edu michael.rosen@utsouthwestern.edu. ; Howard Hughes Medical Institute (HHMI) Summer Institute, Marine Biological Laboratory, Woods Hole, MA 02543, USA. Department of Cellular and Molecular Pharmacology and Howard Hughes Medical Institute, University of California, San Francisco, CA 94158, USA. ron.vale@ucsf.edu michael.rosen@utsouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27056844" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*metabolism ; Adaptor Proteins, Signal Transducing/*metabolism ; Fluorescence Recovery After Photobleaching ; Humans ; Jurkat Cells ; Membrane Proteins/*metabolism ; Mitogen-Activated Protein Kinase Kinases ; Phosphorylation ; Polymerization ; Receptors, Antigen, T-Cell/*agonists ; Signal Transduction ; T-Lymphocytes/*metabolism
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  • 12
    Publication Date: 2016-03-19
    Description: Systemic inflammation, which results from the massive release of proinflammatory molecules into the circulatory system, is a major risk factor for severe illness, but the precise mechanisms underlying its control are not fully understood. We observed that prostaglandin E2 (PGE2), through its receptor EP4, is down-regulated in human systemic inflammatory disease. Mice with reduced PGE2 synthesis develop systemic inflammation, associated with translocation of gut bacteria, which can be prevented by treatment with EP4 agonists. Mechanistically, we demonstrate that PGE2-EP4 signaling acts directly on type 3 innate lymphoid cells (ILCs), promoting their homeostasis and driving them to produce interleukin-22 (IL-22). Disruption of the ILC-IL-22 axis impairs PGE2-mediated inhibition of systemic inflammation. Hence, the ILC-IL-22 axis is essential in protecting against gut barrier dysfunction, enabling PGE2-EP4 signaling to impede systemic inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841390/" 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/PMC4841390/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duffin, Rodger -- O'Connor, Richard A -- Crittenden, Siobhan -- Forster, Thorsten -- Yu, Cunjing -- Zheng, Xiaozhong -- Smyth, Danielle -- Robb, Calum T -- Rossi, Fiona -- Skouras, Christos -- Tang, Shaohui -- Richards, James -- Pellicoro, Antonella -- Weller, Richard B -- Breyer, Richard M -- Mole, Damian J -- Iredale, John P -- Anderton, Stephen M -- Narumiya, Shuh -- Maizels, Rick M -- Ghazal, Peter -- Howie, Sarah E -- Rossi, Adriano G -- Yao, Chengcan -- 106122/Wellcome Trust/United Kingdom -- BB/K091121/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- DK37097/DK/NIDDK NIH HHS/ -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1333-8. doi: 10.1126/science.aad9903.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh EH16 4TJ, UK. ; Division of Pathway Medicine, Edinburgh Infectious Diseases, The University of Edinburgh, Edinburgh EH16 4SB, UK. ; Institute for Immunology and Infection Research, The University of Edinburgh, Edinburgh EH9 3JT, UK. ; MRC Centre for Regenerative Medicine, The University of Edinburgh, Edinburgh EH16 4UU, UK. ; Department of Gastroenterology, First Affiliated Hospital of Jinan University, Guangzhou 510630, China. ; Department of Veterans Affairs, Tennessee Valley Health Authority, Nashville, TN 37212, USA. Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA. ; Center for Innovation in Immunoregulative Technology and Therapeutics (AK Project), Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan. Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST), Tokyo 102-0075, Japan. ; Division of Pathway Medicine, Edinburgh Infectious Diseases, The University of Edinburgh, Edinburgh EH16 4SB, UK. Centre for Synthetic and Systems Biology (SynthSys), The University of Edinburgh, Edinburgh EH9 3JD, UK. ; Medical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh EH16 4TJ, UK. chengcan.yao@ed.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Infections/genetics/immunology ; Dinoprostone/*immunology ; Gene Expression ; Humans ; Immunity, Innate ; Inflammation/drug therapy/*immunology/microbiology ; Interleukins/*immunology ; Intestines/*immunology/microbiology ; Lymphocytes/*immunology ; Mice ; Receptors, Prostaglandin E, EP4 Subtype/antagonists & ; inhibitors/genetics/*immunology ; Signal Transduction
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  • 13
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McNutt, Marcia -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):641. doi: 10.1126/science.aaf4014. Epub 2016 Feb 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Marcia McNutt Editor-in-Chief Science Journals.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912832" target="_blank"〉PubMed〈/a〉
    Keywords: Corrosion ; Federal Government ; Humans ; Michigan ; *Public Health ; Safety/*economics ; Trust ; United States ; United States Environmental Protection Agency ; Water Supply/*economics
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  • 14
    Publication Date: 2016-01-23
    Description: Oligodendrocytes myelinate axons in the central nervous system and develop from oligodendrocyte precursor cells (OPCs) that must first migrate extensively during brain and spinal cord development. We show that OPCs require the vasculature as a physical substrate for migration. We observed that OPCs of the embryonic mouse brain and spinal cord, as well as the human cortex, emerge from progenitor domains and associate with the abluminal endothelial surface of nearby blood vessels. Migrating OPCs crawl along and jump between vessels. OPC migration in vivo was disrupted in mice with defective vascular architecture but was normal in mice lacking pericytes. Thus, physical interactions with the vascular endothelium are required for OPC migration. We identify Wnt-Cxcr4 (chemokine receptor 4) signaling in regulation of OPC-endothelial interactions and propose that this signaling coordinates OPC migration with differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Hui-Hsin -- Niu, Jianqin -- Munji, Roeben -- Davalos, Dimitrios -- Chang, Junlei -- Zhang, Haijing -- Tien, An-Chi -- Kuo, Calvin J -- Chan, Jonah R -- Daneman, Richard -- Fancy, Stephen P J -- 1P01 NS083513/NS/NINDS NIH HHS/ -- 1R01NS064517/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):379-84. doi: 10.1126/science.aad3839.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of California at San Francisco (UCSF), San Francisco, CA 94158, USA. ; Departments of Pharmacology and Neuroscience, University of California at San Diego (UCSD), San Diego, CA 92093, USA. ; Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA. ; Division of Hematology, Department of Medicine, Stanford University, Stanford, CA 94305, USA. ; Division of Hematology, Department of Medicine, Stanford University, Stanford, CA 94305, USA. Department of Urology, Cleveland Clinic Foundation, Cleveland, OH 44195, USA. Howard Hughes Medical Institute (HHMI), Chevy Chase, MD 20815, USA. Duke University School of Medicine, Durham, NC 27710, USA. ; Department of Neurology, UCSF, San Francisco, CA 94158, USA. ; Department of Pediatrics, University of California at San Francisco (UCSF), San Francisco, CA 94158, USA. Department of Neurology, UCSF, San Francisco, CA 94158, USA. Division of Neonatology, UCSF, San Francisco, CA 94158, USA. Newborn Brain Research Institute, UCSF, San Francisco, CA 94158, USA. stephen.fancy@ucsf.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26798014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/cytology/embryology ; *Cell Movement ; Cerebral Cortex/blood supply/*embryology ; Endothelium, Vascular/cytology ; Humans ; Mice ; Neural Stem Cells/cytology/*physiology ; *Neurogenesis ; Oligodendroglia/cytology/*physiology ; *Organogenesis ; Pericytes/cytology/physiology ; Receptors, CXCR4/metabolism ; Signal Transduction ; Spinal Cord/blood supply/cytology/*embryology ; Wnt Proteins/metabolism
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  • 15
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fahlgren, Noah -- Bart, Rebecca -- Herrera-Estrella, Luis -- Rellan-Alvarez, Ruben -- Chitwood, Daniel H -- Dinneny, Jose R -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):824. doi: 10.1126/science.351.6275.824-a. Epub 2016 Feb 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Donald Danforth Plant Science Center, St. Louis, MO 63132, USA. ; Nacional de Genomica para la Biodiversidad, Irapuato, 36821, Mexico. ; Donald Danforth Plant Science Center, St. Louis, MO 63132, USA. jdinneny@carnegiescience.edu dchitwood@danforthcenter.org. ; Carnegie Institution for Science, Stanford, CA 94305, USA. jdinneny@carnegiescience.edu dchitwood@danforthcenter.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912883" target="_blank"〉PubMed〈/a〉
    Keywords: China ; Food, Genetically Modified/*adverse effects ; Genetic Engineering/*utilization ; Health ; Humans ; Plants, Genetically Modified/*adverse effects/genetics ; United States ; Zea mays/genetics
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  • 16
    Publication Date: 2016-02-26
    Description: Astrocytes are specialized and heterogeneous cells that contribute to central nervous system function and homeostasis. However, the mechanisms that create and maintain differences among astrocytes and allow them to fulfill particular physiological roles remain poorly defined. We reveal that neurons actively determine the features of astrocytes in the healthy adult brain and define a role for neuron-derived sonic hedgehog (Shh) in regulating the molecular and functional profile of astrocytes. Thus, the molecular and physiological program of astrocytes is not hardwired during development but, rather, depends on cues from neurons that drive and sustain their specialized properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farmer, W Todd -- Abrahamsson, Therese -- Chierzi, Sabrina -- Lui, Christopher -- Zaelzer, Cristian -- Jones, Emma V -- Bally, Blandine Ponroy -- Chen, Gary G -- Theroux, Jean-Francois -- Peng, Jimmy -- Bourque, Charles W -- Charron, Frederic -- Ernst, Carl -- Sjostrom, P Jesper -- Murai, Keith K -- FDN 143337/Canadian Institutes of Health Research/Canada -- MOP 111152/Canadian Institutes of Health Research/Canada -- MOP 123390/Canadian Institutes of Health Research/Canada -- MOP 126137/Canadian Institutes of Health Research/Canada -- NIA 288936/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):849-54. doi: 10.1126/science.aab3103.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Research in Neuroscience, Department of Neurology and Neurosurgery, Brain Repair and Integrative Neuroscience Program, The Research Institute of the McGill University Health Centre, Montreal General Hospital, Montreal, Quebec, Canada. ; Department of Psychiatry, McGill University, Montreal, Quebec, Canada. McGill Group for Suicide Studies, Douglas Hospital, Montreal, Quebec, Canada. ; Molecular Biology of Neural Development, Institut de Recherches Cliniques de Montreal, Department of Medicine, University of Montreal, Montreal, Quebec, Canada. Department of Biology, McGill University, Montreal, Quebec, Canada. ; Department of Psychiatry, McGill University, Montreal, Quebec, Canada. McGill Group for Suicide Studies, Douglas Hospital, Montreal, Quebec, Canada. Department of Human Genetics, McGill University, Montreal, Quebec, Canada. Douglas Hospital Research Institute, Verdun, Quebec, Canada. ; Centre for Research in Neuroscience, Department of Neurology and Neurosurgery, Brain Repair and Integrative Neuroscience Program, The Research Institute of the McGill University Health Centre, Montreal General Hospital, Montreal, Quebec, Canada. keith.murai@mcgill.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912893" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*metabolism ; Cerebellar Cortex/*cytology ; Female ; Gene Deletion ; Hedgehog Proteins/genetics/*metabolism ; Male ; Mice ; Mice, Mutant Strains ; Neurons/*metabolism ; Receptors, G-Protein-Coupled/genetics/*metabolism ; Signal Transduction
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  • 17
    Publication Date: 2016-01-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mervis, Jeffrey -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):115. doi: 10.1126/science.351.6269.115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744390" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Financing, Organized/*statistics & numerical data ; Humans ; Research Personnel ; Research Support as Topic/*statistics & numerical data ; *Sexism ; United States ; *Women, Working
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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mervis, Jeffrey -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):10-1. doi: 10.1126/science.351.6268.10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉With reporting from Science's news staff.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721980" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/*economics ; Budgets ; Humans ; National Institutes of Health (U.S.)/*economics ; *Research Support as Topic ; United States ; United States National Aeronautics and Space Administration/economics
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):277-8. doi: 10.1126/science.352.6283.277.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081045" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain ; *Datasets as Topic ; European Union ; Humans ; International Cooperation ; Neurosciences/*trends ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varmus, Harold -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):123. doi: 10.1126/science.aaf7301.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harold Varmus is the Lewis Thomas University Professor at the Meyer Cancer Center, Weill Cornell Medicine, New York, NY; Senior Associate Member of the New York Genome Center, New York, NY; and former director of the U.S. National Cancer Institute. varmus@med.cornell.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124426" target="_blank"〉PubMed〈/a〉
    Keywords: Federal Government ; Humans ; Information Dissemination ; *Leadership ; Medical Oncology/economics/*trends ; Neoplasms/diagnosis/drug therapy/prevention & control ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fu, He -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):486. doi: 10.1126/science.352.6284.486.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉He Fu is a Ph.D. candidate in the Department of Microbiology at the University of Illinois, Urbana-Champaign. For more on life and careers, visit sciencecareers.org. Send your story to SciCareerEditor@aaas.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102487" target="_blank"〉PubMed〈/a〉
    Keywords: *Career Choice ; China ; *International Educational Exchange ; Microbiology/*education ; United States
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  • 22
    Publication Date: 2016-02-26
