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  • Humans  (4,682)
  • Animals  (4,471)
  • Inorganic Chemistry
  • LUNAR AND PLANETARY EXPLORATION
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  • 1995-1999  (6,241)
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  • 101
    Publication Date: 2016-04-28
    Description: Riboswitches and attenuators are cis-regulatory RNA elements, most of which control bacterial gene expression via metabolite-mediated, premature transcription termination. We developed an unbiased experimental approach for genome-wide discovery of such ribo-regulators in bacteria. We also devised an experimental platform that quantitatively measures the in vivo activity of all such regulators in parallel and enables rapid screening for ribo-regulators that respond to metabolites of choice. Using this approach, we detected numerous antibiotic-responsive ribo-regulators that control antibiotic resistance genes in pathogens and in the human microbiome. Studying one such regulator in Listeria monocytogenes revealed an attenuation mechanism mediated by antibiotic-stalled ribosomes. Our results expose broad roles for conditional termination in regulating antibiotic resistance and provide a tool for discovering riboswitches and attenuators that respond to previously unknown ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dar, Daniel -- Shamir, Maya -- Mellin, J R -- Koutero, Mikael -- Stern-Ginossar, Noam -- Cossart, Pascale -- Sorek, Rotem -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):aad9822. doi: 10.1126/science.aad9822.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel. ; Institut Pasteur, Unite des Interactions Bacteries-Cellules, Paris, F-75015 France. INSERM, U604, Paris, F-75015 France. Institut National de la Recherche Agronomique, USC2020, Paris, F-75015 France. ; Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel. rotem.sorek@weizmann.ac.il.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27120414" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/genetics ; Anti-Bacterial Agents/pharmacology ; Bacillus subtilis/drug effects/genetics ; Drug Resistance, Bacterial/*genetics ; Enterococcus faecalis/drug effects ; Gastrointestinal Microbiome/drug effects/genetics ; *Gene Expression Regulation, Bacterial ; Genome, Bacterial/genetics ; Genome-Wide Association Study/*methods ; High-Throughput Nucleotide Sequencing/*methods ; Humans ; Listeria monocytogenes/drug effects/genetics ; Ribosomes/metabolism ; Riboswitch/*genetics ; Sequence Analysis, RNA/methods ; *Transcription Termination, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 102
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 103
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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〉Ma, Eric H -- Jones, Russell G -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):670-1. doi: 10.1126/science.aaf1929.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Goodman Cancer Research Centre, Department of Physiology, McGill University, Montreal, QC, H3A 1A3, Canada. Department of Physiology, McGill University, Montreal, QC, H3G 1Y6, Canada. ; Goodman Cancer Research Centre, Department of Physiology, McGill University, Montreal, QC, H3A 1A3, Canada. Department of Physiology, McGill University, Montreal, QC, H3G 1Y6, Canada. russell.jones@mcgill.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Mitochondria/*metabolism ; Multiprotein Complexes/*metabolism ; Purines/*biosynthesis/*metabolism ; TOR Serine-Threonine Kinases/*metabolism ; Tetrahydrofolates/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 104
    Publication Date: 2016-02-26
    Description: The cerebrum of large mammals is convoluted, whereas that of small mammals is smooth. Mota and Herculano-Houzel (Reports, 3 July 2015, p. 74) inspired a model on an old theory that proposed a fractal geometry. I show that their model reduces to the product of gray-matter proportion times the folding index. This proportional relation describes the available data even better than the fractal model.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Lussanet, Marc H E -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):825. doi: 10.1126/science.aad0127.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Sports Science, University of Munster, Horstmarer Landweg 62b, D-48149 Munster, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912885" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cerebral Cortex ; Humans ; Lissencephaly/*pathology ; Neurons/*cytology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 105
    Publication Date: 2016-04-23
    Description: Tissue-resident memory T (Trm) cells permanently localize to portals of pathogen entry, where they provide immediate protection against reinfection. To enforce tissue retention, Trm cells up-regulate CD69 and down-regulate molecules associated with tissue egress; however, a Trm-specific transcriptional regulator has not been identified. Here, we show that the transcription factor Hobit is specifically up-regulated in Trm cells and, together with related Blimp1, mediates the development of Trm cells in skin, gut, liver, and kidney in mice. The Hobit-Blimp1 transcriptional module is also required for other populations of tissue-resident lymphocytes, including natural killer T (NKT) cells and liver-resident NK cells, all of which share a common transcriptional program. Our results identify Hobit and Blimp1 as central regulators of this universal program that instructs tissue retention in diverse tissue-resident lymphocyte populations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mackay, Laura K -- Minnich, Martina -- Kragten, Natasja A M -- Liao, Yang -- Nota, Benjamin -- Seillet, Cyril -- Zaid, Ali -- Man, Kevin -- Preston, Simon -- Freestone, David -- Braun, Asolina -- Wynne-Jones, Erica -- Behr, Felix M -- Stark, Regina -- Pellicci, Daniel G -- Godfrey, Dale I -- Belz, Gabrielle T -- Pellegrini, Marc -- Gebhardt, Thomas -- Busslinger, Meinrad -- Shi, Wei -- Carbone, Francis R -- van Lier, Rene A W -- Kallies, Axel -- van Gisbergen, Klaas P J M -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):459-63. doi: 10.1126/science.aad2035.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, The University of Melbourne, The Peter Doherty Institute for Infection and Immunity, Melbourne, Australia. Australian Research Council (ARC) Centre of Excellence in Advanced Molecular Imaging, University of Melbourne, Melbourne, Australia. lkmackay@unimelb.edu.au kallies@wehi.edu.au k.vangisbergen@sanquin.nl. ; Research Institute of Molecular Pathology (IMP), Vienna Biocenter (VBC), Vienna, Austria. ; Department of Hematopoiesis, Sanquin Research and Landsteiner Laboratory, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, Netherlands. ; The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Department of Medical Biology, The University of Melbourne, Melbourne, Australia. ; Department of Blood Cell Research, Sanquin Research and Landsteiner Laboratory, AMC, University of Amsterdam, Amsterdam, Netherlands. ; Department of Microbiology and Immunology, The University of Melbourne, The Peter Doherty Institute for Infection and Immunity, Melbourne, Australia. ; Department of Hematopoiesis, Sanquin Research and Landsteiner Laboratory, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, Netherlands. The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Department of Medical Biology, The University of Melbourne, Melbourne, Australia. Department of Experimental Immunology, AMC, Amsterdam, Netherlands. ; Department of Microbiology and Immunology, The University of Melbourne, The Peter Doherty Institute for Infection and Immunity, Melbourne, Australia. Australian Research Council (ARC) Centre of Excellence in Advanced Molecular Imaging, University of Melbourne, Melbourne, Australia. ; The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Department of Computing and Information Systems, The University of Melbourne, Melbourne, Australia. ; The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Department of Medical Biology, The University of Melbourne, Melbourne, Australia. lkmackay@unimelb.edu.au kallies@wehi.edu.au k.vangisbergen@sanquin.nl. ; Department of Hematopoiesis, Sanquin Research and Landsteiner Laboratory, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, Netherlands. The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Department of Medical Biology, The University of Melbourne, Melbourne, Australia. Department of Experimental Immunology, AMC, Amsterdam, Netherlands. lkmackay@unimelb.edu.au kallies@wehi.edu.au k.vangisbergen@sanquin.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102484" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gastrointestinal Tract/immunology ; *Gene Expression Regulation ; Genes, Regulator/genetics/*physiology ; Immunologic Memory/*genetics ; Kidney/immunology ; Killer Cells, Natural/*immunology ; Liver/immunology ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Natural Killer T-Cells/*immunology ; Skin/immunology ; Transcription Factors/genetics/*physiology ; Transcription, Genetic ; Up-Regulation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 106
    Publication Date: 2016-03-19
    Description: Sanchez et al.'s textbook k-anonymization example does not prove, or even suggest, that location and other big-data data sets can be anonymized and of general use. The synthetic data set that they "successfully anonymize" bears no resemblance to modern high-dimensional data sets on which their methods fail. Moving forward, deidentification should not be considered a useful basis for policy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Montjoye, Yves-Alexandre -- Pentland, Alex Sandy -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1274. doi: 10.1126/science.aaf1578.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Harvard University, Institute for Quantitative Social Science, Cambridge, MA 02138, USA. yvesalexandre@demontjoye.com. ; 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/26989244" target="_blank"〉PubMed〈/a〉
    Keywords: *Commerce ; *Data Collection ; Female ; Humans ; *Information Dissemination ; Male ; *Privacy
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  • 107
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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〉Magurran, Anne E -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):448-9. doi: 10.1126/science.aad6758.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Biological Diversity, School of Biology, University of St. Andrews, St. Andrews, Scotland, UK. aem1@st-andrews.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823412" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; *Climate Change ; *Conservation of Natural Resources ; Extinction, Biological ; *Fishes ; Introduced Species ; Rivers
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 108
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 109
    Publication Date: 2016-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dejana, Elisabetta -- Betsholtz, Christer -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):341-2. doi: 10.1126/science.aaf1139.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden. FIRC Institute of Molecular Oncology, Milan, Italy. Department of Oncology and Hemato-Oncology, Milan University, Milan, Italy. elisabetta.dejana@igp.uu.se christer.betsholtz@igp.uu.se. ; Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden. Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden. elisabetta.dejana@igp.uu.se christer.betsholtz@igp.uu.se.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26798001" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Movement ; Cerebral Cortex/*embryology ; Humans ; Neural Stem Cells/*physiology ; *Neurogenesis ; Oligodendroglia/*physiology ; *Organogenesis ; Spinal Cord/*embryology
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  • 110
    Publication Date: 2016-01-28
    Description: Hydroxymethylcytosine, well described in DNA, occurs also in RNA. Here, we show that hydroxymethylcytosine preferentially marks polyadenylated RNAs and is deposited by Tet in Drosophila. We map the transcriptome-wide hydroxymethylation landscape, revealing hydroxymethylcytosine in the transcripts of many genes, notably in coding sequences, and identify consensus sites for hydroxymethylation. We found that RNA hydroxymethylation can favor mRNA translation. Tet and hydroxymethylated RNA are found to be most abundant in the Drosophila brain, and Tet-deficient fruitflies suffer impaired brain development, accompanied by decreased RNA hydroxymethylation. This study highlights the distribution, localization, and function of cytosine hydroxymethylation and identifies central roles for this modification in Drosophila.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delatte, Benjamin -- Wang, Fei -- Ngoc, Long Vo -- Collignon, Evelyne -- Bonvin, Elise -- Deplus, Rachel -- Calonne, Emilie -- Hassabi, Bouchra -- Putmans, Pascale -- Awe, Stephan -- Wetzel, Collin -- Kreher, Judith -- Soin, Romuald -- Creppe, Catherine -- Limbach, Patrick A -- Gueydan, Cyril -- Kruys, Veronique -- Brehm, Alexander -- Minakhina, Svetlana -- Defrance, Matthieu -- Steward, Ruth -- Fuks, Francois -- R01 GM089992/GM/NIGMS NIH HHS/ -- T32 CA117846/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):282-5. doi: 10.1126/science.aac5253.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cancer Epigenetics, Faculty of Medicine, ULB Cancer Research Center (U-CRC), Universite Libre de Bruxelles (ULB), Brussels, Belgium. ; Waksman Institute, Department of Molecular Biology and Biochemistry, Cancer Institute of New Jersey, Rutgers University, Piscataway, NJ, USA. ; Laboratory of Molecular Biology of the Gene, Faculty of Sciences, Universite Libre de Bruxelles, Gosselies, Belgium. ; Institut fur Molekularbiologie und Tumorforschung, Philipps-Universitat Marburg, Marburg, Germany. ; Department of Chemistry, University of Cincinnati, Cincinnati, OH, USA. ; Laboratory of Cancer Epigenetics, Faculty of Medicine, ULB Cancer Research Center (U-CRC), Universite Libre de Bruxelles (ULB), Brussels, Belgium. ffuks@ulb.ac.be.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816380" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*abnormalities/metabolism ; Cell Line ; Cytosine/*analogs & derivatives/metabolism ; Dioxygenases/genetics/metabolism ; Drosophila melanogaster/genetics/*growth & development/metabolism ; Methylation ; RNA, Messenger/genetics/*metabolism ; Transcriptome
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  • 111
    Publication Date: 2016-01-09