    Description: Purine biosynthetic enzymes organize into dynamic cellular bodies called purinosomes. Little is known about the spatiotemporal control of these structures. Using super-resolution microscopy, we demonstrated that purinosomes colocalized with mitochondria, and these results were supported by isolation of purinosome enzymes with mitochondria. Moreover, the number of purinosome-containing cells responded to dysregulation of mitochondrial function and metabolism. To explore the role of intracellular signaling, we performed a kinome screen using a label-free assay and found that mechanistic target of rapamycin (mTOR) influenced purinosome assembly. mTOR inhibition reduced purinosome-mitochondria colocalization and suppressed purinosome formation stimulated by mitochondria dysregulation. Collectively, our data suggest an mTOR-mediated link between purinosomes and mitochondria, and a general means by which mTOR regulates nucleotide metabolism by spatiotemporal control over protein association.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉French, Jarrod B -- Jones, Sara A -- Deng, Huayun -- Pedley, Anthony M -- Kim, Doory -- Chan, Chung Yu -- Hu, Haibei -- Pugh, Raymond J -- Zhao, Hong -- Zhang, Youxin -- Huang, Tony Jun -- Fang, Ye -- Zhuang, Xiaowei -- Benkovic, Stephen J -- 1R33EB019785-01/EB/NIBIB NIH HHS/ -- GM024129/GM/NIGMS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):733-7. doi: 10.1126/science.aac6054.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Cell Biology, Department of Chemistry, Stony Brook University, Stony Brook, NY 11794, USA. jarrod.french@stonybrook.edu fangy2@corning.com zhuang@chemistry.harvard.edu sjb1@psu.edu. ; Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA. ; Biochemical Technologies, Science and Technology Division, Corning Incorporated, Corning, NY 14831, USA. ; Department of Chemistry, The Pennsylvania State University, University Park, PA 16802, USA. ; Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA. Howard Hughes Medical Institute, Harvard University, Cambridge, MA 02138, USA. ; Department of Engineering Science and Mechanics, The Pennsylvania State University, University Park, PA 16802, USA. ; Biochemical Technologies, Science and Technology Division, Corning Incorporated, Corning, NY 14831, USA. jarrod.french@stonybrook.edu fangy2@corning.com zhuang@chemistry.harvard.edu sjb1@psu.edu. ; Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA. Howard Hughes Medical Institute, Harvard University, Cambridge, MA 02138, USA. Department of Physics, Harvard University, Cambridge, MA 02138, USA. jarrod.french@stonybrook.edu fangy2@corning.com zhuang@chemistry.harvard.edu sjb1@psu.edu. ; Department of Chemistry, The Pennsylvania State University, University Park, PA 16802, USA. jarrod.french@stonybrook.edu fangy2@corning.com zhuang@chemistry.harvard.edu sjb1@psu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912862" target="_blank"〉PubMed〈/a〉
    Keywords: HeLa Cells ; Humans ; Microscopy ; Mitochondria/*metabolism/ultrastructure ; Purines/*metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases/*metabolism
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alberts, Bruce -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):207. doi: 10.1126/science.aaf2001.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bruce Alberts is the Chancellor's Leadership Chair in Biochemistry and Biophysics for Science and Education at the University of California, San Francisco, CA, and emeritus editor-in-chief of Science. Bruce.Alberts@ucsf.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816352" target="_blank"〉PubMed〈/a〉
    Keywords: *Career Choice ; *Faculty ; Humans ; Leadership ; Policy Making ; *Power (Psychology) ; Schools/*manpower/trends ; Teaching/*manpower/methods/trends ; United States
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  • 24
    Publication Date: 2016-01-23
    Description: The plant root cap, surrounding the very tip of the growing root, perceives and transmits environmental signals to the inner root tissues. In Arabidopsis thaliana, auxin released by the root cap contributes to the regular spacing of lateral organs along the primary root axis. Here, we show that the periodicity of lateral organ induction is driven by recurrent programmed cell death at the most distal edge of the root cap. We suggest that synchronous bursts of cell death in lateral root cap cells release pulses of auxin to surrounding root tissues, establishing the pattern for lateral root formation. The dynamics of root cap turnover may therefore coordinate primary root growth with root branching in order to optimize the uptake of water and nutrients from the soil.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xuan, Wei -- Band, Leah R -- Kumpf, Robert P -- Van Damme, Daniel -- Parizot, Boris -- De Rop, Gieljan -- Opdenacker, Davy -- Moller, Barbara K -- Skorzinski, Noemi -- Njo, Maria F -- De Rybel, Bert -- Audenaert, Dominique -- Nowack, Moritz K -- Vanneste, Steffen -- Beeckman, Tom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):384-7. doi: 10.1126/science.aad2776.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Systems Biology, Vlaams Instituut voor Biotechnologie (VIB), Technologiepark 927, 9052 Ghent, Belgium. Department of Plant Biotechnology and Bioinformatics, Gent University, Technologiepark 927, 9052 Ghent, Belgium. State Key Laboratory of Crop Genetics and Germplasm Enhancement and MOA Key Laboratory of Plant Nutrition and Fertilization in Lower-Middle Reaches of the Yangtze River, Nanjing Agricultural University, Weigang No. 1, Nanjing 210095, PR China. ; Centre for Plant Integrative Biology, University of Nottingham, Nottingham LE12 5RD, UK. ; Department of Plant Systems Biology, Vlaams Instituut voor Biotechnologie (VIB), Technologiepark 927, 9052 Ghent, Belgium. Department of Plant Biotechnology and Bioinformatics, Gent University, Technologiepark 927, 9052 Ghent, Belgium. ; Max Planck Institute for Developmental Biology, Spemannstrasse 35, 72076 Tubingen, Germany. ; Department of Plant Systems Biology, Vlaams Instituut voor Biotechnologie (VIB), Technologiepark 927, 9052 Ghent, Belgium. Department of Plant Biotechnology and Bioinformatics, Gent University, Technologiepark 927, 9052 Ghent, Belgium. Laboratory of Biochemistry, Wageningen University, Dreijenlaan 3, 6703HA Wageningen, Netherlands. ; Department of Plant Systems Biology, Vlaams Instituut voor Biotechnologie (VIB), Technologiepark 927, 9052 Ghent, Belgium. Department of Plant Biotechnology and Bioinformatics, Gent University, Technologiepark 927, 9052 Ghent, Belgium. tobee@psb.vib-ugent.be.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26798015" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Arabidopsis/cytology/*growth & development/metabolism ; Indoleacetic Acids/*metabolism ; Plant Epidermis/cytology/growth & development/metabolism ; Plant Root Cap/cytology/*growth & development/metabolism ; Receptors, TNF-Related Apoptosis-Inducing Ligand/genetics/metabolism ; Signal Transduction ; Soil ; Water/metabolism
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):394-5. doi: 10.1126/science.352.6284.394. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102455" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Evolution, Molecular ; Foundations ; Genes ; Genetic Research/*economics ; Great Britain ; Humans ; *Research Support as Topic ; *Selection, Genetic ; Sweden ; United States
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  • 26
    Publication Date: 2016-02-06
    Description: The intestinal epithelium forms an essential barrier between a host and its microbiota. Protozoa and helminths are members of the gut microbiota of mammals, including humans, yet the many ways that gut epithelial cells orchestrate responses to these eukaryotes remain unclear. Here we show that tuft cells, which are taste-chemosensory epithelial cells, accumulate during parasite colonization and infection. Disruption of chemosensory signaling through the loss of TRMP5 abrogates the expansion of tuft cells, goblet cells, eosinophils, and type 2 innate lymphoid cells during parasite colonization. Tuft cells are the primary source of the parasite-induced cytokine interleukin-25, which indirectly induces tuft cell expansion by promoting interleukin-13 production by innate lymphoid cells. Our results identify intestinal tuft cells as critical sentinels in the gut epithelium that promote type 2 immunity in response to intestinal parasites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Howitt, Michael R -- Lavoie, Sydney -- Michaud, Monia -- Blum, Arthur M -- Tran, Sara V -- Weinstock, Joel V -- Gallini, Carey Ann -- Redding, Kevin -- Margolskee, Robert F -- Osborne, Lisa C -- Artis, David -- Garrett, Wendy S -- F31DK105653/DK/NIDDK NIH HHS/ -- F32DK098826/DK/NIDDK NIH HHS/ -- R01 CA154426/CA/NCI NIH HHS/ -- R01 GM099531/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1329-33. doi: 10.1126/science.aaf1648. Epub 2016 Feb 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Immunology and Infectious Diseases and Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA. ; Division of Gastroenterology, Tufts Medical Center, Boston, MA 02111, USA. ; Monell Chemical Senses Center, Philadelphia, PA 19104, USA. ; Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medical College, Cornell University, New York, NY 10021, USA. ; Departments of Immunology and Infectious Diseases and Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA. Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA 02142, USA. Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. wgarrett@hsph.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26847546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chemoreceptor Cells/*immunology ; Eosinophils/immunology ; Goblet Cells/immunology ; Helminthiasis/immunology/parasitology ; Helminths/immunology ; Immunity, Mucosal ; Interleukin-13/immunology ; Interleukin-17/immunology ; Intestinal Diseases, Parasitic/*immunology/parasitology ; Intestinal Mucosa/*immunology/*parasitology ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Microbiota/*immunology ; Protein-Serine-Threonine Kinases/immunology ; Protozoan Infections/immunology/parasitology ; Signal Transduction ; TRPM Cation Channels/*immunology ; Taste ; Transducin/genetics/immunology ; Tritrichomonas/immunology
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    Publication Date: 2016-02-06
    Description: SH3 and multiple ankyrin repeat domains 3 (SHANK3) haploinsufficiency is causative for the neurological features of Phelan-McDermid syndrome (PMDS), including a high risk of autism spectrum disorder (ASD). We used unbiased, quantitative proteomics to identify changes in the phosphoproteome of Shank3-deficient neurons. Down-regulation of protein kinase B (PKB/Akt)-mammalian target of rapamycin complex 1 (mTORC1) signaling resulted from enhanced phosphorylation and activation of serine/threonine protein phosphatase 2A (PP2A) regulatory subunit, B56beta, due to increased steady-state levels of its kinase, Cdc2-like kinase 2 (CLK2). Pharmacological and genetic activation of Akt or inhibition of CLK2 relieved synaptic deficits in Shank3-deficient and PMDS patient-derived neurons. CLK2 inhibition also restored normal sociability in a Shank3-deficient mouse model. Our study thereby provides a novel mechanistic and potentially therapeutic understanding of deregulated signaling downstream of Shank3 deficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bidinosti, Michael -- Botta, Paolo -- Kruttner, Sebastian -- Proenca, Catia C -- Stoehr, Natacha -- Bernhard, Mario -- Fruh, Isabelle -- Mueller, Matthias -- Bonenfant, Debora -- Voshol, Hans -- Carbone, Walter -- Neal, Sarah J -- McTighe, Stephanie M -- Roma, Guglielmo -- Dolmetsch, Ricardo E -- Porter, Jeffrey A -- Caroni, Pico -- Bouwmeester, Tewis -- Luthi, Andreas -- Galimberti, Ivan -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1199-203. doi: 10.1126/science.aad5487. Epub 2016 Feb 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Molecular Pathways, Novartis Institutes for Biomedical Research, Basel, Switzerland. ; Friedrich Miescher Institute, Basel, Switzerland. ; Analytical Sciences and Imaging, Novartis Institutes for Biomedical Research, Basel, Switzerland. ; Neuroscience, Novartis Institutes for Biomedical Research, Cambridge, USA. ; Developmental Molecular Pathways, Novartis Institutes for Biomedical Research, Basel, Switzerland. ivan.galimberti@novartis.com.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26847545" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Autism Spectrum Disorder/*drug therapy/enzymology/genetics ; Chromosome Deletion ; Chromosome Disorders/genetics ; Chromosomes, Human, Pair 22/genetics ; Disease Models, Animal ; Down-Regulation ; Gene Knockdown Techniques ; Humans ; Insulin-Like Growth Factor I/metabolism ; Mice ; Molecular Sequence Data ; Multiprotein Complexes/metabolism ; Nerve Tissue Proteins/*genetics ; Neurons/enzymology ; Phosphorylation ; Protein Phosphatase 2/metabolism ; Protein-Serine-Threonine Kinases/*antagonists & inhibitors/metabolism ; Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Proteomics ; Proto-Oncogene Proteins c-akt/genetics/metabolism ; Rats ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blum, Arlene -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1117. doi: 10.1126/science.aaf5468. Epub 2016 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Arlene Blum is founder and executive director of the Green Science Policy Institute, Berkeley, CA. arlene@GreenSciencePolicy.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965592" target="_blank"〉PubMed〈/a〉
    Keywords: Consumer Product Safety/*legislation & jurisprudence ; Health ; Household Products/*toxicity ; Humans ; Manufactured Materials/*toxicity ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-29
    Description: Metastatic disease is the leading cause of cancer-related deaths and involves critical interactions between tumor cells and the microenvironment. Hypoxia is a potent microenvironmental factor promoting metastatic progression. Clinically, hypoxia and the expression of the hypoxia-inducible transcription factors HIF-1 and HIF-2 are associated with increased distant metastasis and poor survival in a variety of tumor types. Moreover, HIF signaling in malignant cells influences multiple steps within the metastatic cascade. Here we review research focused on elucidating the mechanisms by which the hypoxic tumor microenvironment promotes metastatic progression. These studies have identified potential biomarkers and therapeutic targets regulated by hypoxia that could be incorporated into strategies aimed at preventing and treating metastatic disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rankin, Erinn B -- Giaccia, Amato J -- CA-197713/CA/NCI NIH HHS/ -- CA-198291/CA/NCI NIH HHS/ -- CA-67166/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):175-80. doi: 10.1126/science.aaf4405. Epub 2016 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University Medical Center, Stanford, CA 94305-5152, USA. Department of Obstetrics and Gynecology, Stanford University Medical Center, Stanford, CA 94305-5152, USA. ; Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University Medical Center, Stanford, CA 94305-5152, USA. giaccia@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124451" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/*metabolism ; Biomarkers, Tumor/analysis/metabolism ; Cell Hypoxia ; Cell Movement ; Disease Progression ; Drug Resistance, Neoplasm ; Epithelial-Mesenchymal Transition ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism ; Neoplasm Invasiveness ; Neoplasm Metastasis/*pathology/*therapy ; Radiation Tolerance ; Signal Transduction ; *Tumor Microenvironment