    Description: The stomach bacterium Helicobacter pylori is one of the most prevalent human pathogens. It has dispersed globally with its human host, resulting in a distinct phylogeographic pattern that can be used to reconstruct both recent and ancient human migrations. The extant European population of H. pylori is known to be a hybrid between Asian and African bacteria, but there exist different hypotheses about when and where the hybridization took place, reflecting the complex demographic history of Europeans. Here, we present a 5300-year-old H. pylori genome from a European Copper Age glacier mummy. The "Iceman" H. pylori is a nearly pure representative of the bacterial population of Asian origin that existed in Europe before hybridization, suggesting that the African population arrived in Europe within the past few thousand years.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4775254/" 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/PMC4775254/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maixner, Frank -- Krause-Kyora, Ben -- Turaev, Dmitrij -- Herbig, Alexander -- Hoopmann, Michael R -- Hallows, Janice L -- Kusebauch, Ulrike -- Vigl, Eduard Egarter -- Malfertheiner, Peter -- Megraud, Francis -- O'Sullivan, Niall -- Cipollini, Giovanna -- Coia, Valentina -- Samadelli, Marco -- Engstrand, Lars -- Linz, Bodo -- Moritz, Robert L -- Grimm, Rudolf -- Krause, Johannes -- Nebel, Almut -- Moodley, Yoshan -- Rattei, Thomas -- Zink, Albert -- 2P50 GM076547/GM/NIGMS NIH HHS/ -- P50 GM076547/GM/NIGMS NIH HHS/ -- R01 GM087221/GM/NIGMS NIH HHS/ -- S10 RR027584/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):162-5. doi: 10.1126/science.aad2545.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Mummies and the Iceman, European Academy of Bozen/Bolzano (EURAC), Viale Druso 1, 39100 Bolzano, Italy. frank.maixner@eurac.edu albert.zink@eurac.edu. ; Institute of Clinical Molecular Biology, Kiel University, Schittenhelmstrasse 12, 24105 Kiel, Germany. ; CUBE-Division of Computational Systems Biology, Department of Microbiology and Ecosystem Science, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria. ; Institute for Archaeological Sciences, University of Tubingen, Rumelinstrasse 23, 72072 Tubingen, Germany. Max Planck Institute for the Science of Human History, Kahlaische Strasse 10, 07745 Jena, Germany. ; Institute for Systems Biology, 401 Terry Avenue North, Seattle, WA 98109, USA. ; Scuola Superiore Sanitaria Provinciale "Claudiana," Via Lorenz Bohler 13, 39100 Bolzano, Italy. ; Department of Gastroenterology, Hepatology, and Infectious Diseases, Otto-von-Guericke University, Leipziger Strasse 44, 39120 Magdeburg, Germany. ; Universite de Bordeaux, Centre National de Reference des Helicobacters et Campylobacters and INSERM U853, 146 rue Leo Saignat, 33076 Bordeaux, France. ; Institute for Mummies and the Iceman, European Academy of Bozen/Bolzano (EURAC), Viale Druso 1, 39100 Bolzano, Italy. ; Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 141 83 Stockholm, Sweden. ; Department of Veterinary and Biomedical Sciences, Pennsylvania State University, University Park, PA 16802, USA. ; Robert Mondavi Institute for Food Science, University of California, Davis, CA 95616, USA. ; Department of Zoology, University of Venda, Private Bag X5050, Thohoyandou 0950, Republic of South Africa. Department of Integrative Biology and Evolution, Konrad Lorenz Institute for Ethology, University of Veterinary Medicine Vienna, Savoyenstrasse 1a, 1160 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744403" target="_blank"〉PubMed〈/a〉
    Keywords: Asia ; Chromosome Mapping ; DNA, Bacterial/genetics/isolation & purification ; Europe ; Genome, Bacterial/*genetics ; Helicobacter Infections/*microbiology ; Helicobacter pylori/*genetics/isolation & purification ; Human Migration ; Humans ; *Hybridization, Genetic ; Ice Cover/microbiology ; Mummies/microbiology ; Phylogeny ; Phylogeography ; Sequence Analysis, DNA ; Stomach/*microbiology
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  • 112
    Publication Date: 2016-03-26
    Description: During cancer metastasis, tumor cells penetrate tissues through tight interstitial spaces, which requires extensive deformation of the cell and its nucleus. Here, we investigated mammalian tumor cell migration in confining microenvironments in vitro and in vivo. Nuclear deformation caused localized loss of nuclear envelope (NE) integrity, which led to the uncontrolled exchange of nucleo-cytoplasmic content, herniation of chromatin across the NE, and DNA damage. The incidence of NE rupture increased with cell confinement and with depletion of nuclear lamins, NE proteins that structurally support the nucleus. Cells restored NE integrity using components of the endosomal sorting complexes required for transport III (ESCRT III) machinery. Our findings indicate that cell migration incurs substantial physical stress on the NE and its content and requires efficient NE and DNA damage repair for cell survival.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4833568/" 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/PMC4833568/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Denais, Celine M -- Gilbert, Rachel M -- Isermann, Philipp -- McGregor, Alexandra L -- te Lindert, Mariska -- Weigelin, Bettina -- Davidson, Patricia M -- Friedl, Peter -- Wolf, Katarina -- Lammerding, Jan -- R01 HL082792/HL/NHLBI NIH HHS/ -- R01 NS059348/NS/NINDS NIH HHS/ -- S10OD018516/OD/NIH HHS/ -- U54 CA143876/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):353-8. doi: 10.1126/science.aad7297. Epub 2016 Mar 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nancy E. and Peter C. Meinig School of Biomedical Engineering and Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA. ; Department of Cell Biology, Radboud University Medical Center, Nijmegen, Netherlands. ; Department of Cell Biology, Radboud University Medical Center, Nijmegen, Netherlands. Department of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Cancer Genomics Center, Netherlands (CGC.nl). ; Nancy E. and Peter C. Meinig School of Biomedical Engineering and Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA. jan.lammerding@cornell.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013428" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; *Cell Movement ; Chromatin/metabolism ; Cytoplasm/metabolism ; DNA Damage ; Endosomal Sorting Complexes Required for Transport/metabolism ; Humans ; Lamins/deficiency ; Neoplasms/metabolism/*pathology ; Nuclear Envelope/metabolism/*pathology ; Stress, Mechanical ; *Tumor Microenvironment
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  • 113
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Desban, Laura -- Wyart, Claire -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):42-3. doi: 10.1126/science.aaf6016.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut du Cerveau et de la Moelle epiniere, GH Pitie-Salpetriere, 75013 Paris, France. ; Institut du Cerveau et de la Moelle epiniere, GH Pitie-Salpetriere, 75013 Paris, France. claire.wyart@icm-institute.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034363" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression/*physiology ; Animals ; *Conflict (Psychology) ; Habenula/*physiology ; *Negotiating
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  • 114
    Publication Date: 2016-04-23
    Description: Pershing et al (Science, 13 November 2015, p. 809) concluded that recent warming in the Gulf of Maine contributed to the collapse of Gulf of Maine cod. We argue that this conclusion is based on a flawed analysis of the population dynamics of this cod stock. We believe that understanding the potential role of climate change in the collapse of this stock requires more defensible analyses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Swain, Douglas P -- Benoit, Hugues P -- Cox, Sean P -- Cadigan, Noel G -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):423. doi: 10.1126/science.aad9346.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fisheries and Oceans Canada, Gulf Fisheries Centre, Moncton, NB E1C 9B6, Canada. ; Fisheries and Oceans Canada, Gulf Fisheries Centre, Moncton, NB E1C 9B6, Canada. hugues.benoit@dfo-mpo.gc.ca. ; School of Resource and Environmental Management, Simon Fraser University, Burnaby, BC V5A 1S6, Canada. ; Centre for Fisheries Ecosystems Research, Marine Institute of Memorial University of Newfoundland, St. John's, NL A1C 5R3, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102474" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; *Fisheries ; Gadus morhua/*physiology ; *Global Warming
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  • 115
    Publication Date: 2016-02-26
    Description: T cell-mediated destruction of insulin-producing beta cells in the pancreas causes type 1 diabetes (T1D). CD4 T cell responses play a central role in beta cell destruction, but the identity of the epitopes recognized by pathogenic CD4 T cells remains unknown. We found that diabetes-inducing CD4 T cell clones isolated from nonobese diabetic mice recognize epitopes formed by covalent cross-linking of proinsulin peptides to other peptides present in beta cell secretory granules. These hybrid insulin peptides (HIPs) are antigenic for CD4 T cells and can be detected by mass spectrometry in beta cells. CD4 T cells from the residual pancreatic islets of two organ donors who had T1D also recognize HIPs. Autoreactive T cells targeting hybrid peptides may explain how immune tolerance is broken in T1D.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delong, Thomas -- Wiles, Timothy A -- Baker, Rocky L -- Bradley, Brenda -- Barbour, Gene -- Reisdorph, Richard -- Armstrong, Michael -- Powell, Roger L -- Reisdorph, Nichole -- Kumar, Nitesh -- Elso, Colleen M -- DeNicola, Megan -- Bottino, Rita -- Powers, Alvin C -- Harlan, David M -- Kent, Sally C -- Mannering, Stuart I -- Haskins, Kathryn -- 1K01DK094941/DK/NIDDK NIH HHS/ -- 1R01DK081166/DK/NIDDK NIH HHS/ -- 5U01DK89572/DK/NIDDK NIH HHS/ -- DK104211/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):711-4. doi: 10.1126/science.aad2791.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Microbiology, University of Colorado School of Medicine, Denver, Anschutz Medical Campus, Aurora, CO 80045, USA. thomas.delong@ucdenver.edu katie.haskins@ucdenver.edu. ; Department of Immunology and Microbiology, University of Colorado School of Medicine, Denver, Anschutz Medical Campus, Aurora, CO 80045, USA. ; Pharmaceutical Sciences, University of Colorado School of Medicine, Aurora, CO 80045, USA. ; Immunology and Diabetes Unit, St. Vincent's Institute of Medical Research, 9 Princes Street, Fitzroy, Victoria 3065, Australia. ; Department of Medicine, Diabetes Division, Diabetes Center of Excellence, University of Massachusetts Medical School, Worcester, MA, USA. ; Institute of Cellular Therapeutics, Allegheny-Singer Research Institute, Allegheny Health Network, Pittsburgh, PA, USA. ; Division of Diabetes, Endocrinology, and Metabolism, Department of Medicine, and Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN, USA. VA Tennessee Valley Healthcare System, Nashville, TN, USA. ; Immunology and Diabetes Unit, St. Vincent's Institute of Medical Research, 9 Princes Street, Fitzroy, Victoria 3065, Australia. University of Melbourne, Department of Medicine, St. Vincent's Hospital, Fitzroy, Victoria 3065, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912858" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; C-Peptide/chemistry/*immunology ; CD4-Positive T-Lymphocytes/*immunology ; Clone Cells ; Diabetes Mellitus, Experimental/*immunology/pathology ; Diabetes Mellitus, Type 1/*immunology/pathology ; Epitopes/*immunology ; Immune Tolerance ; Insulin-Secreting Cells/*immunology/pathology ; Mice ; Mice, Inbred NOD ; Molecular Sequence Data ; Peptides/chemistry/immunology
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  • 116
    Publication Date: 2016-01-02
    Description: Frame-disrupting mutations in the DMD gene, encoding dystrophin, compromise myofiber integrity and drive muscle deterioration in Duchenne muscular dystrophy (DMD). Removing one or more exons from the mutated transcript can produce an in-frame mRNA and a truncated, but still functional, protein. In this study, we developed and tested a direct gene-editing approach to induce exon deletion and recover dystrophin expression in the mdx mouse model of DMD. Delivery by adeno-associated virus (AAV) of clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 endonucleases coupled with paired guide RNAs flanking the mutated Dmd exon23 resulted in excision of intervening DNA and restored the Dmd reading frame in myofibers, cardiomyocytes, and muscle stem cells after local or systemic delivery. AAV-Dmd CRISPR treatment partially recovered muscle functional deficiencies and generated a pool of endogenously corrected myogenic precursors in mdx mouse muscle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tabebordbar, Mohammadsharif -- Zhu, Kexian -- Cheng, Jason K W -- Chew, Wei Leong -- Widrick, Jeffrey J -- Yan, Winston X -- Maesner, Claire -- Wu, Elizabeth Y -- Xiao, Ru -- Ran, F Ann -- Cong, Le -- Zhang, Feng -- Vandenberghe, Luk H -- Church, George M -- Wagers, Amy J -- 1DP2OD004345/OD/NIH HHS/ -- 5DP1-MH100706/DP/NCCDPHP CDC HHS/ -- 5PN2EY018244/EY/NEI NIH HHS/ -- 5R01DK097768-03/DK/NIDDK NIH HHS/ -- 5U01HL100402/HL/NHLBI NIH HHS/ -- P50 HG005550/HG/NHGRI NIH HHS/ -- T2GM007753/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):407-11. doi: 10.1126/science.aad5177. Epub 2015 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Stem Cell and Regenerative Biology, Harvard University, and Harvard Stem Cell Institute, Cambridge, MA 02138, USA. Biological and Biomedical Sciences Program, Harvard Medical School, Boston, MA 02115, USA. ; Department of Stem Cell and Regenerative Biology, Harvard University, and Harvard Stem Cell Institute, Cambridge, MA 02138, USA. Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA. ; Department of Stem Cell and Regenerative Biology, Harvard University, and Harvard Stem Cell Institute, Cambridge, MA 02138, USA. ; Biological and Biomedical Sciences Program, Harvard Medical School, Boston, MA 02115, USA. Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Division of Genetics and Program in Genomics, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. McGovern Institute for Brain Research, Department of Brain and Cognitive Science, and Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Grousbeck Gene Therapy Center, Schepens Eye Research Institute, and Massachusetts Eye and Ear Infirmary, 20 Staniford Street, Boston, MA 02114, USA. ; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Department of Stem Cell and Regenerative Biology, Harvard University, and Harvard Stem Cell Institute, Cambridge, MA 02138, USA. amy_wagers@harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721686" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CRISPR-Cas Systems ; Clustered Regularly Interspaced Short Palindromic Repeats ; Dependovirus ; Disease Models, Animal ; Exons ; Frameshift Mutation ; Genetic Therapy/*methods ; Mice ; Mice, Inbred mdx ; Muscle, Skeletal/metabolism ; Muscular Dystrophy, Duchenne/genetics/*therapy ; Myocardium/metabolism ; RNA, Messenger/genetics ; Satellite Cells, Skeletal Muscle/*metabolism ; Sequence Deletion ; Transduction, Genetic/*methods
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  • 117
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-05-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takamura, Noboru -- Orita, Makiko -- Yamashita, Shunichi -- Chhem, Rethy -- New York, N.Y. -- Science. 2016 May 6;352(6286):666. doi: 10.1126/science.352.6286.666-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, 852-8523 Japan. takamura@nagasaki-u.ac.jp. ; Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, 852-8523 Japan. ; Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, 852-8523 Japan. Cambodia Development Resource Institute, Phnom Penh 622, Cambodia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27151855" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Radiation-Induced/*epidemiology ; *Disasters ; *Epidemics ; Female ; *Fukushima Nuclear Accident ; Humans ; Radiation Exposure/*adverse effects ; Thyroid Gland/*abnormalities/*pathology ; Thyroid Neoplasms/*epidemiology
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  • 118
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Devkota, Suzanne -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):452-3. doi: 10.1126/science.aaf1353.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA. suzanne.devkota@cshs.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823414" target="_blank"〉PubMed〈/a〉
    Keywords: Diabetes Mellitus, Type 2/*microbiology ; Female ; Gastrointestinal Microbiome/*drug effects/*physiology ; Humans ; Male ; Metformin/*pharmacology
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  • 119
    Publication Date: 2016-01-28