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):14. doi: 10.1126/science.351.6268.14.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721983" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Databases, Genetic/*economics ; Financial Support ; Human Genome Project/*economics ; Humans ; Models, Animal ; National Human Genome Research Institute (U.S.)/*economics ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Richmond, Geraldine -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):427. doi: 10.1126/science.aaf2869. Epub 2016 Jan 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Geraldine Richmond is president of AAAS and Presidential Chair in Science and professor in the Department of Chemistry and Biochemistry at the University of Oregon, Eugene, OR. richmond@oregon.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823402" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Asia ; *Food Supply ; Humans ; *Internationality ; United States ; *Water Supply
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):20. doi: 10.1126/science.352.6281.20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034352" target="_blank"〉PubMed〈/a〉
    Keywords: Awards and Prizes ; Biomedical Research/*economics ; *Financing, Government ; National Institute of General Medical Sciences (U.S.) ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 33
    Publication Date: 2016-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):325-6. doi: 10.1126/science.351.6271.325.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26797992" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/*organization & administration ; Federal Government ; Humans ; Neoplasms/*therapy ; Policy ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roman, Joe -- Kraska, James -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1258-60. doi: 10.1126/science.aad4247.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gund Institute for Ecological Economics, University of Vermont, Burlington, VT 05405, USA. jroman@uvm.edu. ; Stockton Center for the Study of International Law, U.S. Naval War College, Newport, RI 02841, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989232" target="_blank"〉PubMed〈/a〉
    Keywords: *Bays ; *Conservation of Natural Resources ; Cuba ; Diplomacy ; United States
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  • 35
    Publication Date: 2016-03-12
    Description: The oncogene MDMX is overexpressed in many cancers, leading to suppression of the tumor suppressor p53. Inhibitors of the oncogene product MDMX therefore might help reactivate p53 and enhance the efficacy of DNA-damaging drugs. However, we currently lack a quantitative understanding of how MDMX inhibition affects the p53 signaling pathway and cell sensitivity to DNA damage. Live cell imaging showed that MDMX depletion triggered two distinct phases of p53 accumulation in single cells: an initial postmitotic pulse, followed by low-amplitude oscillations. The response to DNA damage was sharply different in these two phases; in the first phase, MDMX depletion was synergistic with DNA damage in causing cell death, whereas in the second phase, depletion of MDMX inhibited cell death. Thus a quantitative understanding of signal dynamics and cellular states is important for designing an optimal schedule of dual-drug administration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Sheng-Hong -- Forrester, William -- Lahav, Galit -- F32GM105205/GM/NIGMS NIH HHS/ -- GM083303/GM/NIGMS NIH HHS/ -- R01 GM083303/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1204-8. doi: 10.1126/science.aac5610. Epub 2016 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Systems Biology, Harvard Medical School, Boston, MA, USA. ; Developmental and Molecular Pathways, Novartis Institutes for Biomedical Research, Cambridge, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965628" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/*administration & dosage ; Apoptosis ; *DNA Damage ; Gene Knockdown Techniques ; Humans ; MCF-7 Cells ; Molecular Imaging ; Neoplasms/*drug therapy ; Proto-Oncogene Proteins c-mdm2/*antagonists & inhibitors/genetics ; RNA, Small Interfering/genetics ; Signal Transduction ; Time Factors ; Tumor Suppressor Protein p53/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Publication Date: 2016-01-07
    Description: Endothelial cells (ECs) are plastic cells that can switch between growth states with different bioenergetic and biosynthetic requirements. Although quiescent in most healthy tissues, ECs divide and migrate rapidly upon proangiogenic stimulation. Adjusting endothelial metabolism to the growth state is central to normal vessel growth and function, yet it is poorly understood at the molecular level. Here we report that the forkhead box O (FOXO) transcription factor FOXO1 is an essential regulator of vascular growth that couples metabolic and proliferative activities in ECs. Endothelial-restricted deletion of FOXO1 in mice induces a profound increase in EC proliferation that interferes with coordinated sprouting, thereby causing hyperplasia and vessel enlargement. Conversely, forced expression of FOXO1 restricts vascular expansion and leads to vessel thinning and hypobranching. We find that FOXO1 acts as a gatekeeper of endothelial quiescence, which decelerates metabolic activity by reducing glycolysis and mitochondrial respiration. Mechanistically, FOXO1 suppresses signalling by MYC (also known as c-MYC), a powerful driver of anabolic metabolism and growth. MYC ablation impairs glycolysis, mitochondrial function and proliferation of ECs while its EC-specific overexpression fuels these processes. Moreover, restoration of MYC signalling in FOXO1-overexpressing endothelium normalizes metabolic activity and branching behaviour. Our findings identify FOXO1 as a critical rheostat of vascular expansion and define the FOXO1-MYC transcriptional network as a novel metabolic checkpoint during endothelial growth and proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilhelm, Kerstin -- Happel, Katharina -- Eelen, Guy -- Schoors, Sandra -- Oellerich, Mark F -- Lim, Radiance -- Zimmermann, Barbara -- Aspalter, Irene M -- Franco, Claudio A -- Boettger, Thomas -- Braun, Thomas -- Fruttiger, Marcus -- Rajewsky, Klaus -- Keller, Charles -- Bruning, Jens C -- Gerhardt, Holger -- Carmeliet, Peter -- Potente, Michael -- K08CA090438/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- England -- Nature. 2016 Jan 14;529(7585):216-20. doi: 10.1038/nature16498. Epub 2016 Jan 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Angiogenesis &Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, D-61231 Bad Nauheim, Germany. ; Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, Department of Oncology, University of Leuven, Leuven 3000, Belgium. ; Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, VIB, Leuven 3000, Belgium. ; Vascular Biology Laboratory, London Research Institute, Cancer Research UK, London WC2A 3LY, UK. ; Vascular Morphogenesis Laboratory, Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Lisbon 1649-028, Portugal. ; Department of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, D-61231 Bad Nauheim, Germany. ; UCL Institute of Ophthalmology, University College London, London EC1V 9EL, UK. ; Max Delbruck Center for Molecular Medicine (MDC), D-13125 Berlin, Germany. ; Children's Cancer Therapy Development Institute, Beaverton, Oregon 97005, USA. ; Max Planck Institute for Metabolism Research, Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University of Cologne, D-50931 Cologne, Germany. ; Vascular Patterning Laboratory, Vesalius Research Center, VIB and University of Leuven, Leuven 3000, Belgium. ; DZHK (German Center for Cardiovascular Research), partner site Berlin, D-13347 Berlin, Germany. ; Berlin Institute of Health (BIH), D-10117 Berlin, Germany. ; International Institute of Molecular and Cell Biology, 02-109 Warsaw, Poland. ; DZHK (German Center for Cardiovascular Research), partner site Frankfurt Rhine-Main, D-13347 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26735015" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Cell Respiration ; Endothelium, Vascular/cytology/*growth & development/*metabolism ; Female ; Forkhead Transcription Factors/deficiency/genetics/*metabolism ; Glycolysis ; Human Umbilical Vein Endothelial Cells/cytology/metabolism ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-myc/deficiency/genetics/metabolism ; Signal Transduction
    Print ISSN: 0028-0836
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    Publication Date: 2016-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Check Hayden, Erika -- England -- Nature. 2016 Apr 28;532(7600):424-5. doi: 10.1038/532424a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27121817" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/*economics/legislation & jurisprudence/*trends ; *Federal Government ; Financing, Government/economics/legislation & jurisprudence ; Humans ; Immunotherapy/economics ; Information Dissemination ; Leadership ; Neoplasms/economics/genetics/immunology/*therapy ; *Private Sector/economics ; *Public-Private Sector Partnerships/economics ; United States
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    Publication Date: 2016-01-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, Frank -- England -- Nature. 2016 Jan 14;529(7585):156. doi: 10.1038/529156e.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Calgary, Alberta, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26762447" target="_blank"〉PubMed〈/a〉
    Keywords: Chemical Hazard Release/*prevention & control ; Equipment Safety ; *Materials Testing ; Oil and Gas Industry/*instrumentation/methods ; United States
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    Nature Publishing Group (NPG)
    Publication Date: 2016-01-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 Jan 28;529(7587):437-8. doi: 10.1038/529437b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26819007" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; China ; Cities ; Congo ; Conservation of Natural Resources/*legislation & jurisprudence ; Ecosystem ; Great Britain ; *Parks, Recreational/legislation & jurisprudence ; Pleasure ; Uganda ; United States ; *Wilderness
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    Nature Publishing Group (NPG)
    Publication Date: 2016-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 Feb 18;530(7590):253-4. doi: 10.1038/530253b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26887453" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/*economics/*trends ; Child ; *Federal Government ; *Goals ; Humans ; Immunotherapy ; Information Dissemination ; Neoplasms/*therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; United States
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  • 41
    Publication Date: 2016-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nardone, Roland M -- MacLeod, Roderick A F -- Capes-Davis, Amanda -- England -- Nature. 2016 Apr 21;532(7599):313.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27127813" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; DNA Contamination ; Databases, Factual ; *Disease Models, Animal ; Guidelines as Topic ; Heterografts/*standards ; Humans ; National Cancer Institute (U.S.) ; Neoplasms/*pathology ; Quality Control ; Reproducibility of Results ; United States ; Xenograft Model Antitumor Assays/*standards
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    Nature Publishing Group (NPG)
    Publication Date: 2016-05-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 May 11;533(7602):146. doi: 10.1038/533146a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27172009" target="_blank"〉PubMed〈/a〉
    Keywords: Device Approval/legislation & jurisprudence ; Drug Approval/legislation & jurisprudence ; Electronic Cigarettes/*adverse effects/utilization ; Humans ; Industry/legislation & jurisprudence ; Nicotine/administration & dosage/adverse effects/analysis ; Research Personnel ; Smoking/epidemiology/mortality/*prevention & control ; Tobacco Products/adverse effects/utilization ; United States ; United States Food and Drug Administration/*legislation & jurisprudence
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    Nature Publishing Group (NPG)
    Publication Date: 2016-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roth, Alvin E -- England -- Nature. 2016 Apr 14;532(7598):178. doi: 10.1038/532178a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stanford University, California, USA. He shared the 2012 Nobel Memorial Prize in Economic Sciences with Lloyd Shapley.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27075091" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Economics/*history ; Female ; *Game Theory ; History, 20th Century ; History, 21st Century ; Humans ; Male ; Marketing/history ; Marriage/psychology ; Mathematics/*history ; Nobel Prize ; United States
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    Nature Publishing Group (NPG)
    Publication Date: 2016-05-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 May 11;533(7602):145. doi: 10.1038/533145a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27172008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety ; Biomedical Research/*trends ; Breast Feeding/*adverse effects ; Clinical Trials as Topic/ethics/methods ; Female ; Humans ; Infant ; Infant, Newborn ; Milk, Human/*chemistry/*metabolism ; Mothers/psychology ; Pharmaceutical Preparations/*administration & dosage/*metabolism ; Risk Assessment ; Safety ; *Uncertainty ; United States ; United States Food and Drug Administration
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  • 45
    Publication Date: 2016-03-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lauer, Michael -- Valantine, Hannah -- Collins, Francis S -- England -- Nature. 2016 Mar 3;531(7592):35. doi: 10.1038/531035b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institutes of Health, Bethesda, Maryland, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26935689" target="_blank"〉PubMed〈/a〉
    Keywords: Congresses as Topic ; *National Institutes of Health (U.S.)/economics/organization & administration ; *Organizational Policy ; Sexual Harassment/*prevention & control/statistics & numerical data ; United States ; Workplace
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    Nature Publishing Group (NPG)
    Publication Date: 2016-05-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 May 5;533(7601):7. doi: 10.1038/533007a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27146996" target="_blank"〉PubMed〈/a〉
    Keywords: Americas ; *Bone and Bones/metabolism ; Burial/ethics/*legislation & jurisprudence ; Dissent and Disputes/*legislation & jurisprudence ; *Federal Government ; Genome, Human/genetics ; Genomics ; History, Ancient ; Human Migration/history ; Humans ; Indians, North American/classification/genetics/*legislation & jurisprudence ; Indians, South American/classification/genetics/legislation & jurisprudence ; *Phylogeny ; Research Personnel/*legislation & jurisprudence ; United States ; Washington
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    Nature Publishing Group (NPG)
    Publication Date: 2016-02-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ledford, Heidi -- England -- Nature. 2016 Feb 4;530(7588):17. doi: 10.1038/530017a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26842036" target="_blank"〉PubMed〈/a〉
    Keywords: Attention/drug effects ; Cognition Disorders/*complications/*drug therapy/psychology ; Depression/*complications/drug therapy/*psychology ; *Drug Discovery ; *Drug Industry/legislation & jurisprudence ; Humans ; Memory/drug effects ; Schizophrenia/drug therapy ; United States ; United States Food and Drug Administration/legislation & jurisprudence
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  • 48
    Publication Date: 2016-03-24
    Description: (beta-)Arrestins are important regulators of G-protein-coupled receptors (GPCRs). They bind to active, phosphorylated GPCRs and thereby shut off 'classical' signalling to G proteins, trigger internalization of GPCRs via interaction with the clathrin machinery and mediate signalling via 'non-classical' pathways. In addition to two visual arrestins that bind to rod and cone photoreceptors (termed arrestin1 and arrestin4), there are only two (non-visual) beta-arrestin proteins (beta-arrestin1 and beta-arrestin2, also termed arrestin2 and arrestin3), which regulate hundreds of different (non-visual) GPCRs. Binding of these proteins to GPCRs usually requires the active form of the receptors plus their phosphorylation by G-protein-coupled receptor kinases (GRKs). The binding of receptors or their carboxy terminus as well as certain truncations induce active conformations of (beta-)arrestins that have recently been solved by X-ray crystallography. Here we investigate both the interaction of beta-arrestin with GPCRs, and the beta-arrestin conformational changes in real time and in living human cells, using a series of fluorescence resonance energy transfer (FRET)-based beta-arrestin2 biosensors. We observe receptor-specific patterns of conformational changes in beta-arrestin2 that occur rapidly after the receptor-beta-arrestin2 interaction. After agonist removal, these changes persist for longer than the direct receptor interaction. Our data indicate a rapid, receptor-type-specific, two-step binding and activation process between GPCRs and beta-arrestins. They further indicate that beta-arrestins remain active after dissociation from receptors, allowing them to remain at the cell surface and presumably signal independently. Thus, GPCRs trigger a rapid, receptor-specific activation/deactivation cycle of beta-arrestins, which permits their active signalling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nuber, Susanne -- Zabel, Ulrike -- Lorenz, Kristina -- Nuber, Andreas -- Milligan, Graeme -- Tobin, Andrew B -- Lohse, Martin J -- Hoffmann, Carsten -- 1 R01 DA038882/DA/NIDA NIH HHS/ -- BB/K019864/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- England -- Nature. 2016 Mar 31;531(7596):661-4. doi: 10.1038/nature17198. Epub 2016 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Pharmacology and Toxicology, University of Wurzburg, Versbacher Str. 9, 97078 Wurzburg, Germany. ; Rudolf Virchow Center, University of Wurzburg, Versbacher Str. 9, 97078 Wurzburg, Germany. ; Comprehensive Heart Failure Center, University of Wurzburg, Versbacher Str. 9, 97078 Wurzburg, Germany. ; Molecular Pharmacology Group, Institute of Molecular, Cell and Systems Biology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK. ; MRC Toxicology Unit, University of Leicester, Hodgkin Building, Lancaster Road, Leicester LE1 9HN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27007855" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arrestins/chemistry/*metabolism ; Biosensing Techniques ; Cattle ; Cell Line ; Cell Membrane/metabolism ; Cell Survival ; Crystallography, X-Ray ; Fluorescence Resonance Energy Transfer ; Humans ; Kinetics ; Models, Molecular ; Protein Binding ; Protein Conformation ; Receptors, G-Protein-Coupled/chemistry/*metabolism ; Signal Transduction ; Substrate Specificity ; Time Factors
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  • 49
    Publication Date: 2016-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Callaway, Ewen -- England -- Nature. 2016 Apr 14;532(7598):159-60. doi: 10.1038/nature.2016.19714.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27075075" target="_blank"〉PubMed〈/a〉
    Keywords: Financing, Organized/economics/*legislation & jurisprudence/*organization & ; administration ; Great Britain ; Laboratories/*economics ; National Institutes of Health (U.S.)/legislation & jurisprudence ; Research Personnel/*economics ; United States
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  • 50
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    Nature Publishing Group (NPG)
    Publication Date: 2016-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 Apr 14;532(7598):147-8. doi: 10.1038/532147b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27075057" target="_blank"〉PubMed〈/a〉
    Keywords: Financing, Organized/*legislation & jurisprudence/*organization & administration ; National Institute of Allergy and Infectious Diseases (U.S.) ; *Research Personnel/economics/psychology ; Surveys and Questionnaires ; United States
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  • 51
    Publication Date: 2016-04-30
    Description: As climate change unfolds, weather systems in the United States have been shifting in patterns that vary across regions and seasons. Climate science research typically assesses these changes by examining individual weather indicators, such as temperature or precipitation, in isolation, and averaging their values across the spatial surface. As a result, little is known about population exposure to changes in weather and how people experience and evaluate these changes considered together. Here we show that in the United States from 1974 to 2013, the weather conditions experienced by the vast majority of the population improved. Using previous research on how weather affects local population growth to develop an index of people's weather preferences, we find that 80% of Americans live in counties that are experiencing more pleasant weather than they did four decades ago. Virtually all Americans are now experiencing the much milder winters that they typically prefer, and these mild winters have not been offset by markedly more uncomfortable summers or other negative changes. Climate change models predict that this trend is temporary, however, because US summers will eventually warm more than winters. Under a scenario in which greenhouse gas emissions proceed at an unabated rate (Representative Concentration Pathway 8.5), we estimate that 88% of the US public will experience weather at the end of the century that is less preferable than weather in the recent past. Our results have implications for the public's understanding of the climate change problem, which is shaped in part by experiences with local weather. Whereas weather patterns in recent decades have served as a poor source of motivation for Americans to demand a policy response to climate change, public concern may rise once people's everyday experiences of climate change effects start to become less pleasant.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, Patrick J -- Mullin, Megan -- England -- Nature. 2016 Apr 21;532(7599):357-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27127821" target="_blank"〉PubMed〈/a〉
    Keywords: Climate Change/*statistics & numerical data ; *Forecasting ; Global Warming/statistics & numerical data ; Greenhouse Effect/statistics & numerical data ; Humidity ; Motivation ; *Public Opinion ; Rain ; Seasons ; Temperature ; Time Factors ; United States ; *Weather
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  • 52
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    Nature Publishing Group (NPG)
    Publication Date: 2016-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eisenstein, Michael -- England -- Nature. 2016 May 5;533(7601):S20-1. doi: 10.1038/533S20a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27144604" target="_blank"〉PubMed〈/a〉
    Keywords: Federal Government ; Financing, Government/economics/statistics & numerical data ; Great Britain ; Humans ; Inventions/economics ; Investments/*economics/statistics & numerical data ; National Institutes of Health (U.S.)/economics ; Patents as Topic ; Research/*economics/statistics & numerical data ; Research Support as Topic/economics/statistics & numerical data ; United States
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  • 53
    Publication Date: 2016-04-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewis, Simon L -- England -- Nature. 2016 Apr 21;532(7599):283. doi: 10.1038/532283a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27111605" target="_blank"〉PubMed〈/a〉
    Keywords: China ; Environmental Policy/*legislation & jurisprudence ; Global Warming/*legislation & jurisprudence/*prevention & control ; Human Activities/legislation & jurisprudence ; *International Cooperation ; Islands ; Paris ; *Politics ; *Temperature ; United States
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  • 54
    Publication Date: 2016-04-07
    Description: Neoplastic pancreatic epithelial cells are believed to die through caspase 8-dependent apoptotic cell death, and chemotherapy is thought to promote tumour apoptosis. Conversely, cancer cells often disrupt apoptosis to survive. Another type of programmed cell death is necroptosis (programmed necrosis), but its role in pancreatic ductal adenocarcinoma (PDA) is unclear. There are many potential inducers of necroptosis in PDA, including ligation of tumour necrosis factor receptor 1 (TNFR1), CD95, TNF-related apoptosis-inducing ligand (TRAIL) receptors, Toll-like receptors, reactive oxygen species, and chemotherapeutic drugs. Here we report that the principal components of the necrosome, receptor-interacting protein (RIP)1 and RIP3, are highly expressed in PDA and are further upregulated by the chemotherapy drug gemcitabine. Blockade of the necrosome in vitro promoted cancer cell proliferation and induced an aggressive oncogenic phenotype. By contrast, in vivo deletion of RIP3 or inhibition of RIP1 protected against oncogenic progression in mice and was associated with the development of a highly immunogenic myeloid and T cell infiltrate. The immune-suppressive tumour microenvironment associated with intact RIP1/RIP3 signalling depended in part on necroptosis-induced expression of the chemokine attractant CXCL1, and CXCL1 blockade protected against PDA. Moreover, cytoplasmic SAP130 (a subunit of the histone deacetylase complex) was expressed in PDA in a RIP1/RIP3-dependent manner, and Mincle--its cognate receptor--was upregulated in tumour-infiltrating myeloid cells. Ligation of Mincle by SAP130 promoted oncogenesis, whereas deletion of Mincle protected against oncogenesis and phenocopied the immunogenic reprogramming of the tumour microenvironment that was induced by RIP3 deletion. Cellular depletion suggested that whereas inhibitory macrophages promote tumorigenesis in PDA, they lose their immune-suppressive effects when RIP3 or Mincle is deleted. Accordingly, T cells, which are not protective against PDA progression in mice with intact RIP3 or Mincle signalling, are reprogrammed into indispensable mediators of anti-tumour immunity in the absence of RIP3 or Mincle. Our work describes parallel networks of necroptosis-induced CXCL1 and Mincle signalling that promote macrophage-induced adaptive immune suppression and thereby enable PDA progression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4833566/" 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/PMC4833566/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seifert, Lena -- Werba, Gregor -- Tiwari, Shaun -- Giao Ly, Nancy Ngoc -- Alothman, Sara -- Alqunaibit, Dalia -- Avanzi, Antonina -- Barilla, Rocky -- Daley, Donnele -- Greco, Stephanie H -- Torres-Hernandez, Alejandro -- Pergamo, Matthew -- Ochi, Atsuo -- Zambirinis, Constantinos P -- Pansari, Mridul -- Rendon, Mauricio -- Tippens, Daniel -- Hundeyin, Mautin -- Mani, Vishnu R -- Hajdu, Cristina -- Engle, Dannielle -- Miller, George -- CA155649/CA/NCI NIH HHS/ -- CA168611/CA/NCI NIH HHS/ -- CA193111/CA/NCI NIH HHS/ -- P30CA016087/CA/NCI NIH HHS/ -- R01 CA168611/CA/NCI NIH HHS/ -- T32 CA193111/CA/NCI NIH HHS/ -- UL1 TR000038/TR/NCATS NIH HHS/ -- England -- Nature. 2016 Apr 14;532(7598):245-9. doi: 10.1038/nature17403. Epub 2016 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 550 First Avenue, New York, New York 10016, USA. ; Department of Cell Biology, New York University School of Medicine, 550 First Avenue, New York, New York 10016, USA. ; Department of Pathology, New York University School of Medicine, 550 First Avenue, New York, New York 10016, USA. ; Cold Spring Harbor Laboratories, Cold Spring Harbor, New York 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27049944" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/immunology/metabolism/pathology ; Animals ; Apoptosis/drug effects ; *Carcinogenesis/drug effects ; Carcinoma, Pancreatic Ductal/immunology/metabolism/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Chemokine CXCL1/antagonists & inhibitors/*metabolism ; Deoxycytidine/analogs & derivatives/pharmacology ; Disease Progression ; Female ; GTPase-Activating Proteins/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; *Immune Tolerance ; Lectins, C-Type/immunology/*metabolism ; Male ; Membrane Proteins/immunology/*metabolism ; Mice ; Mice, Inbred C57BL ; *Necrosis ; Pancreatic Neoplasms/*immunology/metabolism/*pathology ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Signal Transduction ; Up-Regulation
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  • 55
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    Nature Publishing Group (NPG)