    Description: Genes encoding human beta-type globin undergo a developmental switch from embryonic to fetal to adult-type expression. Mutations in the adult form cause inherited hemoglobinopathies or globin disorders, including sickle cell disease and thalassemia. Some experimental results have suggested that these diseases could be treated by induction of fetal-type hemoglobin (HbF). However, the mechanisms that repress HbF in adults remain unclear. We found that the LRF/ZBTB7A transcription factor occupies fetal gamma-globin genes and maintains the nucleosome density necessary for gamma-globin gene silencing in adults, and that LRF confers its repressive activity through a NuRD repressor complex independent of the fetal globin repressor BCL11A. Our study may provide additional opportunities for therapeutic targeting in the treatment of hemoglobinopathies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4778394/" 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/PMC4778394/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Masuda, Takeshi -- Wang, Xin -- Maeda, Manami -- Canver, Matthew C -- Sher, Falak -- Funnell, Alister P W -- Fisher, Chris -- Suciu, Maria -- Martyn, Gabriella E -- Norton, Laura J -- Zhu, Catherine -- Kurita, Ryo -- Nakamura, Yukio -- Xu, Jian -- Higgs, Douglas R -- Crossley, Merlin -- Bauer, Daniel E -- Orkin, Stuart H -- Kharchenko, Peter V -- Maeda, Takahiro -- R01 AI084905/AI/NIAID NIH HHS/ -- R01 HL032259/HL/NHLBI NIH HHS/ -- R56 DK105001/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):285-9. doi: 10.1126/science.aad3312.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; Department of Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA. ; Division of Hematology/Oncology, Boston Children's Hospital, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. ; School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW 2052, Australia. ; Medical Research Council, Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, Oxford University, Oxford, UK. ; Cell Engineering Division, RIKEN BioResource Center, Tsukuba, Ibaraki, Japan. ; Cell Engineering Division, RIKEN BioResource Center, Tsukuba, Ibaraki, Japan. Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan. ; Division of Hematology/Oncology, Boston Children's Hospital, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Children's Research Institute, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Division of Hematology/Oncology, Boston Children's Hospital, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Howard Hughes Medical Institute, Boston, MA 02115, USA. ; Department of Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA. peter.kharchenko@post.harvard.edu tmaeda@partners.org. ; Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. peter.kharchenko@post.harvard.edu tmaeda@partners.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816381" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/genetics ; Animals ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Chromatin/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Erythroblasts/cytology ; Erythropoiesis/genetics ; Fetal Hemoglobin/*genetics ; *Gene Silencing ; Humans ; Mice ; Mice, Knockout ; Nuclear Proteins/genetics/*metabolism ; Repressor Proteins/genetics/*metabolism ; Sequence Deletion ; Thalassemia/genetics ; Transcription Factors/genetics/*metabolism ; gamma-Globins/*genetics
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  • 120
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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〉Matacic, Catherine -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):392-3. doi: 10.1126/science.352.6284.392. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102453" target="_blank"〉PubMed〈/a〉
    Keywords: Facial Expression ; Hand ; Head ; Humans ; Israel ; Linguistics/*trends ; Persons With Hearing Impairments/*rehabilitation ; *Sign Language ; Torso
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  • 121
    Publication Date: 2016-04-30
    Description: Wakefulness is driven by the widespread release of neuromodulators by the ascending arousal system. Yet, it is unclear how these substances orchestrate state-dependent, global changes in neuronal activity. Here, we show that neuromodulators induce increases in the extracellular K(+) concentration ([K(+)]e) in cortical slices electrically silenced by tetrodotoxin. In vivo, arousal was linked to AMPA receptor-independent elevations of [K(+)]e concomitant with decreases in [Ca(2+)]e, [Mg(2+)]e, [H(+)]e, and the extracellular volume. Opposite, natural sleep and anesthesia reduced [K(+)]e while increasing [Ca(2+)]e, [Mg(2+)]e, and [H(+)]e as well as the extracellular volume. Local cortical activity of sleeping mice could be readily converted to the stereotypical electroencephalography pattern of wakefulness by simply imposing a change in the extracellular ion composition. Thus, extracellular ions control the state-dependent patterns of neural activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, Fengfei -- O'Donnell, John -- Xu, Qiwu -- Kang, Ning -- Goldman, Nanna -- Nedergaard, Maiken -- NS078167/NS/NINDS NIH HHS/ -- NS078304/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):550-5. doi: 10.1126/science.aad4821.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Translational Neuromedicine, University of Rochester Medical Center, Rochester, NY 14642, USA. Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. ; Center for Translational Neuromedicine, University of Rochester Medical Center, Rochester, NY 14642, USA. ; Center for Translational Neuromedicine, University of Rochester Medical Center, Rochester, NY 14642, USA. Center for Basic and Translational Neuroscience, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen 2200, Denmark. nedergaard@urmc.rochester.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126038" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/analysis/metabolism ; Cations/analysis/*metabolism ; Cerebral Cortex/chemistry/drug effects/*physiology ; Electroencephalography ; Magnesium/analysis/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Neurons/drug effects/metabolism/physiology ; Neurotransmitter Agents/metabolism/pharmacology ; Potassium/*metabolism ; Receptors, AMPA/metabolism ; Sleep/drug effects/*physiology ; Sodium Channel Blockers/pharmacology ; Tetrodotoxin/pharmacology ; Wakefulness/drug effects/*physiology
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  • 122
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dobson, Stephen L -- Bordenstein, Seth R -- Rose, Robert I -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):526-7. doi: 10.1126/science.352.6285.526-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Kentucky, Lexington, KY 40546, USA. MosquitoMate Inc., Lexington, KY 40503, USA. sdobson@uky.edu. ; Vanderbilt University, Nashville, TN, 37235, USA. ; Biotechnology Regulatory Consulting, Frederick, MD 21704, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126029" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Culicidae/*microbiology ; Dengue/*prevention & control ; Mosquito Control/*methods ; *Wolbachia
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  • 123
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 124
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maxmen, Amy -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1378-80. doi: 10.1126/science.351.6280.1378.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013707" target="_blank"〉PubMed〈/a〉
    Keywords: Anal Canal/*anatomy & histology ; Animals ; *Biological Evolution ; Ctenophora/*anatomy & histology/genetics ; Sequence Analysis, DNA
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  • 125
    Publication Date: 2016-04-29
    Description: When asked to perform the same task, different individuals exhibit markedly different patterns of brain activity. This variability is often attributed to volatile factors, such as task strategy or compliance. We propose that individual differences in brain responses are, to a large degree, inherent to the brain and can be predicted from task-independent measurements collected at rest. Using a large set of task conditions, spanning several behavioral domains, we train a simple model that relates task-independent measurements to task activity and evaluate the model by predicting task activation maps for unseen subjects using magnetic resonance imaging. Our model can accurately predict individual differences in brain activity and highlights a coupling between brain connectivity and function that can be captured at the level of individual subjects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tavor, I -- Parker Jones, O -- Mars, R B -- Smith, S M -- Behrens, T E -- Jbabdi, S -- 098369/Z/12/Z/Wellcome Trust/United Kingdom -- 1U54MH091657/MH/NIMH NIH HHS/ -- MR/L009013/1/Medical Research Council/United Kingdom -- WT104765MA/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):216-20. doi: 10.1126/science.aad8127. Epub 2016 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Oxford Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB), Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford OX3 9DU, UK. Department of Diagnostic Imaging, Sheba Medical Center, Tel Hashomer, 52621, Israel. ; Oxford Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB), Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford OX3 9DU, UK. ; Oxford Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB), Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford OX3 9DU, UK. Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen, 6525 EZ Nijmegen, Netherlands. ; Oxford Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB), Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford OX3 9DU, UK. Wellcome Trust Centre for Neuroimaging, University College London, London, WC1N 3BG, UK. ; Oxford Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB), Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford OX3 9DU, UK. saad@fmrib.ox.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124457" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/*physiology ; Brain Mapping/*methods ; Humans ; Individuality ; Language ; Magnetic Resonance Imaging/*methods ; *Task Performance and Analysis
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  • 126
    Publication Date: 2016-03-26
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4838154/" 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/PMC4838154/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dove, Edward S -- Townend, David -- Meslin, Eric M -- Bobrow, Martin -- Littler, Katherine -- Nicol, Dianne -- de Vries, Jantina -- Junker, Anne -- Garattini, Chiara -- Bovenberg, Jasper -- Shabani, Mahsa -- Levesque, Emmanuelle -- Knoppers, Bartha M -- 099313/Wellcome Trust/United Kingdom -- 103360/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1399-400. doi: 10.1126/science.aad5269.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉J. Kenyon Mason Institute for Medicine, Life Sciences and the Law, School of Law, University of Edinburgh, UK. edward.dove@ed.ac.uk. ; Department of Health, Ethics & Society, CAPHRI Research School, Maastricht University, The Netherlands. ; Indiana University Center for Bioethics, Indiana University School of Medicine, Indianapolis, Indiana, USA. ; Honorary Faculty, Wellcome Trust Sanger Institute, Hinxton, UK. Department of Medical Genetics, University of Cambridge, UK. ; Wellcome Trust, London, UK. ; Centre for Law and Genetics, Faculty of Law, University of Tasmania, Australia. ; Department of Medicine, Faculty of Health Sciences, University of Cape Town, South Africa. ; Department of Pediatrics, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada. ; Intel Corporation, Health and Life Sciences, London, UK. ; Legal Pathways, Aerdenhout, The Netherlands. ; Centre for Biomedical Ethics and Law, KU Leuven, Leuven, Belgium. ; Centre of Genomics and Policy, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013718" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/*ethics ; Datasets as Topic/ethics ; Ethical Review/*standards ; Genetics, Medical ; Genome, Human ; Humans ; Information Dissemination/*ethics ; Internationality ; Neoplasms
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  • 127
    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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  • 128
    Publication Date: 2016-02-26
    Description: 5-Methylthioadenosine phosphorylase (MTAP) is a key enzyme in the methionine salvage pathway. The MTAP gene is frequently deleted in human cancers because of its chromosomal proximity to the tumor suppressor gene CDKN2A. By interrogating data from a large-scale short hairpin RNA-mediated screen across 390 cancer cell line models, we found that the viability of MTAP-deficient cancer cells is impaired by depletion of the protein arginine methyltransferase PRMT5. MTAP-deleted cells accumulate the metabolite methylthioadenosine (MTA), which we found to inhibit PRMT5 methyltransferase activity. Deletion of MTAP in MTAP-proficient cells rendered them sensitive to PRMT5 depletion. Conversely, reconstitution of MTAP in an MTAP-deficient cell line rescued PRMT5 dependence. Thus, MTA accumulation in MTAP-deleted cancers creates a hypomorphic PRMT5 state that is selectively sensitized toward further PRMT5 inhibition. Inhibitors of PRMT5 that leverage this dysregulated metabolic state merit further investigation as a potential therapy for MTAP/CDKN2A-deleted tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mavrakis, Konstantinos J -- McDonald, E Robert 3rd -- Schlabach, Michael R -- Billy, Eric -- Hoffman, Gregory R -- deWeck, Antoine -- Ruddy, David A -- Venkatesan, Kavitha -- Yu, Jianjun -- McAllister, Gregg -- Stump, Mark -- deBeaumont, Rosalie -- Ho, Samuel -- Yue, Yingzi -- Liu, Yue -- Yan-Neale, Yan -- Yang, Guizhi -- Lin, Fallon -- Yin, Hong -- Gao, Hui -- Kipp, D Randal -- Zhao, Songping -- McNamara, Joshua T -- Sprague, Elizabeth R -- Zheng, Bing -- Lin, Ying -- Cho, Young Shin -- Gu, Justin -- Crawford, Kenneth -- Ciccone, David -- Vitari, Alberto C -- Lai, Albert -- Capka, Vladimir -- Hurov, Kristen -- Porter, Jeffery A -- Tallarico, John -- Mickanin, Craig -- Lees, Emma -- Pagliarini, Raymond -- Keen, Nicholas -- Schmelzle, Tobias -- Hofmann, Francesco -- Stegmeier, Frank -- Sellers, William R -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1208-13. doi: 10.1126/science.aad5944. Epub 2016 Feb 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Novartis Institutes for Biomedical Research, Cambridge, MA 02139, USA. ; Novartis Institutes for Biomedical Research, Basel CH-4002, Switzerland. ; Novartis Institutes for Biomedical Research, Emeryville, CA 94608, USA. ; China Novartis Institutes for Biomedical Research, Shanghai 201203, China. ; Novartis Institutes for Biomedical Research, Cambridge, MA 02139, USA. william.sellers@novartis.com fstegmeier@ksqtx.com.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912361" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; Cell Survival ; Cyclin-Dependent Kinase Inhibitor p16/genetics/*metabolism ; Deoxyadenosines/metabolism ; Gene Deletion ; Humans ; Methionine/*metabolism ; Neoplasms/drug therapy/genetics/*metabolism ; Protein-Arginine N-Methyltransferases/genetics/*metabolism ; Purine-Nucleoside Phosphorylase/genetics/*metabolism ; RNA, Small Interfering/genetics ; Thionucleosides/metabolism
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  • 129
    Publication Date: 2016-03-05
    Description: During corticogenesis, excitatory neurons are born from progenitors located in the ventricular zone (VZ), from where they migrate to assemble into circuits. How neuronal identity is dynamically specified upon progenitor division is unknown. Here, we study this process using a high-temporal-resolution technology allowing fluorescent tagging of isochronic cohorts of newborn VZ cells. By combining this in vivo approach with single-cell transcriptomics in mice, we identify and functionally characterize neuron-specific primordial transcriptional programs as they dynamically unfold. Our results reveal early transcriptional waves that instruct the sequence and pace of neuronal differentiation events, guiding newborn neurons toward their final fate, and contribute to a road map for the reverse engineering of specific classes of cortical neurons from undifferentiated cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Telley, Ludovic -- Govindan, Subashika -- Prados, Julien -- Stevant, Isabelle -- Nef, Serge -- Dermitzakis, Emmanouil -- Dayer, Alexandre -- Jabaudon, Denis -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1443-6. doi: 10.1126/science.aad8361. Epub 2016 Mar 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Basic Neurosciences, University of Geneva, Switzerland. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Switzerland. ; Department of Genetic Medicine and Development, University of Geneva, Switzerland. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Switzerland. ; Department of Genetic Medicine and Development, University of Geneva, Switzerland. Biomedical Research Foundation Academy of Athens, Greece. Center of Excellence in Genomic Medicine Research, King Abdulaziz University, Saudi Arabia. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Switzerland. ; Department of Basic Neurosciences, University of Geneva, Switzerland. Department of Psychiatry, Geneva University Hospital, Switzerland. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Switzerland. ; Department of Basic Neurosciences, University of Geneva, Switzerland. Clinic of Neurology, Geneva University Hospital, Switzerland. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Switzerland. denis.jabaudon@unige.ch.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26940868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Cerebral Ventricles/cytology/embryology ; DNA-Binding Proteins/genetics ; Female ; GPI-Linked Proteins/genetics ; Green Fluorescent Proteins/genetics ; Male ; Mice ; Neocortex/cytology/*embryology ; Nerve Tissue Proteins/genetics ; Neural Stem Cells/cytology ; Neurogenesis/*genetics ; Neurons/*cytology ; Neuropeptides/genetics ; SOXB1 Transcription Factors/genetics ; *Transcription, Genetic ; Transcriptome
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  • 130
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McLaughlin, Kathleen -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):506. doi: 10.1126/science.352.6285.506.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126018" target="_blank"〉PubMed〈/a〉
    Keywords: Child, Preschool ; China ; *Counterfeit Drugs ; *Drug Industry ; Hand, Foot and Mouth Disease/prevention & control ; Hepatitis B/prevention & control ; Humans ; Rabies/virology ; *Viral Vaccines
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  • 131
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dustin, Michael L -- Muller, James -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):516-7. doi: 10.1126/science.aaf8179.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kennedy Institute of Rheumatology, The University of Oxford, Oxford, UK. Skirball Institute, New York University School of Medicine, New York, NY, USA. michael.dustin@kennedy.ox.ac.uk. ; Skirball Institute, New York University School of Medicine, New York, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126023" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*metabolism ; Adaptor Proteins, Signal Transducing/*metabolism ; Humans ; Membrane Proteins/*metabolism ; Receptors, Antigen, T-Cell/*agonists ; T-Lymphocytes/*metabolism
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  • 132
    Publication Date: 2016-03-05
    Description: As tumors grow, they acquire mutations, some of which create neoantigens that influence the response of patients to immune checkpoint inhibitors. We explored the impact of neoantigen intratumor heterogeneity (ITH) on antitumor immunity. Through integrated analysis of ITH and neoantigen burden, we demonstrate a relationship between clonal neoantigen burden and overall survival in primary lung adenocarcinomas. CD8(+)tumor-infiltrating lymphocytes reactive to clonal neoantigens were identified in early-stage non-small cell lung cancer and expressed high levels of PD-1. Sensitivity to PD-1 and CTLA-4 blockade in patients with advanced NSCLC and melanoma was enhanced in tumors enriched for clonal neoantigens. T cells recognizing clonal neoantigens were detectable in patients with durable clinical benefit. Cytotoxic chemotherapy-induced subclonal neoantigens, contributing to an increased mutational load, were enriched in certain poor responders. These data suggest that neoantigen heterogeneity may influence immune surveillance and support therapeutic developments targeting clonal neoantigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGranahan, Nicholas -- Furness, Andrew J S -- Rosenthal, Rachel -- Ramskov, Sofie -- Lyngaa, Rikke -- Saini, Sunil Kumar -- Jamal-Hanjani, Mariam -- Wilson, Gareth A -- Birkbak, Nicolai J -- Hiley, Crispin T -- Watkins, Thomas B K -- Shafi, Seema -- Murugaesu, Nirupa -- Mitter, Richard -- Akarca, Ayse U -- Linares, Joseph -- Marafioti, Teresa -- Henry, Jake Y -- Van Allen, Eliezer M -- Miao, Diana -- Schilling, Bastian -- Schadendorf, Dirk -- Garraway, Levi A -- Makarov, Vladimir -- Rizvi, Naiyer A -- Snyder, Alexandra -- Hellmann, Matthew D -- Merghoub, Taha -- Wolchok, Jedd D -- Shukla, Sachet A -- Wu, Catherine J -- Peggs, Karl S -- Chan, Timothy A -- Hadrup, Sine R -- Quezada, Sergio A -- Swanton, Charles -- 12100/Cancer Research UK/United Kingdom -- 1R01CA155010-02/CA/NCI NIH HHS/ -- 1R01CA182461-01/CA/NCI NIH HHS/ -- 1R01CA184922-01/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1463-9. doi: 10.1126/science.aaf1490. Epub 2016 Mar 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Francis Crick Institute, London WC2A 3LY, UK. Centre for Mathematics and Physics in the Life Sciences and Experimental Biology (CoMPLEX), University College London (UCL), London WC1E 6BT, UK. Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. ; Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. Cancer Immunology Unit, UCL Cancer Institute, UCL, London WC1E 6BT, UK. ; Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. ; Section for Immunology and Vaccinology, National Veterinary Institute, Technical University of Denmark, 1970 Frederiksberg C, Denmark. ; The Francis Crick Institute, London WC2A 3LY, UK. Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. ; The Francis Crick Institute, London WC2A 3LY, UK. ; Cancer Immunology Unit, UCL Cancer Institute, UCL, London WC1E 6BT, UK. Department of Cellular Pathology, UCL, London WC1E 6BT, UK. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Center for Cancer Precision Medicine, Dana-Farber Cancer Institute, Boston, MA 02215, USA. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Department of Dermatology, University Hospital, University Duisburg-Essen, 45147 Essen, Germany. German Cancer Consortium (DKTK), 69121 Heidelberg, Germany. ; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Hematology/Oncology Division, 177 Fort Washington Avenue, Columbia University, New York, NY 10032, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Weill Cornell Medical College, New York, NY 10065, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Ludwig Collaborative Laboratory, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Weill Cornell Medical College, New York, NY 10065, USA. Ludwig Collaborative Laboratory, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Department of Medicine, Harvard Medical School, Boston, MA 02115, USA. Department of Internal Medicine, Brigham and Woman's Hospital, Boston, MA 02115, USA. ; Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. Cancer Immunology Unit, UCL Cancer Institute, UCL, London WC1E 6BT, UK. s.quezada@ucl.ac.uk charles.swanton@crick.ac.uk. ; The Francis Crick Institute, London WC2A 3LY, UK. Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. s.quezada@ucl.ac.uk charles.swanton@crick.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26940869" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/drug therapy/genetics/*immunology ; Aged ; Aged, 80 and over ; Antigens, Neoplasm/genetics/*immunology ; Antineoplastic Agents/therapeutic use ; CD4-Positive T-Lymphocytes/*immunology ; CTLA-4 Antigen/immunology ; Carcinoma, Non-Small-Cell Lung/genetics/immunology ; Cell Cycle Checkpoints/immunology ; Female ; Humans ; *Immunologic Surveillance ; Lung Neoplasms/drug therapy/genetics/*immunology ; Lymphocytes, Tumor-Infiltrating/immunology ; Male ; Melanoma/immunology ; Middle Aged ; Mutation ; Programmed Cell Death 1 Receptor/immunology ; Skin Neoplasms/immunology
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  • 133
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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〉Edwards, Marc -- Bernstein, Rachel -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1230. doi: 10.1126/science.351.6278.1230.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rachel Bernstein is the editor of Science Careers. Send your story to SciCareerEditor@aaas.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965630" target="_blank"〉PubMed〈/a〉
    Keywords: Drinking Water/*analysis ; Humans ; Lead/*analysis ; Michigan ; *Water Purification
    Print ISSN: 0036-8075
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  • 134
    Publication Date: 2016-04-29
    Description: A decline in electron transport chain (ETC) activity is associated with many human diseases. Although diminished mitochondrial adenosine triphosphate production is recognized as a source of pathology, the contribution of the associated reduction in the ratio of the amount of oxidized nicotinamide adenine dinucleotide (NAD(+)) to that of its reduced form (NADH) is less clear. We used a water-forming NADH oxidase from Lactobacillus brevis (LbNOX) as a genetic tool for inducing a compartment-specific increase of the NAD(+)/NADH ratio in human cells. We used LbNOX to demonstrate the dependence of key metabolic fluxes, gluconeogenesis, and signaling on the cytosolic or mitochondrial NAD(+)/NADH ratios. Expression of LbNOX in the cytosol or mitochondria ameliorated proliferative and metabolic defects caused by an impaired ETC. The results underscore the role of reductive stress in mitochondrial pathogenesis and demonstrate the utility of targeted LbNOX for direct, compartment-specific manipulation of redox state.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850741/" 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/PMC4850741/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Titov, Denis V -- Cracan, Valentin -- Goodman, Russell P -- Peng, Jun -- Grabarek, Zenon -- Mootha, Vamsi K -- R01 GM099683/GM/NIGMS NIH HHS/ -- R01GM099683/GM/NIGMS NIH HHS/ -- T32 DK007191/DK/NIDDK NIH HHS/ -- T32DK007191/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):231-5. doi: 10.1126/science.aad4017. Epub 2016 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA. Department of Systems Biology, Harvard Medical School, Boston, MA, USA. Broad Institute, Cambridge, MA, USA. ; Howard Hughes Medical Institute and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA. Division of Gastroenterology, Massachusetts General Hospital, Boston, MA, USA. ; Howard Hughes Medical Institute and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA. ; Howard Hughes Medical Institute and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA. Broad Institute, Cambridge, MA, USA. ; Howard Hughes Medical Institute and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA. Department of Systems Biology, Harvard Medical School, Boston, MA, USA. Broad Institute, Cambridge, MA, USA. vamsi@hms.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124460" target="_blank"〉PubMed〈/a〉
    Keywords: Catalysis ; Cytosol/enzymology ; Electron Transport ; Electron Transport Chain Complex Proteins/genetics/*metabolism ; Genetic Complementation Test ; Gluconeogenesis/*genetics ; HeLa Cells ; Humans ; Lactobacillus brevis/enzymology/genetics ; Mitochondria/*metabolism ; Mitochondrial Diseases/enzymology/genetics ; Multienzyme Complexes/genetics/*metabolism ; NAD/*metabolism ; NADH, NADPH Oxidoreductases/genetics/*metabolism ; Oxidation-Reduction
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  • 135
    Publication Date: 2016-04-29
    Description: To explore the distinct genotypic and phenotypic states of melanoma tumors, we applied single-cell RNA sequencing (RNA-seq) to 4645 single cells isolated from 19 patients, profiling malignant, immune, stromal, and endothelial cells. Malignant cells within the same tumor displayed transcriptional heterogeneity associated with the cell cycle, spatial context, and a drug-resistance program. In particular, all tumors harbored malignant cells from two distinct transcriptional cell states, such that tumors characterized by high levels of the MITF transcription factor also contained cells with low MITF and elevated levels of the AXL kinase. Single-cell analyses suggested distinct tumor microenvironmental patterns, including cell-to-cell interactions. Analysis of tumor-infiltrating T cells revealed exhaustion programs, their connection to T cell activation and clonal expansion, and their variability across patients. Overall, we begin to unravel the cellular ecosystem of tumors and how single-cell genomics offers insights with implications for both targeted and immune therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tirosh, Itay -- Izar, Benjamin -- Prakadan, Sanjay M -- Wadsworth, Marc H 2nd -- Treacy, Daniel -- Trombetta, John J -- Rotem, Asaf -- Rodman, Christopher -- Lian, Christine -- Murphy, George -- Fallahi-Sichani, Mohammad -- Dutton-Regester, Ken -- Lin, Jia-Ren -- Cohen, Ofir -- Shah, Parin -- Lu, Diana -- Genshaft, Alex S -- Hughes, Travis K -- Ziegler, Carly G K -- Kazer, Samuel W -- Gaillard, Aleth -- Kolb, Kellie E -- Villani, Alexandra-Chloe -- Johannessen, Cory M -- Andreev, Aleksandr Y -- Van Allen, Eliezer M -- Bertagnolli, Monica -- Sorger, Peter K -- Sullivan, Ryan J -- Flaherty, Keith T -- Frederick, Dennie T -- Jane-Valbuena, Judit -- Yoon, Charles H -- Rozenblatt-Rosen, Orit -- Shalek, Alex K -- Regev, Aviv -- Garraway, Levi A -- 1U24CA180922/CA/NCI NIH HHS/ -- DP2 OD020839/OD/NIH HHS/ -- K99 CA194163/CA/NCI NIH HHS/ -- K99CA194163/CA/NCI NIH HHS/ -- P01CA163222/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- P50GM107618/GM/NIGMS NIH HHS/ -- R35CA197737/CA/NCI NIH HHS/ -- U54CA112962/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):189-96. doi: 10.1126/science.aad0501.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. Center for Cancer Precision Medicine, Dana-Farber Cancer Institute, Boston, MA 02215, USA. bizar@partners.org aregev@broadinstitute.org levi_garraway@dfci.harvard.edu. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Institute for Medical Engineering and Science, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA. Department of Chemistry, MIT, Cambridge, MA 02142, USA. Ragon Institute of Massachusetts General Hospital, MIT and Harvard University, Cambridge, MA 02139, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. Center for Cancer Precision Medicine, Dana-Farber Cancer Institute, Boston, MA 02215, USA. ; Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; Program in Therapeutic Sciences, Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia. ; HMS LINCS Center and Laboratory of Systems Pharmacology, Harvard Medical School, Boston, MA 02115, USA. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Institute for Medical Engineering and Science, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA. Ragon Institute of Massachusetts General Hospital, MIT and Harvard University, Cambridge, MA 02139, USA. Division of Health Sciences and Technology, Harvard Medical School, Boston, MA 02115, USA. ; Department of Surgical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. Department of Surgical Oncology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; Program in Therapeutic Sciences, Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA. HMS LINCS Center and Laboratory of Systems Pharmacology, Harvard Medical School, Boston, MA 02115, USA. Ludwig Center at Harvard, Boston, MA 02215, USA. ; Division of Medical Oncology, Massachusetts General Hospital Cancer Center, Boston, MA 02114, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Institute for Medical Engineering and Science, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA. Department of Chemistry, MIT, Cambridge, MA 02142, USA. Ragon Institute of Massachusetts General Hospital, MIT and Harvard University, Cambridge, MA 02139, USA. Division of Health Sciences and Technology, Harvard Medical School, Boston, MA 02115, USA. Department of Immunology, Massachusetts General Hospital, Boston, MA 02114, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Department of Biology and Koch Institute, MIT, Boston, MA 02142, USA. Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. bizar@partners.org aregev@broadinstitute.org levi_garraway@dfci.harvard.edu. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. bizar@partners.org aregev@broadinstitute.org levi_garraway@dfci.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124452" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Communication ; Cell Cycle ; Drug Resistance, Neoplasm/genetics ; Endothelial Cells/pathology ; Genomics ; Humans ; Immunotherapy ; Lymphocyte Activation ; Melanoma/*genetics/*secondary/therapy ; Microphthalmia-Associated Transcription Factor/metabolism ; Neoplasm Metastasis ; RNA/genetics ; Sequence Analysis, RNA ; Single-Cell Analysis ; Skin Neoplasms/*pathology ; Stromal Cells/pathology ; T-Lymphocytes/immunology/pathology ; Transcriptome ; *Tumor Microenvironment