    Publication Date: 2016-03-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 Mar 10;531(7593):140. doi: 10.1038/531140a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26961620" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CRISPR-Cas Systems/*genetics ; Directed Molecular Evolution/methods ; Dual Use Research/ethics/legislation & jurisprudence ; Embryo Research/ethics ; *Genetic Engineering/ethics/legislation & jurisprudence/trends ; Genome, Human/genetics ; Genomics/ethics/trends ; Germ-Line Mutation/ethics/genetics ; Government Regulation ; Humans ; Public Opinion ; Risk Assessment ; *Security Measures/legislation & jurisprudence ; United States
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  • 56
    Publication Date: 2016-02-11
    Description: The enteric nervous system (ENS) is the largest component of the autonomic nervous system, with neuron numbers surpassing those present in the spinal cord. The ENS has been called the 'second brain' given its autonomy, remarkable neurotransmitter diversity and complex cytoarchitecture. Defects in ENS development are responsible for many human disorders including Hirschsprung disease (HSCR). HSCR is caused by the developmental failure of ENS progenitors to migrate into the gastrointestinal tract, particularly the distal colon. Human ENS development remains poorly understood owing to the lack of an easily accessible model system. Here we demonstrate the efficient derivation and isolation of ENS progenitors from human pluripotent stem (PS) cells, and their further differentiation into functional enteric neurons. ENS precursors derived in vitro are capable of targeted migration in the developing chick embryo and extensive colonization of the adult mouse colon. The in vivo engraftment and migration of human PS-cell-derived ENS precursors rescue disease-related mortality in HSCR mice (Ednrb(s-l/s-l)), although the mechanism of action remains unclear. Finally, EDNRB-null mutant ENS precursors enable modelling of HSCR-related migration defects, and the identification of pepstatin A as a candidate therapeutic target. Our study establishes the first, to our knowledge, human PS-cell-based platform for the study of human ENS development, and presents cell- and drug-based strategies for the treatment of HSCR.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4846424/" 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/PMC4846424/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fattahi, Faranak -- Steinbeck, Julius A -- Kriks, Sonja -- Tchieu, Jason -- Zimmer, Bastian -- Kishinevsky, Sarah -- Zeltner, Nadja -- Mica, Yvonne -- El-Nachef, Wael -- Zhao, Huiyong -- de Stanchina, Elisa -- Gershon, Michael D -- Grikscheit, Tracy C -- Chen, Shuibing -- Studer, Lorenz -- DP2 DK098093-01/DK/NIDDK NIH HHS/ -- NS15547/NS/NINDS NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R01 NS015547/NS/NINDS NIH HHS/ -- England -- Nature. 2016 Mar 3;531(7592):105-9. doi: 10.1038/nature16951. Epub 2016 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Center for Stem Cell Biology, New York, New York 10065, USA. ; Developmental Biology Program, Sloan-Kettering Institute for Cancer Research, New York, New York 10065, USA. ; Weill Graduate School of Medical Sciences of Cornell University, New York, New York 10065, USA. ; Molecular Pharmacology Program, New York, New York 10065, USA. ; Department of Pathology and Cell Biology, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA. ; Children's Hospital Los Angeles, Pediatric Surgery, Los Angeles, California 90027, USA. ; Department of Surgery, Weill Medical College of Cornell University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26863197" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Cell Differentiation ; Cell Line ; *Cell Lineage ; Cell Movement ; Cell Separation ; *Cell- and Tissue-Based Therapy/methods ; Chick Embryo ; Colon/drug effects/pathology ; Disease Models, Animal ; Drug Discovery/*methods ; Enteric Nervous System/*pathology ; Female ; Gastrointestinal Tract/drug effects/pathology ; Hirschsprung Disease/*drug therapy/*pathology/therapy ; Humans ; Male ; Mice ; Neurons/drug effects/*pathology ; Pepstatins/metabolism ; Pluripotent Stem Cells/pathology ; Receptor, Endothelin B/metabolism ; Signal Transduction
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  • 57
    Publication Date: 2016-04-07
    Description: Microglia are damage sensors for the central nervous system (CNS), and the phagocytes responsible for routine non-inflammatory clearance of dead brain cells. Here we show that the TAM receptor tyrosine kinases Mer and Axl regulate these microglial functions. We find that adult mice deficient in microglial Mer and Axl exhibit a marked accumulation of apoptotic cells specifically in neurogenic regions of the CNS, and that microglial phagocytosis of the apoptotic cells generated during adult neurogenesis is normally driven by both TAM receptor ligands Gas6 and protein S. Using live two-photon imaging, we demonstrate that the microglial response to brain damage is also TAM-regulated, as TAM-deficient microglia display reduced process motility and delayed convergence to sites of injury. Finally, we show that microglial expression of Axl is prominently upregulated in the inflammatory environment that develops in a mouse model of Parkinson's disease. Together, these results establish TAM receptors as both controllers of microglial physiology and potential targets for therapeutic intervention in CNS disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fourgeaud, Lawrence -- Traves, Paqui G -- Tufail, Yusuf -- Leal-Bailey, Humberto -- Lew, Erin D -- Burrola, Patrick G -- Callaway, Perri -- Zagorska, Anna -- Rothlin, Carla V -- Nimmerjahn, Axel -- Lemke, Greg -- DP2 NS083038/DP/NCCDPHP CDC HHS/ -- DP2 NS083038/NS/NINDS NIH HHS/ -- P30CA014195/CA/NCI NIH HHS/ -- R01 AI089824/AI/NIAID NIH HHS/ -- R01 AI101400/AI/NIAID NIH HHS/ -- R01 NS085296/NS/NINDS NIH HHS/ -- R01 NS085938/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Apr 14;532(7598):240-4. doi: 10.1038/nature17630. Epub 2016 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA. ; Instituto de Investigaciones Biomedicas Alberto Sols (CSIC-UAM), Madrid 28029, Spain. ; Waitt Advanced Biophotonics Center, The Salk Institute for Biological Studies, La Jolla, California 92037, USA. ; Joint Master in Neuroscience Program, University of Strasbourg, Strasbourg 67081, France. ; Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. ; Immunobiology and Microbial Pathogenesis Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27049947" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Brain/blood supply/cytology/*metabolism/pathology ; Brain Injuries/metabolism/pathology ; Disease Models, Animal ; Female ; Inflammation/metabolism ; Intercellular Signaling Peptides and Proteins/metabolism ; Ligands ; Male ; Mice ; Microglia/*physiology ; Neurogenesis ; Parkinson Disease/metabolism ; Phagocytosis ; Protein S/metabolism ; Proto-Oncogene Proteins/deficiency/*metabolism ; Receptor Protein-Tyrosine Kinases/deficiency/*metabolism ; Signal Transduction ; Stem Cell Niche ; Up-Regulation
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  • 58
    Publication Date: 2016-04-15
    Description: Accurate modelling and prediction of the local to continental-scale hydroclimate response to global warming is essential given the strong impact of hydroclimate on ecosystem functioning, crop yields, water resources, and economic security. However, uncertainty in hydroclimate projections remains large, in part due to the short length of instrumental measurements available with which to assess climate models. Here we present a spatial reconstruction of hydroclimate variability over the past twelve centuries across the Northern Hemisphere derived from a network of 196 at least millennium-long proxy records. We use this reconstruction to place recent hydrological changes and future precipitation scenarios in a long-term context of spatially resolved and temporally persistent hydroclimate patterns. We find a larger percentage of land area with relatively wetter conditions in the ninth to eleventh and the twentieth centuries, whereas drier conditions are more widespread between the twelfth and nineteenth centuries. Our reconstruction reveals that prominent seesaw patterns of alternating moisture regimes observed in instrumental data across the Mediterranean, western USA, and China have operated consistently over the past twelve centuries. Using an updated compilation of 128 temperature proxy records, we assess the relationship between the reconstructed centennial-scale Northern Hemisphere hydroclimate and temperature variability. Even though dry and wet conditions occurred over extensive areas under both warm and cold climate regimes, a statistically significant co-variability of hydroclimate and temperature is evident for particular regions. We compare the reconstructed hydroclimate anomalies with coupled atmosphere-ocean general circulation model simulations and find reasonable agreement during pre-industrial times. However, the intensification of the twentieth-century-mean hydroclimate anomalies in the simulations, as compared to previous centuries, is not supported by our new multi-proxy reconstruction. This finding suggests that much work remains before we can model hydroclimate variability accurately, and highlights the importance of using palaeoclimate data to place recent and predicted hydroclimate changes in a millennium-long context.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ljungqvist, Fredrik Charpentier -- Krusic, Paul J -- Sundqvist, Hanna S -- Zorita, Eduardo -- Brattstrom, Gudrun -- Frank, David -- England -- Nature. 2016 Apr 7;532(7597):94-8. doi: 10.1038/nature17418.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of History, Stockholm University, SE-10691 Stockholm, Sweden. ; Centre for Medieval Studies, Stockholm University, SE-10691 Stockholm, Sweden. ; Bolin Centre for Climate Research, Stockholm University, SE-10691 Stockholm, Sweden. ; Navarino Environmental Observatory, GR-24001 Messinia, Greece. ; Department of Physical Geography, Stockholm University, SE-10691 Stockholm, Sweden. ; Helmholtz-Zentrum Geesthacht, Institute for Coastal Research, DE-21502 Geesthacht, Germany. ; Department of Mathematics, Stockholm University, SE-10691 Stockholm, Sweden. ; Swiss Federal Research Institute WSL, CH-8903 Birmensdorf, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27078569" target="_blank"〉PubMed〈/a〉
    Keywords: Atmosphere ; China ; *Climate ; Climate Change/*statistics & numerical data ; Ecosystem ; Geographic Mapping ; Geologic Sediments/chemistry ; History, 15th Century ; History, 16th Century ; History, 17th Century ; History, 18th Century ; History, 19th Century ; History, 20th Century ; History, 21st Century ; History, Medieval ; Hydrology ; Ice/analysis ; Mediterranean Region ; Models, Theoretical ; *Rain ; Soil/chemistry ; Spatio-Temporal Analysis ; Temperature ; Trees/anatomy & histology/growth & development ; Uncertainty ; United States
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  • 59
    Publication Date: 2016-04-26
    Description: The evolution of novel cell types led to the emergence of new tissues and organs during the diversification of animals. The origin of the chondrocyte, the cell type that synthesizes cartilage matrix, was central to the evolution of the vertebrate endoskeleton. Cartilage-like tissues also exist outside the vertebrates, although their relationship to vertebrate cartilage is enigmatic. Here we show that protostome and deuterostome cartilage share structural and chemical properties, and that the mechanisms of cartilage development are extensively conserved--from induction of chondroprogenitor cells by Hedgehog and beta-catenin signalling, to chondrocyte differentiation and matrix synthesis by SoxE and SoxD regulation of clade A fibrillar collagen (ColA) genes--suggesting that the chondrogenic gene regulatory network evolved in the common ancestor of Bilateria. These results reveal deep homology of the genetic program for cartilage development in Bilateria and suggest that activation of this ancient core chondrogenic network underlies the parallel evolution of cartilage tissues in Ecdysozoa, Lophotrochozoa and Deuterostomia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tarazona, Oscar A -- Slota, Leslie A -- Lopez, Davys H -- Zhang, GuangJun -- Cohn, Martin J -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 May 5;533(7601):86-9. doi: 10.1038/nature17398. Epub 2016 Apr 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, UF Genetics Institute, University of Florida, PO Box 103610, Gainesville, Florida 32610, USA. ; Department of Biology, University of Florida, PO Box 103610, Gainesville, Florida 32610, USA. ; Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, PO Box 103610, Gainesville, Florida 32610, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27111511" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cartilage/anatomy & histology/embryology/metabolism ; Chondrocytes/cytology ; Chondrogenesis/*genetics ; Conserved Sequence/*genetics ; Decapodiformes/cytology/embryology/genetics/metabolism ; *Evolution, Molecular ; Fibrillar Collagens/genetics ; Gene Expression Regulation, Developmental/*genetics ; Gene Regulatory Networks ; Hedgehog Proteins/metabolism ; Invertebrates/cytology/*embryology/*genetics/metabolism ; *Phylogeny ; Signal Transduction ; Stem Cells/cytology ; Vertebrates/anatomy & histology/genetics ; beta Catenin/metabolism
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    Nature Publishing Group (NPG)
    Publication Date: 2016-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Winston, Patrick Henry -- England -- Nature. 2016 Feb 18;530(7590):282. doi: 10.1038/530282a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. He was a graduate student of Marvin Minsky's in the 1960s, and thereafter an admiring friend and colleague.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26887486" target="_blank"〉PubMed〈/a〉
    Keywords: Artificial Intelligence/*history ; Child ; History, 20th Century ; History, 21st Century ; Humans ; Microscopy, Confocal/history ; Neural Networks (Computer) ; Robotics/history ; Software/history ; United States
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  • 61
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    Nature Publishing Group (NPG)
    Publication Date: 2016-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Witze, Alexandra -- England -- Nature. 2016 Apr 7;532(7597):17. doi: 10.1038/532017a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27078544" target="_blank"〉PubMed〈/a〉
    Keywords: Aircraft ; Arctic Regions ; Climate Change/statistics & numerical data ; Ecosystem ; Environmental Monitoring/*instrumentation/*methods ; Geographic Mapping ; Ice Cover ; Satellite Communications ; *Snow ; United States ; United States National Aeronautics and Space Administration ; Water Supply/*statistics & numerical data
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  • 62
    Publication Date: 2016-03-24