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  • 136
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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〉Enserink, Martin -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1128-9. doi: 10.1126/science.351.6278.1128.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965600" target="_blank"〉PubMed〈/a〉
    Keywords: Blood Stains ; *Criminal Law ; DNA Fingerprinting/standards ; Evidence-Based Medicine/*legislation & jurisprudence/*trends ; Forensic Medicine/*legislation & jurisprudence/*trends ; Humans
    Print ISSN: 0036-8075
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  • 137
    Publication Date: 2016-01-28
    Description: Mitochondria undergo fragmentation in response to electron transport chain (ETC) poisons and mitochondrial DNA-linked disease mutations, yet how these stimuli mechanistically connect to the mitochondrial fission and fusion machinery is poorly understood. We found that the energy-sensing adenosine monophosphate (AMP)-activated protein kinase (AMPK) is genetically required for cells to undergo rapid mitochondrial fragmentation after treatment with ETC inhibitors. Moreover, direct pharmacological activation of AMPK was sufficient to rapidly promote mitochondrial fragmentation even in the absence of mitochondrial stress. A screen for substrates of AMPK identified mitochondrial fission factor (MFF), a mitochondrial outer-membrane receptor for DRP1, the cytoplasmic guanosine triphosphatase that catalyzes mitochondrial fission. Nonphosphorylatable and phosphomimetic alleles of the AMPK sites in MFF revealed that it is a key effector of AMPK-mediated mitochondrial fission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Toyama, Erin Quan -- Herzig, Sebastien -- Courchet, Julien -- Lewis, Tommy L Jr -- Loson, Oliver C -- Hellberg, Kristina -- Young, Nathan P -- Chen, Hsiuchen -- Polleux, Franck -- Chan, David C -- Shaw, Reuben J -- K99 NS091526/NS/NINDS NIH HHS/ -- K99NS091526/NS/NINDS NIH HHS/ -- P01 CA120964/CA/NCI NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- R01CA172229/CA/NCI NIH HHS/ -- R01DK080425/DK/NIDDK NIH HHS/ -- R01GM062967/GM/NIGMS NIH HHS/ -- R01GM110039/GM/NIGMS NIH HHS/ -- R01NS089456/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):275-81. doi: 10.1126/science.aab4138.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cell Biology Laboratory and Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, CA 92037, USA. ; Department of Neuroscience, Zuckerman Mind Brain Behavior Institute and Kavli Institute for Brain Science, Columbia University, New York, NY 10032, USA. ; Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA. ; Molecular and Cell Biology Laboratory and Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, CA 92037, USA. shaw@salk.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816379" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/chemistry/genetics/*metabolism ; Adenosine Monophosphate/metabolism ; Amino Acid Motifs ; Cell Line, Tumor ; Cytoplasm/enzymology ; Dactinomycin/analogs & derivatives/pharmacology ; *Energy Metabolism ; Enzyme Activation ; GTP Phosphohydrolases/genetics/metabolism ; Humans ; Microtubule-Associated Proteins/genetics/metabolism ; Mitochondria/drug effects/enzymology/*physiology ; *Mitochondrial Dynamics ; Mitochondrial Proteins/genetics/metabolism ; Molecular Sequence Data ; Rotenone/pharmacology ; *Stress, Physiological
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  • 138
    Publication Date: 2016-02-26
    Description: Transposable elements (TEs) are both a boon and a bane to eukaryotic organisms, depending on where they integrate into the genome and how their sequences function once integrated. We focus on two types of TEs: long interspersed elements (LINEs) and short interspersed elements (SINEs). LINEs and SINEs are retrotransposons; that is, they transpose via an RNA intermediate. We discuss how LINEs and SINEs have expanded in eukaryotic genomes and contribute to genome evolution. An emerging body of evidence indicates that LINEs and SINEs function to regulate gene expression by affecting chromatin structure, gene transcription, pre-mRNA processing, or aspects of mRNA metabolism. We also describe how adenosine-to-inosine editing influences SINE function and how ongoing retrotransposition is countered by the body's defense mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elbarbary, Reyad A -- Lucas, Bronwyn A -- Maquat, Lynne E -- P30 AR061307/AR/NIAMS NIH HHS/ -- R37 GM074593/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):aac7247. doi: 10.1126/science.aac7247. Epub 2016 Feb 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA. Center for RNA Biology, University of Rochester, Rochester, NY, USA. ; Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA. Center for RNA Biology, University of Rochester, Rochester, NY, USA. Department of Oncology, Wilmot Cancer Institute, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA. lynne_maquat@urmc.rochester.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912865" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/ultrastructure ; Disease/genetics ; Evolution, Molecular ; *Gene Expression Regulation ; Humans ; Long Interspersed Nucleotide Elements/genetics/*physiology ; Mice ; Protein Biosynthesis ; RNA Precursors/metabolism ; RNA Processing, Post-Transcriptional ; RNA Stability ; RNA, Messenger/metabolism ; Short Interspersed Nucleotide Elements/genetics/*physiology ; Transcription, Genetic
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  • 139
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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〉McLaughlin, Kathleen -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):283. doi: 10.1126/science.352.6283.283.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kathleen McLaughlin is a writer in Beijing.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081050" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Aging ; China/epidemiology ; *Family Relations ; Female ; Human Migration ; Humans ; Male ; Rural Population/*statistics & numerical data ; Sociology ; Suicide/*statistics & numerical data
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  • 140
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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 19;351(6275):791. doi: 10.1126/science.aaf4216.〈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/26912866" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Leadership ; Male ; Policy ; Sexual Harassment/*prevention & control ; Societies ; Students ; Women
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  • 141
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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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  • 142
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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〉Escobar, Herton -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):18. doi: 10.1126/science.352.6281.18.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034350" target="_blank"〉PubMed〈/a〉
    Keywords: *Antineoplastic Agents/chemical synthesis/chemistry/therapeutic use ; Brazil ; Clinical Trials as Topic ; Dosage Forms ; *Drug Approval ; Ethanolamines/chemical synthesis/chemistry/*therapeutic use ; Federal Government ; Humans ; Neoplasms/*drug therapy
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  • 143
    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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  • 144
    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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  • 145
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-29
    Description: Therapeutic advances in oncology have not fully translated to the treatment of metastatic disease, which remains largely incurable. Metastatic subclones can emerge both early and late in the life of the primary tumor. A better understanding of the genetic evolution of metastatic disease has the potential to reveal differences in the therapeutic vulnerabilities of primary and metastatic tumors, shed light on the temporal patterns of and routes to metastatic colonization, and provide insight into the biology of the metastatic process. Here we review recent comparative studies of primary and metastatic tumors, including data suggesting that macroevolutionary shifts (the onset of chromosomal instability) contribute to the evolution of metastatic disease. We also discuss the practical challenges associated with these studies and how they might be overcome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turajlic, Samra -- Swanton, Charles -- C50947/A18176/Cancer Research UK/United Kingdom -- Department of Health/United Kingdom -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):169-75. doi: 10.1126/science.aaf2784.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY2, UK. Renal and Skin Units, The Royal Marsden Hospital, London SW3 6JJ, UK. ; The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY2, UK. University College London Hospitals and Cancer Institute, Cancer Research UK Lung Cancer Centre of Excellence, Huntley Street, London WC1, UK. charles.swanton@crick.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124450" target="_blank"〉PubMed〈/a〉
    Keywords: Clone Cells/pathology ; *Evolution, Molecular ; Genetic Variation ; Humans ; Neoplasm Metastasis/*genetics/*pathology ; Neoplasms/classification/genetics/pathology ; Phylogeny
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  • 146
    Publication Date: 2016-01-30
    Description: Infection elicits CD4(+) memory T lymphocytes that participate in protective immunity. Although memory cells are the progeny of naive T cells, it is unclear that all naive cells from a polyclonal repertoire have memory cell potential. Using a single-cell adoptive transfer and spleen biopsy method, we found that in mice, essentially all microbe-specific naive cells produced memory cells during infection. Different clonal memory cell populations had different B cell or macrophage helper compositions that matched effector cell populations generated much earlier in the response. Thus, each microbe-specific naive CD4(+) T cell produces a distinctive ratio of effector cell types early in the immune response that is maintained as some cells in the clonal population become memory cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4776317/" 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/PMC4776317/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tubo, Noah J -- Fife, Brian T -- Pagan, Antonio J -- Kotov, Dmitri I -- Goldberg, Michael F -- Jenkins, Marc K -- F32 AI107995/AI/NIAID NIH HHS/ -- R01 AI039614/AI/NIAID NIH HHS/ -- R01 AI106791/AI/NIAID NIH HHS/ -- T32 HL007062/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):511-4. doi: 10.1126/science.aad0483.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immune Mediated Disease Therapy Group, Genzyme, a Sanofi Company, Framingham, MA 01701, USA. ; Department of Medicine, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. ; Department of Medicine, MRC Laboratory of Molecular Biology, Cambridge, UK. ; Department of Microbiology and Immunology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. ; Department of Microbiology and Immunology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. jenki002@umn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823430" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; B-Lymphocytes/immunology ; Bacterial Toxins/immunology ; CD4-Positive T-Lymphocytes/*immunology/*microbiology ; Clone Cells/immunology ; Heat-Shock Proteins/immunology ; Hemolysin Proteins/immunology ; *Immunologic Memory ; Listeria monocytogenes/*immunology ; Listeriosis/*immunology ; Mice ; Mice, Inbred C57BL ; Receptors, CXCR5/genetics/immunology ; Single-Cell Analysis
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  • 147
    Publication Date: 2016-04-30
    Description: Fecal microbiome variation in the average, healthy population has remained under-investigated. Here, we analyzed two independent, extensively phenotyped cohorts: the Belgian Flemish Gut Flora Project (FGFP; discovery cohort; N = 1106) and the Dutch LifeLines-DEEP study (LLDeep; replication; N = 1135). Integration with global data sets (N combined = 3948) revealed a 14-genera core microbiota, but the 664 identified genera still underexplore total gut diversity. Sixty-nine clinical and questionnaire-based covariates were found associated to microbiota compositional variation with a 92% replication rate. Stool consistency showed the largest effect size, whereas medication explained largest total variance and interacted with other covariate-microbiota associations. Early-life events such as birth mode were not reflected in adult microbiota composition. Finally, we found that proposed disease marker genera associated to host covariates, urging inclusion of the latter in study design.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Falony, Gwen -- Joossens, Marie -- Vieira-Silva, Sara -- Wang, Jun -- Darzi, Youssef -- Faust, Karoline -- Kurilshikov, Alexander -- Bonder, Marc Jan -- Valles-Colomer, Mireia -- Vandeputte, Doris -- Tito, Raul Y -- Chaffron, Samuel -- Rymenans, Leen -- Verspecht, Chloe -- De Sutter, Lise -- Lima-Mendez, Gipsi -- D'hoe, Kevin -- Jonckheere, Karl -- Homola, Daniel -- Garcia, Roberto -- Tigchelaar, Ettje F -- Eeckhaudt, Linda -- Fu, Jingyuan -- Henckaerts, Liesbet -- Zhernakova, Alexandra -- Wijmenga, Cisca -- Raes, Jeroen -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):560-4. doi: 10.1126/science.aad3503. Epub 2016 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉KU Leuven-University of Leuven, Department of Microbiology and Immunology, Leuven, Belgium. VIB, Center for the Biology of Disease, Leuven, Belgium. ; KU Leuven-University of Leuven, Department of Microbiology and Immunology, Leuven, Belgium. VIB, Center for the Biology of Disease, Leuven, Belgium. Vrije Universiteit Brussel, Faculty of Sciences and Bioengineering Sciences, Microbiology Unit, Brussels, Belgium. ; Institute of Chemical Biology and Fundamental Medicine SB RAS, Novosibirsk, Russia. Novosibirsk State University, Novosibirsk, Russia. ; University of Groningen, University Medical Center Groningen, Department of Genetics, 9700 RB Groningen, Netherlands. ; VIB, Center for the Biology of Disease, Leuven, Belgium. Vrije Universiteit Brussel, Faculty of Sciences and Bioengineering Sciences, Microbiology Unit, Brussels, Belgium. ; University of Groningen, University Medical Center Groningen, Department of Genetics, 9700 RB Groningen, Netherlands. Top Institute Food and Nutrition, Wageningen, Netherlands. ; University of Groningen, University Medical Center Groningen, Department of Genetics, 9700 RB Groningen, Netherlands. University of Groningen, University Medical Center Groningen, Department of Pediatrics, 9700 RB Groningen, Netherlands. ; KU Leuven-University of Leuven, Department of Microbiology and Immunology, Leuven, Belgium. KU Leuven-University Hospitals Leuven, Department of General Internal Medicine, Leuven, Belgium. ; KU Leuven-University of Leuven, Department of Microbiology and Immunology, Leuven, Belgium. VIB, Center for the Biology of Disease, Leuven, Belgium. Vrije Universiteit Brussel, Faculty of Sciences and Bioengineering Sciences, Microbiology Unit, Brussels, Belgium. jeroen.raes@kuleuven.be.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126039" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteria/*classification/genetics/isolation & purification ; Belgium ; Cohort Studies ; Drug Interactions ; Feces/microbiology ; *Gastrointestinal Microbiome ; Humans
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  • 148
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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〉Tuting, Thomas -- de Visser, Karin E -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):145-6. doi: 10.1126/science.aaf7300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, University Hospital Magdeburg, Magdeburg, Germany. ; Division of Immunology, The Netherlands Cancer Institute, Amsterdam, Netherlands. k.d.visser@nki.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124439" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bystander Effect ; Humans ; Immunotherapy/methods ; Leukocyte Count ; Mice ; Mice, Transgenic ; Neoplasm Metastasis/*immunology/*therapy ; Neoplasms, Experimental/immunology/pathology/therapy ; Neutrophils/*immunology/*pathology
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  • 149
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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〉Underwood, Emily -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):799-800. doi: 10.1126/science.351.6275.799.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912871" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Brain Mapping/economics/*methods ; DNA/*analysis ; Financing, Organized ; Fluorescence ; Mice ; Nerve Net/physiology ; Neurons/*chemistry ; Neurosciences/economics/trends ; RNA/*analysis ; Synapses/*physiology
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  • 150
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farrell, Anthony P -- Franklin, Craig E -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):132-3. doi: 10.1126/science.351.6269.132-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of British Columbia, Vancouver, BC V6T1Z4, Canada. farrellt@mail.ubc.ca. ; School of Biological Sciences, The University of Queensland, St. Lucia, QLD 4072, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744399" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds/*classification ; *Climate Change ; *Endangered Species ; Fishes/*classification ; Mammals/*classification ; Turtles/*classification
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  • 151
    Publication Date: 2016-03-26
    Description: Brazil has experienced an unprecedented epidemic of Zika virus (ZIKV), with ~30,000 cases reported to date. ZIKV was first detected in Brazil in May 2015, and cases of microcephaly potentially associated with ZIKV infection were identified in November 2015. We performed next-generation sequencing to generate seven Brazilian ZIKV genomes sampled from four self-limited cases, one blood donor, one fatal adult case, and one newborn with microcephaly and congenital malformations. Results of phylogenetic and molecular clock analyses show a single introduction of ZIKV into the Americas, which we estimated to have occurred between May and December 2013, more than 12 months before the detection of ZIKV in Brazil. The estimated date of origin coincides with an increase in air passengers to Brazil from ZIKV-endemic areas, as well as with reported outbreaks in the Pacific Islands. ZIKV genomes from Brazil are phylogenetically interspersed with those from other South American and Caribbean countries. Mapping mutations onto existing structural models revealed the context of viral amino acid changes present in the outbreak lineage; however, no shared amino acid changes were found among the three currently available virus genomes from microcephaly cases. Municipality-level incidence data indicate that reports of suspected microcephaly in Brazil best correlate with ZIKV incidence around week 17 of pregnancy, although this correlation does not demonstrate causation. Our genetic description and analysis of ZIKV isolates in Brazil provide a baseline for future studies of the evolution and molecular epidemiology of this emerging virus in the Americas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faria, Nuno Rodrigues -- Azevedo, Raimunda do Socorro da Silva -- Kraemer, Moritz U G -- Souza, Renato -- Cunha, Mariana Sequetin -- Hill, Sarah C -- Theze, Julien -- Bonsall, Michael B -- Bowden, Thomas A -- Rissanen, Ilona -- Rocco, Iray Maria -- Nogueira, Juliana Silva -- Maeda, Adriana Yurika -- Vasami, Fernanda Giseli da Silva -- Macedo, Fernando Luiz de Lima -- Suzuki, Akemi -- Rodrigues, Sueli Guerreiro -- Cruz, Ana Cecilia Ribeiro -- Nunes, Bruno Tardeli -- Medeiros, Daniele Barbosa de Almeida -- Rodrigues, Daniela Sueli Guerreiro -- Nunes Queiroz, Alice Louize -- da Silva, Eliana Vieira Pinto -- Henriques, Daniele Freitas -- Travassos da Rosa, Elisabeth Salbe -- de Oliveira, Consuelo Silva -- Martins, Livia Caricio -- Vasconcelos, Helena Baldez -- Casseb, Livia Medeiros Neves -- Simith, Darlene de Brito -- Messina, Jane P -- Abade, Leandro -- Lourenco, Jose -- Carlos Junior Alcantara, Luiz -- de Lima, Maricelia Maia -- Giovanetti, Marta -- Hay, Simon I -- de Oliveira, Rodrigo Santos -- Lemos, Poliana da Silva -- de Oliveira, Layanna Freitas -- de Lima, Clayton Pereira Silva -- da Silva, Sandro Patroca -- de Vasconcelos, Janaina Mota -- Franco, Luciano -- Cardoso, Jedson Ferreira -- Vianez-Junior, Joao Lidio da Silva Goncalves -- Mir, Daiana -- Bello, Gonzalo -- Delatorre, Edson -- Khan, Kamran -- Creatore, Marisa -- Coelho, Giovanini Evelim -- de Oliveira, Wanderson Kleber -- Tesh, Robert -- Pybus, Oliver G -- Nunes, Marcio R T -- Vasconcelos, Pedro F C -- 090532/Z/09/Z/Wellcome Trust/United Kingdom -- 095066/Wellcome Trust/United Kingdom -- 102427/Wellcome Trust/United Kingdom -- MR/L009528/1/Medical Research Council/United Kingdom -- R24 AT 120942/AT/NCCIH NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):345-9. doi: 10.1126/science.aaf5036. Epub 2016 Mar 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Technological Innovation, Evandro Chagas Institute, Ministry of Health, Ananindeua, PA 67030-000, Brazil. Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. ; Department of Arbovirology and Hemorrhagic Fevers, Evandro Chagas Institute, Ministry of Health, Ananindeua, Para State, Brazil. ; Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. ; Instituto Adolfo Lutz, University of Sao Paulo, Sao Paulo, Brazil. ; Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK. ; Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. Metabiota, San Francisco, CA 94104, USA. ; Oswaldo Cruz Foundation (FIOCRUZ), Salvador, Bahia, Brazil. ; Centre of Post Graduation in Collective Health, Department of Health, Universidade Estadual de Feira de Santana, Feira de Santana, Bahia, Brazil. ; Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA 98121, USA. Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK. ; Center for Technological Innovation, Evandro Chagas Institute, Ministry of Health, Ananindeua, PA 67030-000, Brazil. ; Laboratorio de AIDS and Imunologia Molecular, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil. ; Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada. Department of Medicine, Division of Infectious Diseases, University of Toronto, Toronto, Ontario, Canada. ; Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada. ; Brazilian Ministry of Health, Brasilia, Brazil. ; Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA. ; Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. Metabiota, San Francisco, CA 94104, USA. oliver.pybus@zoo.ox.ac.uk marcionunesbrasil@yahoo.com.br pedrovasconcelos@iec.pa.gov.br. ; Center for Technological Innovation, Evandro Chagas Institute, Ministry of Health, Ananindeua, PA 67030-000, Brazil. Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA. oliver.pybus@zoo.ox.ac.uk marcionunesbrasil@yahoo.com.br pedrovasconcelos@iec.pa.gov.br. ; Department of Arbovirology and Hemorrhagic Fevers, Evandro Chagas Institute, Ministry of Health, Ananindeua, Para State, Brazil. oliver.pybus@zoo.ox.ac.uk marcionunesbrasil@yahoo.com.br pedrovasconcelos@iec.pa.gov.br.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013429" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/virology ; Americas/epidemiology ; Animals ; *Disease Outbreaks ; Female ; Genome, Viral/genetics ; Humans ; Incidence ; Insect Vectors/virology ; Microcephaly/*epidemiology/virology ; Molecular Epidemiology ; Molecular Sequence Data ; Mutation ; Pacific Islands/epidemiology ; Phylogeny ; Pregnancy ; RNA, Viral/genetics ; Sequence Analysis, RNA ; Travel ; Zika Virus/classification/*genetics/isolation & purification ; Zika Virus Infection/*epidemiology/transmission/*virology
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  • 152
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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〉Underwood, Emily -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):212-3. doi: 10.1126/science.351.6270.212.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816355" target="_blank"〉PubMed〈/a〉
    Keywords: Advertising as Topic/legislation & jurisprudence ; Brain/*physiology ; Cognition ; Humans ; *Learning ; Neuronal Plasticity ; Neurosciences/*legislation & jurisprudence ; Simulation Training/*legislation & jurisprudence ; Software/*legislation & jurisprudence ; Video Games/*legislation & jurisprudence
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  • 153
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):116-9. doi: 10.1126/science.351.6269.116.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744391" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies/*therapeutic use ; Clinical Trials as Topic ; *Cortical Spreading Depression/drug effects/immunology/physiology ; Drug Design ; Drug Industry ; Female ; Humans ; Male ; Migraine Disorders/*immunology/physiopathology/*therapy ; Receptors, Calcitonin Gene-Related Peptide/*antagonists & inhibitors/immunology ; Sex Ratio
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  • 154
    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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  • 155
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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〉Fearnside, Philip M -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):456-7. doi: 10.1126/science.351.6272.456-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute for Research in Amazonia (INPA), Manaus, Amazonas, 69067-375, Brazil. pmfearn@inpa.gov.br.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823417" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; *Fishes ; *Power Plants ; *Rivers
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  • 156
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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〉Underwood, Emily -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):397. doi: 10.1126/science.352.6284.397.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102458" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/*physiology ; Cadaver ; Humans ; Neurosciences/*trends ; *Transcranial Direct Current Stimulation
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  • 157
    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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  • 158
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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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  • 159
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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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  • 160
    Publication Date: 2016-01-02
    Description: Motivation for reward drives adaptive behaviors, whereas impairment of reward perception and experience (anhedonia) can contribute to psychiatric diseases, including depression and schizophrenia. We sought to test the hypothesis that the medial prefrontal cortex (mPFC) controls interactions among specific subcortical regions that govern hedonic responses. By using optogenetic functional magnetic resonance imaging to locally manipulate but globally visualize neural activity in rats, we found that dopamine neuron stimulation drives striatal activity, whereas locally increased mPFC excitability reduces this striatal response and inhibits the behavioral drive for dopaminergic stimulation. This chronic mPFC overactivity also stably suppresses natural reward-motivated behaviors and induces specific new brainwide functional interactions, which predict the degree of anhedonia in individuals. These findings describe a mechanism by which mPFC modulates expression of reward-seeking behavior, by regulating the dynamical interactions between specific distant subcortical regions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772156/" 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/PMC4772156/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferenczi, Emily A -- Zalocusky, Kelly A -- Liston, Conor -- Grosenick, Logan -- Warden, Melissa R -- Amatya, Debha -- Katovich, Kiefer -- Mehta, Hershel -- Patenaude, Brian -- Ramakrishnan, Charu -- Kalanithi, Paul -- Etkin, Amit -- Knutson, Brian -- Glover, Gary H -- Deisseroth, Karl -- 1F31MH105151_01/MH/NIMH NIH HHS/ -- P41 EB015891/EB/NIBIB NIH HHS/ -- R00 MH097822/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):aac9698. doi: 10.1126/science.aac9698.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, Stanford University, Stanford, CA 94305, USA. Neurosciences Program, Stanford University, Stanford, CA 94305, USA. ; Brain Mind Research Institute, Weill Cornell Medical College, New York, NY 10065, USA. ; Department of Neurobiology and Behavior, Cornell University, Ithaca, NY 14853, USA. ; Department of Bioengineering, Stanford University, Stanford, CA 94305, USA. ; Department of Psychology, Stanford University, Stanford, CA 94305, USA. ; Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA 94305, USA. ; Department of Neurosurgery, Stanford University, Stanford, CA 94305, USA. ; Department of Radiology, Stanford University, Stanford, CA, 94305, USA. ; Department of Bioengineering, Stanford University, Stanford, CA 94305, USA. Department of Neurobiology and Behavior, Cornell University, Ithaca, NY 14853, USA. Howard Hughes Medical Institute, Stanford University, Stanford, CA, 94305, USA. deissero@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26722001" target="_blank"〉PubMed〈/a〉
    Keywords: Anhedonia/*physiology ; Animals ; Brain Mapping ; Corpus Striatum/cytology/drug effects/*physiology ; Depressive Disorder/physiopathology ; Dopamine/pharmacology ; Dopaminergic Neurons/drug effects/*physiology ; Female ; Magnetic Resonance Imaging ; Male ; Mesencephalon/cytology/drug effects/physiology ; *Motivation ; Nerve Net/physiology ; Oxygen/blood ; Prefrontal Cortex/cytology/drug effects/*physiology ; Rats ; Rats, Inbred LEC ; Rats, Sprague-Dawley ; *Reward ; Schizophrenia/physiopathology
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  • 161
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    Publication Date: 2016-01-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mervis, Jeffrey -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):216. doi: 10.1126/science.351.6270.216. Epub 2016 Jan 14.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816359" target="_blank"〉PubMed〈/a〉
    Keywords: Astronomy/education ; California ; *Faculty ; Humans ; Male ; Sexual Harassment/*legislation & jurisprudence ; Universities
    Print ISSN: 0036-8075
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  • 162
    Publication Date: 2016-01-28