    Description: A marked bias towards risk aversion has been observed in nearly every species tested. A minority of individuals, however, instead seem to prefer risk (repeatedly choosing uncertain large rewards over certain but smaller rewards), and even risk-averse individuals sometimes opt for riskier alternatives. It is not known how neural activity underlies such important shifts in decision-making--either as a stable trait across individuals or at the level of variability within individuals. Here we describe a model of risk-preference in rats, in which stable individual differences, trial-by-trial choices, and responses to pharmacological agents all parallel human behaviour. By combining new genetic targeting strategies with optical recording of neural activity during behaviour in this model, we identify relevant temporally specific signals from a genetically and anatomically defined population of neurons. This activity occurred within dopamine receptor type-2 (D2R)-expressing cells in the nucleus accumbens (NAc), signalled unfavourable outcomes from the recent past at a time appropriate for influencing subsequent decisions, and also predicted subsequent choices made. Having uncovered this naturally occurring neural correlate of risk selection, we then mimicked the temporally specific signal with optogenetic control during decision-making and demonstrated its causal effect in driving risk-preference. Specifically, risk-preferring rats could be instantaneously converted to risk-averse rats with precisely timed phasic stimulation of NAc D2R cells. These findings suggest that individual differences in risk-preference, as well as real-time risky decision-making, can be largely explained by the encoding in D2R-expressing NAc cells of prior unfavourable outcomes during decision-making.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zalocusky, Kelly A -- Ramakrishnan, Charu -- Lerner, Talia N -- Davidson, Thomas J -- Knutson, Brian -- Deisseroth, Karl -- 1F31MH105151-01/MH/NIMH NIH HHS/ -- 1F32MH105053-01/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Mar 31;531(7596):642-6. doi: 10.1038/nature17400. Epub 2016 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bioengineering Department, Stanford University, Stanford, California 94305, USA. ; Neurosciences Program, Stanford University, Stanford, California 94305, USA. ; CNC Program, Stanford University, Stanford, California 94305, USA. ; Psychology Department, Stanford University, Stanford, California 94305, USA. ; Howard Hughes Medical Institute, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27007845" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Choice Behavior ; *Decision Making ; Humans ; Individuality ; Male ; Models, Animal ; Models, Neurological ; Models, Psychological ; Neurons/*metabolism ; Nucleus Accumbens/*cytology/*metabolism ; Rats ; Rats, Long-Evans ; Receptors, Dopamine D2/*metabolism ; Reward ; *Risk Management ; Signal Transduction ; Uncertainty
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  • 63
    Publication Date: 2016-03-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cressey, Daniel -- England -- Nature. 2016 Mar 10;531(7593):152. doi: 10.1038/531152a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26961636" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; *Climate Change ; Conservation of Natural Resources/*methods ; Ecology/*methods ; *Plants ; Research ; *Seed Bank ; Seeds/*growth & development ; United States
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  • 64
    Publication Date: 2016-02-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reardon, Sara -- England -- Nature. 2016 Feb 11;530(7589):142. doi: 10.1038/nature.2016.19290.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26863962" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Embryo Research/*legislation & jurisprudence ; Extrachromosomal Inheritance/genetics ; Female ; Follow-Up Studies ; Genetic Therapy/*legislation & jurisprudence/*methods ; Great Britain ; Haplorhini/genetics ; Heredity/genetics/physiology ; Humans ; Male ; Mitochondrial Diseases/genetics/*prevention & control ; Mitochondrial Replacement Therapy/adverse effects/*legislation & ; jurisprudence/*methods ; Mutation/genetics ; *Patient Safety ; Sex Factors ; United States ; United States Food and Drug Administration/legislation & jurisprudence
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  • 65
    Publication Date: 2016-04-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reardon, Sara -- England -- Nature. 2016 Mar 31;531(7596):560. doi: 10.1038/531560a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27029280" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adolescent Behavior/*drug effects/physiology/*psychology ; Child ; *Clinical Trials as Topic/economics ; Decision Making ; Gonadotropin-Releasing Hormone/agonists ; Humans ; National Institutes of Health (U.S.)/economics ; Puberty/*drug effects/*physiology/psychology ; Time Factors ; Transgender Persons/*psychology ; Treatment Outcome ; United States
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    Nature Publishing Group (NPG)
    Publication Date: 2016-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kogleck, Larissa -- England -- Nature. 2016 Mar 17;531(7594):S102-3. doi: 10.1038/531S102a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982019" target="_blank"〉PubMed〈/a〉
    Keywords: China ; Cooperative Behavior ; Great Britain ; Italy ; Japan ; Journal Impact Factor ; Research/economics/*organization & administration/standards/*statistics & ; numerical data ; Switzerland ; United States
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  • 67
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    Nature Publishing Group (NPG)
    Publication Date: 2016-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 Feb 18;530(7590):253. doi: 10.1038/530253a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26887454" target="_blank"〉PubMed〈/a〉
    Keywords: Aircraft/*instrumentation/*legislation & jurisprudence/standards ; Global Warming/*legislation & jurisprudence/*prevention & control ; Internationality ; United States ; United States Environmental Protection Agency/*legislation & jurisprudence
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    Nature Publishing Group (NPG)
    Publication Date: 2016-02-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wagner, Erwin F -- England -- Nature. 2016 Feb 4;530(7588):42-3. doi: 10.1038/530042a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Research Centre (CNIO), Department of Cancer Cell Biology, E-28029 Madrid, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26842052" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Disease Progression ; Fibroblasts/*cytology/*pathology ; I-kappa B Kinase/deficiency/genetics/metabolism ; Inflammation/immunology/pathology ; Intestinal Neoplasms/*immunology/*pathology/therapy ; Mice ; NF-kappa B/metabolism ; Signal Transduction ; Tumor Microenvironment/*physiology ; Uncertainty
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  • 69
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    Publication Date: 2016-02-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 Feb 4;530(7588):6. doi: 10.1038/530006a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26842020" target="_blank"〉PubMed〈/a〉
    Keywords: Ecology/*economics/*legislation & jurisprudence ; Environmental Policy/*legislation & jurisprudence ; Politics ; Research Support as Topic/*economics/*legislation & jurisprudence ; United States
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  • 70
    Publication Date: 2016-04-14
    Description: Blood vessels define local microenvironments in the skeletal system, play crucial roles in osteogenesis and provide niches for haematopoietic stem cells. The properties of niche-forming vessels and their changes in the ageing organism remain incompletely understood. Here we show that Notch signalling in endothelial cells leads to the expansion of haematopoietic stem cell niches in bone, which involves increases in CD31-positive capillaries and platelet-derived growth factor receptor-beta (PDGFRbeta)-positive perivascular cells, arteriole formation and elevated levels of cellular stem cell factor. Although endothelial hypoxia-inducible factor signalling promotes some of these changes, it fails to enhance vascular niche function because of a lack of arterialization and expansion of PDGFRbeta-positive cells. In ageing mice, niche-forming vessels in the skeletal system are strongly reduced but can be restored by activation of endothelial Notch signalling. These findings indicate that vascular niches for haematopoietic stem cells are part of complex, age-dependent microenvironments involving multiple cell populations and vessel subtypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kusumbe, Anjali P -- Ramasamy, Saravana K -- Itkin, Tomer -- Mae, Maarja Andaloussi -- Langen, Urs H -- Betsholtz, Christer -- Lapidot, Tsvee -- Adams, Ralf H -- England -- Nature. 2016 Apr 21;532(7599):380-4. doi: 10.1038/nature17638. Epub 2016 Apr 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, and University of Munster, Faculty of Medicine, D-48149 Munster, Germany. ; Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel. ; Vascular Biology Program, Department of Immunology, Genetics and Pathology, Uppsala University, SE-751 85 Uppsala, Sweden. ; Department of Medical Biochemistry and Biophysics, Division of Vascular Biology, Karolinska Institute, Scheeles vag 2, SE-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27074508" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Antigens, CD31/metabolism ; Arterioles/cytology/*physiology ; Bone and Bones/*blood supply/cytology/metabolism ; Capillaries/cytology/*physiology ; Cell Count ; Endothelial Cells/metabolism ; Hematopoietic Stem Cells/*cytology ; Hypoxia-Inducible Factor 1/metabolism ; Male ; Mice ; Osteogenesis ; Receptor, Platelet-Derived Growth Factor beta/metabolism ; Receptors, Notch/metabolism ; Signal Transduction ; Stem Cell Factor/metabolism ; *Stem Cell Niche
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  • 71
    Publication Date: 2016-03-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuzma, Jennifer -- England -- Nature. 2016 Mar 10;531(7593):165-7. doi: 10.1038/531165a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetic Engineering and Society Center at North Carolina State University, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26961641" target="_blank"〉PubMed〈/a〉
    Keywords: CRISPR-Cas Systems/genetics ; Crops, Agricultural/genetics ; *Dissent and Disputes ; Genetic Engineering/*legislation & jurisprudence ; *Government Regulation ; *Policy Making ; United States ; United States Department of Agriculture/legislation & jurisprudence ; United States Environmental Protection Agency/legislation & jurisprudence ; United States Food and Drug Administration/legislation & jurisprudence
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  • 72
    Publication Date: 2016-04-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waltz, Emily -- England -- Nature. 2016 Apr 21;532(7599):293. doi: 10.1038/nature.2016.19754.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27111611" target="_blank"〉PubMed〈/a〉
    Keywords: Agaricus/enzymology/*genetics ; CRISPR-Cas Systems/*genetics ; Catechol Oxidase/genetics/metabolism ; Crops, Agricultural/economics/enzymology/genetics ; Food, Genetically Modified ; Gene Deletion ; Genetic Engineering/economics/*legislation & jurisprudence ; Patents as Topic ; United States ; United States Department of Agriculture/*legislation & jurisprudence
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  • 73
    Publication Date: 2016-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ward, Alyssa -- Baldwin, Thomas O -- Antin, Parker B -- England -- Nature. 2016 Apr 14;532(7598):177. doi: 10.1038/532177d.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. ; University of California, Riverside, USA. ; University of Arizona, Tucson, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27075087" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Confounding Factors (Epidemiology) ; *Learning ; Mice ; Mice, Transgenic/genetics ; National Institutes of Health (U.S.)/economics ; Reproducibility of Results ; Research/*standards ; United States
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    Publication Date: 2016-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wapner, Jessica -- England -- Nature. 2016 May 5;533(7601):S13-5. doi: 10.1038/533S13a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27144603" target="_blank"〉PubMed〈/a〉
    Keywords: Industry/*economics ; Inventions/*economics ; Licensure/economics/legislation & jurisprudence ; Patents as Topic/legislation & jurisprudence ; Science/*economics ; *Technology Transfer ; United States ; Universities/*economics
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  • 75
    Publication Date: 2016-04-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nowogrodzki, Anna -- England -- Nature. 2016 Mar 31;531(7596):561. doi: 10.1038/nature.2016.19599.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27029258" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Specimen Banks/*economics/trends ; Climate Change ; Financing, Government/*economics/trends ; Financing, Organized/economics ; Museums ; Research Support as Topic/*economics/trends ; Time Factors ; United States ; United States Government Agencies/economics/trends
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    Publication Date: 2016-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 Apr 28;532(7600):414. doi: 10.1038/532414a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27121803" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/economics/manpower/*organization & administration/*trends ; *Federal Government ; Humans ; International Cooperation ; National Cancer Institute (U.S.) ; Neoplasms/*therapy ; Research Personnel/organization & administration ; United States
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  • 77
    Publication Date: 2016-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ledford, Heidi -- England -- Nature. 2016 Apr 7;532(7597):13-4. doi: 10.1038/532013a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27078541" target="_blank"〉PubMed〈/a〉
    Keywords: Emigrants and Immigrants/legislation & jurisprudence/psychology ; Emigration and Immigration/*legislation & jurisprudence ; *Fear ; Internationality ; Islam/*psychology ; *Politics ; Research Personnel/*psychology ; Science/*manpower/standards ; *Uncertainty ; United States
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  • 78
    Publication Date: 2016-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ledford, Heidi -- England -- Nature. 2016 Apr 14;532(7598):158-9. doi: 10.1038/532158a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27075074" target="_blank"〉PubMed〈/a〉
    Keywords: CRISPR-Cas Systems/*genetics ; Crops, Agricultural/*genetics ; Food, Genetically Modified ; Genetic Engineering/*legislation & jurisprudence/*trends ; *Government Regulation ; Internationality ; Plant Breeding/legislation & jurisprudence/methods ; United States ; United States Department of Agriculture/legislation & jurisprudence
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  • 79
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    Publication Date: 2016-03-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ledford, Heidi -- England -- Nature. 2016 Mar 10;531(7593):149. doi: 10.1038/531149a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26961633" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CRISPR-Cas Systems/*genetics ; Europe ; Humans ; Patents as Topic/*legislation & jurisprudence ; Time Factors ; United States
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    Publication Date: 2016-05-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Savage, Neil -- England -- Nature. 2016 May 11;533(7602):S56-8. doi: 10.1038/533S56a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27167391" target="_blank"〉PubMed〈/a〉
    Keywords: Access to Information ; Competitive Behavior ; *Cooperative Behavior ; Drug Discovery/economics/manpower/*methods/*organization & administration ; Drug Industry/economics/manpower/*methods/*organization & administration ; *Efficiency, Organizational ; Humans ; *Information Dissemination ; Public-Private Sector Partnerships/organization & administration ; Time Factors ; United States ; United States Food and Drug Administration
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 81
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    Nature Publishing Group (NPG)
    Publication Date: 2016-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Savage, Neil -- England -- Nature. 2016 May 5;533(7601):S10-2. doi: 10.1038/533S10a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27144602" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Science Disciplines/economics ; Entrepreneurship/*economics/*organization & administration/statistics & numerical ; data/trends ; Europe ; Humans ; Inventions/economics/statistics & numerical data ; Investments/economics ; Laboratories/economics/organization & administration ; Licensure/economics ; Marketing/economics ; Patents as Topic ; Private Sector/economics/organization & administration/statistics & numerical ; data/trends ; Research/*economics/organization & administration ; Technology Transfer ; United States ; Universities/economics/organization & administration ; Vaccines/economics
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  • 82
    Publication Date: 2016-02-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, Monya -- England -- Nature. 2016 Feb 11;530(7589):141. doi: 10.1038/nature.2016.19269.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26863961" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/*standards ; *Biotechnology ; Drug Industry ; *Open Access Publishing ; Reproducibility of Results ; *Uncertainty ; United States
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 83
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    Nature Publishing Group (NPG)
    Publication Date: 2016-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macilwain, Colin -- England -- Nature. 2016 Mar 17;531(7594):277. doi: 10.1038/531277a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26983505" target="_blank"〉PubMed〈/a〉
    Keywords: *Democracy ; Europe ; *Politics ; *Research Personnel/psychology ; Social Change ; United States
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  • 84
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-08-16
    Description: Author: L. Bryan Ray
    Keywords: Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 85
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-10-14
    Description: Authors: Caroline Ash, L. Bryan Ray
    Keywords: Signal Transduction
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 86
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-10-14
    Description: Reversible protein phosphorylation plays a fundamental role in signal transduction networks. Phosphorylation alters protein function by regulating enzymatic activity, stability, cellular localization, or binding partners. Over three-quarters of human proteins may be phosphorylated, with many targeted at multiple sites. Such multisite phosphorylation substantially increases the scope for modulating protein function—a protein with n phosphorylation sites has the potential to exist in 2n distinct phosphorylation states, each of which could, in theory, display modified functionality. Proteins can be substrates for several protein kinases, thereby integrating distinct signals to provide a coherent biological response. However, they can also be phosphorylated at multiple sites by a single protein kinase to promote a specific functional output that can be reversed by dephosphorylation by protein phosphatases. On page 233 of this issue, Mylona et al. (1) reveal an unexpected role for multisite phosphorylation, whereby a protein kinase progressively phosphorylates sites on a transcription factor to promote and then subsequently limit its activity independently of dephosphorylation. Authors: Alan J. Whitmarsh, Roger J. Davis
    Keywords: Signal Transduction
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  • 87
    Publication Date: 2015-12-10
    Description: Epithelial regeneration is critical for barrier maintenance and organ function after intestinal injury. The intestinal stem cell (ISC) niche provides Wnt, Notch and epidermal growth factor (EGF) signals supporting Lgr5(+) crypt base columnar ISCs for normal epithelial maintenance. However, little is known about the regulation of the ISC compartment after tissue damage. Using ex vivo organoid cultures, here we show that innate lymphoid cells (ILCs), potent producers of interleukin-22 (IL-22) after intestinal injury, increase the growth of mouse small intestine organoids in an IL-22-dependent fashion. Recombinant IL-22 directly targeted ISCs, augmenting the growth of both mouse and human intestinal organoids, increasing proliferation and promoting ISC expansion. IL-22 induced STAT3 phosphorylation in Lgr5(+) ISCs, and STAT3 was crucial for both organoid formation and IL-22-mediated regeneration. Treatment with IL-22 in vivo after mouse allogeneic bone marrow transplantation enhanced the recovery of ISCs, increased epithelial regeneration and reduced intestinal pathology and mortality from graft-versus-host disease. ATOH1-deficient organoid culture demonstrated that IL-22 induced epithelial regeneration independently of the Paneth cell niche. Our findings reveal a fundamental mechanism by which the immune system is able to support the intestinal epithelium, activating ISCs to promote regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4720437/" 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/PMC4720437/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lindemans, Caroline A -- Calafiore, Marco -- Mertelsmann, Anna M -- O'Connor, Margaret H -- Dudakov, Jarrod A -- Jenq, Robert R -- Velardi, Enrico -- Young, Lauren F -- Smith, Odette M -- Lawrence, Gillian -- Ivanov, Juliet A -- Fu, Ya-Yuan -- Takashima, Shuichiro -- Hua, Guoqiang -- Martin, Maria L -- O'Rourke, Kevin P -- Lo, Yuan-Hung -- Mokry, Michal -- Romera-Hernandez, Monica -- Cupedo, Tom -- Dow, Lukas E -- Nieuwenhuis, Edward E -- Shroyer, Noah F -- Liu, Chen -- Kolesnick, Richard -- van den Brink, Marcel R M -- Hanash, Alan M -- HHSN272200900059C/PHS HHS/ -- K08 HL115355/HL/NHLBI NIH HHS/ -- K08-HL115355/HL/NHLBI NIH HHS/ -- K99 CA176376/CA/NCI NIH HHS/ -- K99-CA176376/CA/NCI NIH HHS/ -- P01 CA023766/CA/NCI NIH HHS/ -- P01-CA023766/CA/NCI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- P30-CA008748/CA/NCI NIH HHS/ -- R01 AI080455/AI/NIAID NIH HHS/ -- R01 AI100288/AI/NIAID NIH HHS/ -- R01 AI101406/AI/NIAID NIH HHS/ -- R01 HL069929/HL/NHLBI NIH HHS/ -- R01 HL125571/HL/NHLBI NIH HHS/ -- R01-AI080455/AI/NIAID NIH HHS/ -- R01-AI100288/AI/NIAID NIH HHS/ -- R01-AI101406/AI/NIAID NIH HHS/ -- R01-HL069929/HL/NHLBI NIH HHS/ -- R01-HL125571/HL/NHLBI NIH HHS/ -- U19 AI116497/AI/NIAID NIH HHS/ -- England -- Nature. 2015 Dec 24;528(7583):560-4. doi: 10.1038/nature16460. Epub 2015 Dec 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Pediatrics, University Medical Center Utrecht, 3508 AB Utrecht, The Netherlands. ; Department of Immunology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Anatomy and Developmental Biology, Monash University, Clayton 3800, Australia. ; Department of Medicine, Weill Cornell Medicine, New York, New York 10021, USA. ; Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Molecular Pharmacology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Cancer Biology &Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Hematology, Erasmus University Medical Center, 3000 CA Rotterdam, The Netherlands. ; Department of Pathology, Immunology and Laboratory Medicine, University of Florida College of Medicine, Gainesville, Florida 32610, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26649819" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Epithelial Cells/*cytology/immunology/pathology ; Female ; Graft vs Host Disease/pathology ; Humans ; Immunity, Mucosal ; Interleukins/deficiency/*immunology ; Intestinal Mucosa/*cytology/immunology/pathology ; Intestine, Small/*cytology/immunology/pathology ; Mice ; Organoids/cytology/growth & development/immunology ; Paneth Cells/cytology ; Phosphorylation ; *Regeneration ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Stem Cell Niche ; Stem Cells/*cytology/*metabolism
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  • 88
    Publication Date: 2015-07-15
    Description: Surface polysaccharides are important for bacterial interactions with multicellular organisms, and some are virulence factors in pathogens. In the legume-rhizobium symbiosis, bacterial exopolysaccharides (EPS) are essential for the development of infected root nodules. We have identified a gene in Lotus japonicus, Epr3, encoding a receptor-like kinase that controls this infection. We show that epr3 mutants are defective in perception of purified EPS, and that EPR3 binds EPS directly and distinguishes compatible and incompatible EPS in bacterial competition studies. Expression of Epr3 in epidermal cells within the susceptible root zone shows that the protein is involved in bacterial entry, while rhizobial and plant mutant studies suggest that Epr3 regulates bacterial passage through the plant's epidermal cell layer. Finally, we show that Epr3 expression is inducible and dependent on host perception of bacterial nodulation (Nod) factors. Plant-bacterial compatibility and bacterial access to legume roots is thus regulated by a two-stage mechanism involving sequential receptor-mediated recognition of Nod factor and EPS signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawaharada, Y -- Kelly, S -- Nielsen, M Wibroe -- Hjuler, C T -- Gysel, K -- Muszynski, A -- Carlson, R W -- Thygesen, M B -- Sandal, N -- Asmussen, M H -- Vinther, M -- Andersen, S U -- Krusell, L -- Thirup, S -- Jensen, K J -- Ronson, C W -- Blaise, M -- Radutoiu, S -- Stougaard, J -- England -- Nature. 2015 Jul 16;523(7560):308-12. doi: 10.1038/nature14611. Epub 2015 Jul 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Centre for Carbohydrate Recognition and Signalling. Aarhus University, Aarhus 8000 C, Denmark [2] Department of Molecular Biology and Genetics, Aarhus University, Aarhus 8000 C, Denmark. ; 1] Centre for Carbohydrate Recognition and Signalling. Aarhus University, Aarhus 8000 C, Denmark [2] Department of Molecular Biology and Genetics, Aarhus University, Aarhus 8000 C, Denmark [3] Department of Microbiology and Immunology, University of Otago, Dunedin 9054, New Zealand. ; 1] Centre for Carbohydrate Recognition and Signalling. Aarhus University, Aarhus 8000 C, Denmark [2] Department of Chemistry, University of Copenhagen, Frederiksberg 1871 C, Denmark. ; Complex Carbohydrate Research Center, University of Georgia, Athens, Georgia 30602, USA. ; 1] Centre for Carbohydrate Recognition and Signalling. Aarhus University, Aarhus 8000 C, Denmark [2] Department of Microbiology and Immunology, University of Otago, Dunedin 9054, New Zealand.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26153863" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Carbohydrate Sequence ; Lipopolysaccharides/chemistry/*metabolism ; Lotus/genetics/*metabolism/*microbiology ; Molecular Sequence Data ; Mutation/genetics ; Phenotype ; Plant Epidermis/metabolism/microbiology ; Plant Proteins/chemistry/genetics/*metabolism ; Plant Root Nodulation ; Protein Kinases/chemistry/genetics/metabolism ; Protein Structure, Tertiary ; Receptors, Cell Surface/chemistry/genetics/*metabolism ; Rhizobium/*metabolism ; Root Nodules, Plant/metabolism/microbiology ; Signal Transduction ; Species Specificity ; Suppression, Genetic/genetics ; *Symbiosis
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  • 89
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    Nature Publishing Group (NPG)
    Publication Date: 2015-01-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schaefer, Henry F -- England -- Nature. 2015 Jan 1;517(7532):22. doi: 10.1038/517022a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Georgia, Athens, Georgia, USA. He was a colleague of Paul Schleyer's for 24 years.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25557708" target="_blank"〉PubMed〈/a〉
    Keywords: Adamantane/analogs & derivatives/chemical synthesis ; Chemistry/*history ; Dipeptides/chemical synthesis ; Germany ; History, 20th Century ; Memantine/chemical synthesis ; Nobel Prize ; United States
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  • 90
    Publication Date: 2015-10-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tollefson, Jeff -- England -- Nature. 2015 Oct 22;526(7574):488-9. doi: 10.1038/526488a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26490598" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodiversity ; Conservation of Natural Resources/economics/*legislation & jurisprudence ; Cuba ; Gulf of Mexico ; International Cooperation/*legislation & jurisprudence ; Mexico ; *Sharks ; United States
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  • 91
    Publication Date: 2015-04-22