    Description: Vocal imitation involves incorporating instructive auditory information into relevant motor circuits through processes that are poorly understood. In zebra finches, we found that exposure to a tutor's song drives spiking activity within premotor neurons in the juvenile, whereas inhibition suppresses such responses upon learning in adulthood. We measured inhibitory currents evoked by the tutor song throughout development while simultaneously quantifying each bird's learning trajectory. Surprisingly, we found that the maturation of synaptic inhibition onto premotor neurons is correlated with learning but not age. We used synthetic tutoring to demonstrate that inhibition is selective for specific song elements that have already been learned and not those still in refinement. Our results suggest that structured inhibition plays a crucial role during song acquisition, enabling a piece-by-piece mastery of complex tasks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vallentin, Daniela -- Kosche, Georg -- Lipkind, Dina -- Long, Michael A -- R01NS075044/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):267-71. doi: 10.1126/science.aad3023.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉NYU Neuroscience Institute and Department of Otolaryngology, New York University Langone Medical Center, New York, NY 10016, USA. Center for Neural Science, New York University, New York, NY 10003, USA. ; Laboratory of Vocal Learning, Department of Psychology, Hunter College, New York, NY 10065, USA. ; NYU Neuroscience Institute and Department of Otolaryngology, New York University Langone Medical Center, New York, NY 10016, USA. Center for Neural Science, New York University, New York, NY 10003, USA. mlong@med.nyu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816377" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Finches/*physiology ; High Vocal Center/*physiology ; *Learning ; Male ; Motor Neurons/physiology ; Music ; *Neural Inhibition ; Neural Pathways/*physiology ; Prosencephalon/physiology ; Synapses/physiology ; *Vocalization, Animal
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  • 163
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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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  • 164
    Publication Date: 2016-03-19
    Description: Although Neandertal sequences that persist in the genomes of modern humans have been identified in Eurasians, comparable studies in people whose ancestors hybridized with both Neandertals and Denisovans are lacking. We developed an approach to identify DNA inherited from multiple archaic hominin ancestors and applied it to whole-genome sequences from 1523 geographically diverse individuals, including 35 previously unknown Island Melanesian genomes. In aggregate, we recovered 1.34 gigabases and 303 megabases of the Neandertal and Denisovan genome, respectively. We use these maps of archaic sequences to show that Neandertal admixture occurred multiple times in different non-African populations, characterize genomic regions that are significantly depleted of archaic sequences, and identify signatures of adaptive introgression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vernot, Benjamin -- Tucci, Serena -- Kelso, Janet -- Schraiber, Joshua G -- Wolf, Aaron B -- Gittelman, Rachel M -- Dannemann, Michael -- Grote, Steffi -- McCoy, Rajiv C -- Norton, Heather -- Scheinfeldt, Laura B -- Merriwether, David A -- Koki, George -- Friedlaender, Jonathan S -- Wakefield, Jon -- Paabo, Svante -- Akey, Joshua M -- 5R01GM110068/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):235-9. doi: 10.1126/science.aad9416. Epub 2016 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genome Sciences, University of Washington, Seattle, Washington, USA. ; Department of Genome Sciences, University of Washington, Seattle, Washington, USA. Department of Life Sciences and Biotechnology, University of Ferrara, Italy. ; Department of Evolutionary Genetics, Max-Planck-Institute for Evolutionary Anthropology, Leipzig, Germany. ; Department of Anthropology, University of Cincinnati, Cincinnati, OH, USA. ; Department of Biology and Institute for Genomics and Evolutionary Medicine, Temple University, Philadelphia, PA, USA. ; Department of Anthropology, Binghamton University, Binghamton, NY, USA. ; Institute for Medical Research, Goroka, Eastern Highlands Province, Papua New Guinea. ; Department of Anthropology, Temple University, Philadelphia PA, USA. ; Department of Statistics, University of Washington, Seattle, Washington, USA. ; Department of Evolutionary Genetics, Max-Planck-Institute for Evolutionary Anthropology, Leipzig, Germany. paabo@eva.mpg.de akeyj@uw.edu. ; Department of Genome Sciences, University of Washington, Seattle, Washington, USA. paabo@eva.mpg.de akeyj@uw.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989198" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA/*genetics ; Genetic Variation ; Genome, Human/*genetics ; Humans ; Melanesia ; Neanderthals/*genetics ; Oceanic Ancestry Group/*genetics ; Sequence Analysis, DNA
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  • 165
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: Berkowitz et al. (Reports, 9 October 2015, p. 196) described a randomized field experiment testing whether a math app designed to increase parent-child interaction could also bring academic benefits. A reanalysis of the data suggests that this well-designed trial failed to find strong evidence for the efficacy of the intervention. In particular, there was no significant effect of the intervention on math performance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frank, Michael C -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1161. doi: 10.1126/science.aad8008. Epub 2016 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Stanford University, Stanford, CA, USA. mcfrank@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965619" target="_blank"〉PubMed〈/a〉
    Keywords: *Educational Status ; Female ; Humans ; *Intergenerational Relations ; Male ; Mathematics/*education ; *Parent-Child Relations ; Students/*psychology
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  • 166
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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〉Michelucci, Pietro -- Dickinson, Janis L -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):32-3. doi: 10.1126/science.aad6499.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Computation Institute, Fairfax, VA 22032, USA. pem@humancomputation.org. ; Cornell Lab of Ornithology, Cornell University, Ithaca, NY 14850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721991" target="_blank"〉PubMed〈/a〉
    Keywords: *Computers ; Humans ; *Problem Solving ; Task Performance and Analysis
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  • 167
    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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    Publication Date: 2016-05-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Midorikawa, Sanae -- Suzuki, Satoru -- Ohtsuru, Akira -- New York, N.Y. -- Science. 2016 May 6;352(6286):666-7. doi: 10.1126/science.352.6286.666-c.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Radiation Medical Science Center, Fukushima Medical University, Fukushima, 960-1295, Japan. Department of Radiation Health Management, Fukushima Medical University, Fukushima, 960-1295, Japan. hana@fmu.ac.jp. ; Radiation Medical Science Center, Fukushima Medical University, Fukushima, 960-1295, Japan. Department of Thyroid and Endocrinology, Fukushima Medical University, Fukushima, 960-1295, Japan. ; Radiation Medical Science Center, Fukushima Medical University, Fukushima, 960-1295, Japan. Department of Radiation Health Management, Fukushima Medical University, Fukushima, 960-1295, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27151857" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Radiation-Induced/*epidemiology ; *Disasters ; *Epidemics ; Female ; *Fukushima Nuclear Accident ; Humans ; Radiation Exposure/*adverse effects ; Thyroid Gland/*abnormalities/*pathology ; Thyroid Neoplasms/*epidemiology
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  • 169
    Publication Date: 2016-03-19
    Description: Steroids regulate cell proliferation, tissue development, and cell signaling via two pathways: a nuclear receptor mechanism and genome-independent signaling. Sperm activation, egg maturation, and steroid-induced anesthesia are executed via the latter pathway, the key components of which remain unknown. Here, we present characterization of the human sperm progesterone receptor that is conveyed by the orphan enzyme alpha/beta hydrolase domain-containing protein 2 (ABHD2). We show that ABHD2 is highly expressed in spermatozoa, binds progesterone, and acts as a progesterone-dependent lipid hydrolase by depleting the endocannabinoid 2-arachidonoylglycerol (2AG) from plasma membrane. The 2AG inhibits the sperm calcium channel (CatSper), and its removal leads to calcium influx via CatSper and ensures sperm activation. This study reveals that progesterone-activated endocannabinoid depletion by ABHD2 is a general mechanism by which progesterone exerts its genome-independent action and primes sperm for fertilization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Melissa R -- Mannowetz, Nadja -- Iavarone, Anthony T -- Safavi, Rojin -- Gracheva, Elena O -- Smith, James F -- Hill, Rose Z -- Bautista, Diana M -- Kirichok, Yuriy -- Lishko, Polina V -- 1S10OD020062-01/OD/NIH HHS/ -- R01 AR059385/AR/NIAMS NIH HHS/ -- R01AR059385/AR/NIAMS NIH HHS/ -- R01GM111802/GM/NIGMS NIH HHS/ -- R01HD068914/HD/NICHD NIH HHS/ -- R21HD081403/HD/NICHD NIH HHS/ -- S10RR025622/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):555-9. doi: 10.1126/science.aad6887. Epub 2016 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA. ; QB3/Chemistry Mass Spectrometry Facility, University of California, Berkeley, CA 94720, USA. ; Department of Cellular and Molecular Physiology; Department of Neuroscience, Program in Cellular Neuroscience, Neurodegeneration, and Repair (CNNR), Yale School of Medicine, Yale University, New Haven, CT 06536, USA. ; Department of Urology, University of California, San Francisco, CA 94143, USA. ; Department of Physiology, University of California, San Francisco, CA 94158, USA. ; Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA. lishko@berkeley.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989199" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Arachidonic Acids/*deficiency ; Calcium/metabolism ; Calcium Channels/metabolism ; Calcium Signaling ; Cell Membrane/metabolism ; Endocannabinoids/*deficiency ; Fertilization ; Glycerides/*deficiency ; Humans ; Hydrolases/genetics/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Progesterone/*metabolism/pharmacology ; Rats ; Rats, Wistar ; Receptors, Progesterone/genetics/*metabolism ; Sperm Motility/drug effects/*physiology ; Spermatozoa/drug effects/metabolism/*physiology ; Young Adult
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  • 170
    Publication Date: 2016-02-27
    Description: Ebola virus causes hemorrhagic fever with a high case fatality rate for which there is no approved therapy. Two human monoclonal antibodies, mAb100 and mAb114, in combination, protect nonhuman primates against all signs of Ebola virus disease, including viremia. Here, we demonstrate that mAb100 recognizes the base of the Ebola virus glycoprotein (GP) trimer, occludes access to the cathepsin-cleavage loop, and prevents the proteolytic cleavage of GP that is required for virus entry. We show that mAb114 interacts with the glycan cap and inner chalice of GP, remains associated after proteolytic removal of the glycan cap, and inhibits binding of cleaved GP to its receptor. These results define the basis of neutralization for two protective antibodies and may facilitate development of therapies and vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Misasi, John -- Gilman, Morgan S A -- Kanekiyo, Masaru -- Gui, Miao -- Cagigi, Alberto -- Mulangu, Sabue -- Corti, Davide -- Ledgerwood, Julie E -- Lanzavecchia, Antonio -- Cunningham, James -- Muyembe-Tamfun, Jean Jacques -- Baxa, Ulrich -- Graham, Barney S -- Xiang, Ye -- Sullivan, Nancy J -- McLellan, Jason S -- 5K08AI079381/AI/NIAID NIH HHS/ -- HHSN261200800001E/PHS HHS/ -- T32GM008704/GM/NIGMS NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1343-6. doi: 10.1126/science.aad6117. Epub 2016 Feb 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Division of Infectious Diseases, Boston Children's Hospital, Boston, MA 02215, USA. ; Department of Biochemistry, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA. ; Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. ; Centre for Infectious Diseases Research, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Beijing Advanced Innovation Center for Structural Biology, Department of Basic Medical Sciences, School of Medicine, Tsinghua University, Beijing 100084 China. ; Institute for Research in Biomedicine, Universita della Svizzera Italiana, CH-6500 Bellinzona, Switzerland. ; Institute for Research in Biomedicine, Universita della Svizzera Italiana, CH-6500 Bellinzona, Switzerland. Institute of Microbiology, ETH Zurich, CH-8093 Zurich, Switzerland. ; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; National Institute for Biomedical Research, National Laboratory of Public Health, Kinshasa B.P. 1197, Democratic Republic of the Congo. ; Electron Microscopy Laboratory, Cancer Research Technology Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA. ; Centre for Infectious Diseases Research, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Beijing Advanced Innovation Center for Structural Biology, Department of Basic Medical Sciences, School of Medicine, Tsinghua University, Beijing 100084 China. njsull@mail.nih.gov yxiang@mail.tsinghua.edu.cn. ; Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. njsull@mail.nih.gov yxiang@mail.tsinghua.edu.cn.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26917592" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal/*chemistry/immunology ; Antibodies, Neutralizing/*chemistry/immunology ; Antibodies, Viral/*chemistry/immunology ; Cathepsins/chemistry ; Cryoelectron Microscopy ; Crystallography, X-Ray ; Ebolavirus/*immunology ; Hemorrhagic Fever, Ebola/immunology/*prevention & control ; Humans ; Protein Conformation ; Proteolysis ; Viral Envelope Proteins/chemistry/*immunology
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  • 171
    Publication Date: 2016-04-23
    Description: Progression through the stages of lymphocyte development requires coordination of the cell cycle. Such coordination ensures genomic integrity while cells somatically rearrange their antigen receptor genes [in a process called variable-diversity-joining (VDJ) recombination] and, upon successful rearrangement, expands the pools of progenitor lymphocytes. Here we show that in developing B lymphocytes, the RNA-binding proteins (RBPs) ZFP36L1 and ZFP36L2 are critical for maintaining quiescence before precursor B cell receptor (pre-BCR) expression and for reestablishing quiescence after pre-BCR-induced expansion. These RBPs suppress an evolutionarily conserved posttranscriptional regulon consisting of messenger RNAs whose protein products cooperatively promote transition into the S phase of the cell cycle. This mechanism promotes VDJ recombination and effective selection of cells expressing immunoglobulin-mu at the pre-BCR checkpoint.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galloway, Alison -- Saveliev, Alexander -- Lukasiak, Sebastian -- Hodson, Daniel J -- Bolland, Daniel -- Balmanno, Kathryn -- Ahlfors, Helena -- Monzon-Casanova, Elisa -- Mannurita, Sara Ciullini -- Bell, Lewis S -- Andrews, Simon -- Diaz-Munoz, Manuel D -- Cook, Simon J -- Corcoran, Anne -- Turner, Martin -- Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):453-9. doi: 10.1126/science.aad5978.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Cambridge CB22 3AT, UK. ; Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Cambridge CB22 3AT, UK. Department of Haematology, University of Cambridge, The Clifford Allbutt Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0AH, UK. ; Laboratory of Nuclear Dynamics, The Babraham Institute, Cambridge CB22 3AT, UK. ; Laboratory of Signalling, The Babraham Institute, Cambridge CB22 3AT, UK. ; Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Cambridge CB22 3AT, UK. Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK. ; Bioinformatics Group, The Babraham Institute, Cambridge CB22 3AT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102483" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*cytology ; Conserved Sequence ; Cyclins/metabolism ; G0 Phase/genetics/physiology ; G1 Phase/genetics/physiology ; Gene Expression Regulation ; Immunoglobulin mu-Chains/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nuclear Proteins/genetics/*physiology ; Pre-B Cell Receptors ; RNA, Messenger/metabolism ; RNA-Binding Proteins/genetics/*physiology ; S Phase/genetics/*physiology ; Selection, Genetic ; Transcription, Genetic ; Tristetraprolin/genetics/*physiology ; V(D)J Recombination