    Description: Impaired mitochondrial maintenance in disparate cell types is a shared hallmark of many human pathologies and ageing. How mitochondrial biogenesis coordinates with the removal of damaged or superfluous mitochondria to maintain cellular homeostasis is not well understood. Here we show that mitophagy, a selective type of autophagy targeting mitochondria for degradation, interfaces with mitochondrial biogenesis to regulate mitochondrial content and longevity in Caenorhabditis elegans. We find that DCT-1 is a key mediator of mitophagy and longevity assurance under conditions of stress in C. elegans. Impairment of mitophagy compromises stress resistance and triggers mitochondrial retrograde signalling through the SKN-1 transcription factor that regulates both mitochondrial biogenesis genes and mitophagy by enhancing DCT-1 expression. Our findings reveal a homeostatic feedback loop that integrates metabolic signals to coordinate the biogenesis and turnover of mitochondria. Uncoupling of these two processes during ageing contributes to overproliferation of damaged mitochondria and decline of cellular function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palikaras, Konstantinos -- Lionaki, Eirini -- Tavernarakis, Nektarios -- England -- Nature. 2015 May 28;521(7553):525-8. doi: 10.1038/nature14300. Epub 2015 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology - Hellas, Nikolaou Plastira 100, Heraklion 70013, Crete, Greece [2] Department of Biology, University of Crete, Heraklion 70013, Crete, Greece. ; Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology - Hellas, Nikolaou Plastira 100, Heraklion 70013, Crete, Greece. ; 1] Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology - Hellas, Nikolaou Plastira 100, Heraklion 70013, Crete, Greece [2] Department of Basic Sciences, Faculty of Medicine, University of Crete, Heraklion 71110, Crete, Greece.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25896323" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/pathology/*physiology ; Animals ; Caenorhabditis elegans/*cytology/genetics/*physiology ; Caenorhabditis elegans Proteins/metabolism ; DNA-Binding Proteins/metabolism ; Homeostasis ; Insulin/metabolism ; Insulin-Like Growth Factor I/metabolism ; Longevity ; Membrane Proteins/metabolism ; Mitochondria/genetics/*metabolism/pathology ; *Mitochondrial Degradation/genetics ; Signal Transduction ; Stress, Physiological ; Transcription Factors/metabolism
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  • 92
    Publication Date: 2015-02-20
    Description: Pluripotent stem cells provide a powerful system to dissect the underlying molecular dynamics that regulate cell fate changes during mammalian development. Here we report the integrative analysis of genome-wide binding data for 38 transcription factors with extensive epigenome and transcriptional data across the differentiation of human embryonic stem cells to the three germ layers. We describe core regulatory dynamics and show the lineage-specific behaviour of selected factors. In addition to the orchestrated remodelling of the chromatin landscape, we find that the binding of several transcription factors is strongly associated with specific loss of DNA methylation in one germ layer, and in many cases a reciprocal gain in the other layers. Taken together, our work shows context-dependent rewiring of transcription factor binding, downstream signalling effectors, and the epigenome during human embryonic stem cell differentiation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4499331/" 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/PMC4499331/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsankov, Alexander M -- Gu, Hongcang -- Akopian, Veronika -- Ziller, Michael J -- Donaghey, Julie -- Amit, Ido -- Gnirke, Andreas -- Meissner, Alexander -- 5F32DK095537/DK/NIDDK NIH HHS/ -- P01 GM099117/GM/NIGMS NIH HHS/ -- P01GM099117/GM/NIGMS NIH HHS/ -- P50HG006193/HG/NHGRI NIH HHS/ -- U01 ES017155/ES/NIEHS NIH HHS/ -- U01ES017155/ES/NIEHS NIH HHS/ -- England -- Nature. 2015 Feb 19;518(7539):344-9. doi: 10.1038/nature14233.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA [2] Harvard Stem Cell Institute, Cambridge, Massachusetts 02138, USA [3] Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, Massachusetts 02138, USA. ; Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA. ; 1] Harvard Stem Cell Institute, Cambridge, Massachusetts 02138, USA [2] Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, Massachusetts 02138, USA. ; 1] Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA [2] Department of Immunology, Weizmann Institute, Rehovot, 76100 Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25693565" target="_blank"〉PubMed〈/a〉
    Keywords: *Cell Differentiation/genetics ; Cell Lineage ; Chromatin/chemistry/genetics/metabolism ; Chromatin Assembly and Disassembly/genetics ; DNA Methylation ; Embryonic Stem Cells/*cytology/*metabolism ; Enhancer Elements, Genetic/genetics ; Epigenesis, Genetic/genetics ; Epigenomics ; Genome, Human/genetics ; Germ Layers/cytology/metabolism ; Histones/chemistry/metabolism ; Humans ; Protein Binding ; Signal Transduction ; Transcription Factors/*metabolism ; Transcription, Genetic/genetics
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  • 93
    Publication Date: 2015-10-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tollefson, Jeff -- England -- Nature. 2015 Oct 1;526(7571):13-4. doi: 10.1038/nature.2015.18440.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26432216" target="_blank"〉PubMed〈/a〉
    Keywords: Carbon Dioxide/analysis/*economics/*supply & distribution ; China ; Environmental Policy/*economics/*trends ; *International Cooperation ; Renewable Energy/statistics & numerical data ; United Nations ; United States
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  • 94
    Publication Date: 2015-03-25
    Description: Wing polyphenism is an evolutionarily successful feature found in a wide range of insects. Long-winged morphs can fly, which allows them to escape adverse habitats and track changing resources, whereas short-winged morphs are flightless, but usually possess higher fecundity than the winged morphs. Studies on aphids, crickets and planthoppers have revealed that alternative wing morphs develop in response to various environmental cues, and that the response to these cues may be mediated by developmental hormones, although research in this area has yielded equivocal and conflicting results about exactly which hormones are involved. As it stands, the molecular mechanism underlying wing morph determination in insects has remained elusive. Here we show that two insulin receptors in the migratory brown planthopper Nilaparvata lugens, InR1 and InR2, have opposing roles in controlling long wing versus short wing development by regulating the activity of the forkhead transcription factor Foxo. InR1, acting via the phosphatidylinositol-3-OH kinase (PI(3)K)-protein kinase B (Akt) signalling cascade, leads to the long-winged morph if active and the short-winged morph if inactive. InR2, by contrast, functions as a negative regulator of the InR1-PI(3)K-Akt pathway: suppression of InR2 results in development of the long-winged morph. The brain-secreted ligand Ilp3 triggers development of long-winged morphs. Our findings provide the first evidence of a molecular basis for the regulation of wing polyphenism in insects, and they are also the first demonstration--to our knowledge--of binary control over alternative developmental outcomes, and thus deepen our understanding of the development and evolution of phenotypic plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Hai-Jun -- Xue, Jian -- Lu, Bo -- Zhang, Xue-Chao -- Zhuo, Ji-Chong -- He, Shu-Fang -- Ma, Xiao-Fang -- Jiang, Ya-Qin -- Fan, Hai-Wei -- Xu, Ji-Yu -- Ye, Yu-Xuan -- Pan, Peng-Lu -- Li, Qiao -- Bao, Yan-Yuan -- Nijhout, H Frederik -- Zhang, Chuan-Xi -- England -- Nature. 2015 Mar 26;519(7544):464-7. doi: 10.1038/nature14286. Epub 2015 Mar 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Rice Biology and Ministry of Agriculture Key Laboratory of Agricultural Entomology, Institute of Insect Sciences, Zhejiang University, Hangzhou 310058, China. ; Department of Biology, Duke University, Durham, North Carolina 27708, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25799997" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Forkhead Transcription Factors/deficiency/metabolism ; Hemiptera/*anatomy & histology/enzymology/genetics/*metabolism ; Insulin/metabolism ; Male ; Molecular Sequence Data ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Receptor, Insulin/deficiency/*metabolism ; Signal Transduction ; Wings, Animal/anatomy & histology/enzymology/*growth & development/*metabolism
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  • 95
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    Nature Publishing Group (NPG)
    Publication Date: 2015-11-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macilwain, Colin -- England -- Nature. 2015 Nov 19;527(7578):277. doi: 10.1038/527277a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26581256" target="_blank"〉PubMed〈/a〉
    Keywords: Faculty/standards ; *Freedom ; Germany ; Great Britain ; Scotland ; Students ; United States ; Universities/legislation & jurisprudence/*manpower/*organization & administration
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  • 96
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    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2015-08-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tollefson, Jeff -- England -- Nature. 2015 Jul 30;523(7562):510-1. doi: 10.1038/523510a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26223603" target="_blank"〉PubMed〈/a〉
    Keywords: Aircraft ; Atmosphere/chemistry ; Climate Change ; *Expeditions ; *Geography ; Greenland ; Ice Cover/*chemistry ; Models, Theoretical ; Oceans and Seas ; Reproducibility of Results ; *Research ; Seawater/chemistry ; Ships ; United States ; *United States National Aeronautics and Space Administration ; Water/*analysis/chemistry
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 97
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    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2015-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zastrow, Mark -- England -- Nature. 2015 Jan 15;517(7534):256-7. doi: 10.1038/517256a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25592515" target="_blank"〉PubMed〈/a〉
    Keywords: Climate ; *Earth (Planet) ; Environmental Monitoring/*instrumentation ; Environmental Pollution/analysis ; Extraterrestrial Environment/chemistry ; Models, Theoretical ; Politics ; Seasons ; *Spacecraft ; United States ; United States National Aeronautics and Space Administration
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 98
    Publication Date: 2015-07-07
    Description: Stem cells integrate inputs from multiple sources. Stem cell niches provide signals that promote stem cell maintenance, while differentiated daughter cells are known to provide feedback signals to regulate stem cell replication and differentiation. Recently, stem cells have been shown to regulate themselves using an autocrine mechanism. The existence of a 'stem cell niche' was first postulated by Schofield in 1978 to define local environments necessary for the maintenance of haematopoietic stem cells. Since then, an increasing body of work has focused on defining stem cell niches. Yet little is known about how progenitor cell and differentiated cell numbers and proportions are maintained. In the airway epithelium, basal cells function as stem/progenitor cells that can both self-renew and produce differentiated secretory cells and ciliated cells. Secretory cells also act as transit-amplifying cells that eventually differentiate into post-mitotic ciliated cells . Here we describe a mode of cell regulation in which adult mammalian stem/progenitor cells relay a forward signal to their own progeny. Surprisingly, this forward signal is shown to be necessary for daughter cell maintenance. Using a combination of cell ablation, lineage tracing and signalling pathway modulation, we show that airway basal stem/progenitor cells continuously supply a Notch ligand to their daughter secretory cells. Without these forward signals, the secretory progenitor cell pool fails to be maintained and secretory cells execute a terminal differentiation program and convert into ciliated cells. Thus, a parent stem/progenitor cell can serve as a functional daughter cell niche.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4521991/" 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/PMC4521991/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pardo-Saganta, Ana -- Tata, Purushothama Rao -- Law, Brandon M -- Saez, Borja -- Chow, Ryan Dz-Wei -- Prabhu, Mythili -- Gridley, Thomas -- Rajagopal, Jayaraj -- 5P30HL101287-02/HL/NHLBI NIH HHS/ -- R01 HL118185/HL/NHLBI NIH HHS/ -- R01HL118185/HL/NHLBI NIH HHS/ -- England -- Nature. 2015 Jul 30;523(7562):597-601. doi: 10.1038/nature14553. Epub 2015 Jul 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Center for Regenerative Medicine, Massachusetts General Hospital, 185 Cambridge Street, Boston, Massachusetts 02114, USA [2] Departments of Internal Medicine and Pediatrics, Pulmonary and Critical Care Unit, Massachusetts General Hospital, Boston, Massachusetts 02114, USA [3] Harvard Stem Cell Institute, Cambridge, Massachusetts 02138, USA. ; 1] Center for Regenerative Medicine, Massachusetts General Hospital, 185 Cambridge Street, Boston, Massachusetts 02114, USA [2] Harvard Stem Cell Institute, Cambridge, Massachusetts 02138, USA [3] Stem Cell and Regenerative Biology Department, Harvard University, Cambridge, Massachusetts 02138, USA. ; Center for Molecular Medicine, Maine Medical Center Research Institute, 81 Research Drive, Scarborough, Maine 04074, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26147083" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication ; Cell Differentiation ; Cell Division ; Cilia/metabolism ; Female ; Male ; Membrane Proteins/metabolism ; Mice ; Receptor, Notch2/metabolism ; Signal Transduction ; Stem Cell Niche/*physiology ; Stem Cells/*cytology/metabolism/secretion ; Trachea/cytology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 99
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    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2015-07-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deng, Boer -- England -- Nature. 2015 Jul 2;523(7558):16. doi: 10.1038/523016a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26135427" target="_blank"〉PubMed〈/a〉
    Keywords: Botany/economics/*trends ; United States
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 100
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    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2015-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tollefson, Jeff -- England -- Nature. 2015 Apr 23;520(7548):420. doi: 10.1038/520420a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25903606" target="_blank"〉PubMed〈/a〉
    Keywords: Astronomy/*manpower ; Exobiology/*manpower ; *Extraterrestrial Environment ; Meteorology/*manpower ; Planets ; Research/*manpower/*organization & administration ; *Research Personnel ; United States ; United States National Aeronautics and Space Administration/organization & ; administration
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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