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  • 172
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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〉Vogel, Gretchen -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1123-4. doi: 10.1126/science.351.6278.1123.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965596" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/*abnormalities/*virology ; Female ; Humans ; Infant ; Microcephaly/*virology ; Pregnancy ; Pregnancy Complications, Infectious/*virology ; World Health Organization ; *Zika Virus ; Zika Virus Infection/*complications
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  • 173
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-05-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyazaki, Makoto -- Tanigawa, Koichi -- Murakami, Michio -- New York, N.Y. -- Science. 2016 May 6;352(6286):666. doi: 10.1126/science.352.6286.666-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Health Management, Fukushima Medical University, Fukushima, 960-1295, Japan. ; Fukushima Global Medical Science Center, Fukushima Medical University, Fukushima, 960-1295, Japan. tanigawa@fmu.ac.jp. ; Department of Risk Communication, Fukushima Medical University, Fukushima, 960-1295, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27151856" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Radiation-Induced/*epidemiology ; *Disasters ; *Epidemics ; Female ; *Fukushima Nuclear Accident ; Humans ; Radiation Exposure/*adverse effects ; Thyroid Gland/*abnormalities/*pathology ; Thyroid Neoplasms/*epidemiology
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  • 174
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):110-1. doi: 10.1126/science.351.6269.110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744386" target="_blank"〉PubMed〈/a〉
    Keywords: Brazil/epidemiology ; Communicable Diseases, Emerging/*epidemiology/*virology ; *Disease Outbreaks ; Female ; Fetal Blood/virology ; Flavivirus/isolation & purification/physiology ; Flavivirus Infections/diagnosis/*epidemiology ; Humans ; Infant ; Infant, Newborn ; Microcephaly/diagnosis/*epidemiology/*virology ; Pregnancy ; Pregnancy Complications, Infectious/*virology ; Virus Activation
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  • 175
    Publication Date: 2016-01-23
    Description: Ecological intensification, or the improvement of crop yield through enhancement of biodiversity, may be a sustainable pathway toward greater food supplies. Such sustainable increases may be especially important for the 2 billion people reliant on small farms, many of which are undernourished, yet we know little about the efficacy of this approach. Using a coordinated protocol across regions and crops, we quantify to what degree enhancing pollinator density and richness can improve yields on 344 fields from 33 pollinator-dependent crop systems in small and large farms from Africa, Asia, and Latin America. For fields less than 2 hectares, we found that yield gaps could be closed by a median of 24% through higher flower-visitor density. For larger fields, such benefits only occurred at high flower-visitor richness. Worldwide, our study demonstrates that ecological intensification can create synchronous biodiversity and yield outcomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garibaldi, Lucas A -- Carvalheiro, Luisa G -- Vaissiere, Bernard E -- Gemmill-Herren, Barbara -- Hipolito, Juliana -- Freitas, Breno M -- Ngo, Hien T -- Azzu, Nadine -- Saez, Agustin -- Astrom, Jens -- An, Jiandong -- Blochtein, Betina -- Buchori, Damayanti -- Chamorro Garcia, Fermin J -- Oliveira da Silva, Fabiana -- Devkota, Kedar -- Ribeiro, Marcia de Fatima -- Freitas, Leandro -- Gaglianone, Maria C -- Goss, Maria -- Irshad, Mohammad -- Kasina, Muo -- Pacheco Filho, Alipio J S -- Kiill, Lucia H Piedade -- Kwapong, Peter -- Parra, Guiomar Nates -- Pires, Carmen -- Pires, Viviane -- Rawal, Ranbeer S -- Rizali, Akhmad -- Saraiva, Antonio M -- Veldtman, Ruan -- Viana, Blandina F -- Witter, Sidia -- Zhang, Hong -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):388-91. doi: 10.1126/science.aac7287.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instituto de Investigaciones en Recursos Naturales, Agroecologia y Desarrollo Rural (IRNAD), Sede Andina, Universidad Nacional de Rio Negro (UNRN) and Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET), Mitre 630, CP 8400, San Carlos de Bariloche, Rio Negro, Argentina. lgaribaldi@unrn.edu.ar. ; Departamento de Ecologia, Universidade de Brasilia, Campus Universitario Darcy Ribeiro, Brasilia - DF, 70910-900, Brazil; Centre for Ecology, Evolution and Environmental Changes (CE3C), Faculdade de Ciencias da Universidade de Lisboa 1749-016 Lisboa, Portugal & Naturalis Biodiversity Center, postbus 9517, 2300, RA, Leiden, Netherlands. ; Institut national de la recherche agronomique, UR406 Abeilles et Environnement, 228 route de l'Aerodrome, CS40509, F84914, Avignon Cedex 9, France. ; Food and Agriculture Organization of the United Nations, Viale delle Terme di Caracalla 00153, Rome, Italy. ; Departamento de Zoologia, Universidade Federal da Bahia, Instituto de Biologia, Rua Barao de Geremoabo, S/N, Campus de Ondina, CEP 40170110, Salvador, BA, Brazil. ; Departamento de Zootecnia-Centro de Ciencias Agrarias, Universidade Federal do Ceara, Campus Universitario do Pici, CEP 60021970, Fortaleza, CE, Brazil. ; IPBES Secretariat, Intergovernmental Platform on Biodiversity and Ecosystem Services (IPBES), UN Campus, Platz der Vereinten Nationen 1, D-53113, Bonn, Germany. ; Laboratorio Ecotono, Universidad Nacional del Comahue-CONICET, Instituto de Investigaciones en Biodiversidad y Medioambiente, Quintral 1250, CP 8400, San Carlos de Bariloche, Rio Negro, Argentina. ; Norwegian Institute for Nature Research, Post Office Box 5685 Sluppen, NO-7485, Trondheim, Norway. ; Key Laboratory for Insect-Pollinator Biology of the Ministry of Agriculture, Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, 100093, Beijing, China. ; Pontificia Universidade Catolica do Rio Grande do Sul (PUCRS), Av. Ipiranga, 6681, CEP 90619900, Porto Alegre, RS, Brazil. ; Department of Plant Protection, Faculty of Agriculture, Bogor Agricultural University. Jln. Kamper, Darmaga, Bogor, 16680, West Java, Indonesia. ; Laboratorio investigaciones en Abejas (LABUN), Departamento de Biologia, Universidad Nacional de Colombia, Sede Bogota, CP11001, Bogota, Colombia. ; Departamento de Educacao em Ciencias Agrarias e da Terra, Universidade Federal de Sergipe, Campus do Sertao, Rodovia Engenheiro Jorge Neto. Silos KM 0, CEP 49680000, Nossa Senhora da Gloria, SE, Brazil. ; Institute of Agriculture and Animal Science, Rampur, Chitwan, Nepal. ; Embrapa Semiarido, BR 428, Km 152, C.P. 23, zona rural, CEP 56302970, Petrolina, PE, Brazil. ; Jardim Botanico do Rio de Janeiro (JBRJ), Rua Pacheco Leao 915, CEP 22460030, Rio de Janeiro, RJ, Brazil. ; Laboratorio de Ciencias Ambientais, Universidade Estadual do Norte Fluminense Darcy Ribeiro, CEP 28013620, Campos dos Goytacazes, RJ, Brazil. ; University of Zimbabwe, Faculty of Agriculture, Crop Science Department, Post Office Box MP167, Mt Pleasant, Harare, Zimbabwe. ; Conservation and Management of Pollinators for Sustainable Agriculture through Ecosystem Approach project, Honey Bee Research Institute, National Agricultural Research Centre, Park Road, Post Office Box 44000, Islamabad, Pakistan. ; Kenya Agricultural and Livestock Research Organisation-Sericulture, Post Office Box 7816 code 01000 Thika, Kenya. ; College of Agriculture and Natural Sciences, School of Biological Sciences, University of Cape Coast, Cape Coast, Ghana. ; Embrapa Recursos Geneticos e Biotecnologia, Parque Estacao Biologica, W5 Norte (final), CEP 70770917, Brasilia, DF, Brazil. ; Instituto do Meio Ambiente e Recursos Hidricos (INEMA)-UR Extremo Sul, Rua Viena, no. 425, Bairro Dinnah Borges, CEP 45820970, Eunapolis, BA, Brazil. ; G.B. Pant Institute of Himalayan Environment and Development, Kosi-Katarmal, Almora-263 643, Uttarakhand. India. ; Department of Plant Pest Diseases, Faculty of Agriculture, University of Brawijaya. Jl. Veteran, Malang 65145, East Java, Indonesia. ; Universidade de Sao Paulo, Escola Politecnica, Av. Prof. Luciano Gualberto Travessa 3, n.158, CEP 05508010, Sao Paulo, SP, Brazil. ; South African National Biodiversity Institute, Kirstenbosch Research Centre, Private Bag X7, Claremont, 7735, South Africa. Conservation Ecology and Entomology, Stellenbosch University, Private Bag X1, 7602, Matieland, South Africa. ; Centro de Pesquisa Emilio Schenk, Fundacao Estadual de Pesquisa Agropecuaria (Fepagro Vale do Taquari), 1 degrees Distrito, Fonte Grande, Caixa Postal 12, CEP 95860000, Taquari, RS, Brazil.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26798016" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Animals ; Asia ; *Bees ; *Biodiversity ; *Crop Production ; Crops, Agricultural/*growth & development ; Flowers/growth & development ; *Pollination
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  • 176
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-02
    Description: Secreted and integral membrane proteins compose up to one-third of the biological proteome. These proteins contain hydrophobic signals that direct their translocation across or insertion into the lipid bilayer by the Sec61 protein-conducting channel. The molecular basis of how hydrophobic signals within a nascent polypeptide trigger channel opening is not understood. Here, we used cryo-electron microscopy to determine the structure of an active Sec61 channel that has been opened by a signal sequence. The signal supplants helix 2 of Sec61alpha, which triggers a rotation that opens the central pore both axially across the membrane and laterally toward the lipid bilayer. Comparisons with structures of Sec61 in other states suggest a pathway for how hydrophobic signals engage the channel to gain access to the lipid bilayer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4700591/" 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/PMC4700591/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Voorhees, Rebecca M -- Hegde, Ramanujan S -- MC_UP_A022_1007/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):88-91. doi: 10.1126/science.aad4992.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Laboratory of Molecular Biology, Medical Research Council, Francis Crick Avenue, Cambridge CB2 0QH, UK. ; MRC Laboratory of Molecular Biology, Medical Research Council, Francis Crick Avenue, Cambridge CB2 0QH, UK. rhegde@mrc-lmb.cam.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721998" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cryoelectron Microscopy ; Crystallography, X-Ray ; Dogs ; Hydrophobic and Hydrophilic Interactions ; Lipid Bilayers/chemistry ; Membrane Proteins/*chemistry ; Protein Sorting Signals ; Protein Structure, Secondary ; Ribosomes/chemistry
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  • 177
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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〉Monahan, Patrick -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):395. doi: 10.1126/science.352.6284.395. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102456" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Development ; Bone and Bones/*anatomy & histology ; Dinosaurs/*anatomy & histology/*growth & development
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  • 178
    Publication Date: 2016-01-30
    Description: In several human pathogens, thyX-encoded flavin-dependent thymidylate synthase (FDTS) catalyzes the last step in the biosynthesis of thymidylate, one of the four DNA nucleotides. ThyX is absent in humans, rendering FDTS an attractive antibiotic target; however, the lack of mechanistic understanding prohibits mechanism-based drug design. Here, we report trapping and characterization of two consecutive intermediates, which together with previous crystal structures indicate that the enzyme's reduced flavin relays a methylene from the folate carrier to the nucleotide acceptor. Furthermore, these results corroborate an unprecedented activation of the nucleotide that involves no covalent modification but only electrostatic polarization by the enzyme's active site. These findings indicate a mechanism that is very different from thymidylate biosynthesis in humans, underscoring the promise of FDTS as an antibiotic target.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4744818/" 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/PMC4744818/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mishanina, Tatiana V -- Yu, Liping -- Karunaratne, Kalani -- Mondal, Dibyendu -- Corcoran, John M -- Choi, Michael A -- Kohen, Amnon -- R01 GM110775/GM/NIGMS NIH HHS/ -- T32 GM008365/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):507-10. doi: 10.1126/science.aad0300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Iowa, Iowa City, IA 52242, USA. amnon-kohen@uiowa.edu. ; Nuclear Magnetic Resonance (NMR) Core Facility and Department of Biochemistry, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA. ; Department of Chemistry, University of Iowa, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823429" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/*chemistry ; Catalysis ; Catalytic Domain ; *DNA Methylation ; Flavins/chemistry ; Folic Acid/chemistry ; Folic Acid Transporters/chemistry ; Humans ; Kinetics ; Thermotoga maritima/enzymology ; Thymidine Monophosphate/*biosynthesis/chemistry ; Thymidylate Synthase/*chemistry
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  • 179
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1377-8. doi: 10.1126/science.351.6280.1377.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013706" target="_blank"〉PubMed〈/a〉
    Keywords: Brazil/epidemiology ; Genome, Viral ; Humans ; *Sports ; *Travel ; Zika Virus/*genetics ; Zika Virus Infection/epidemiology/*transmission/*virology
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  • 180
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wade, Lizzie -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):507. doi: 10.1126/science.352.6285.507.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126019" target="_blank"〉PubMed〈/a〉
    Keywords: *Career Mobility ; Genomics/education/*organization & administration ; Human Genome Project/economics/*organization & administration ; Humans ; Mexico ; Sequence Analysis, DNA/economics
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  • 181
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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〉Gebauer, Fatima -- Hentze, Matthias W -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):228. doi: 10.1126/science.aad8540.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Regulation, Stem Cells and Cancer Programme, Centre for Genomic Regulation, Barcelona Institute of Science and Technology, 08003 Barcelona, Spain. Universitat Pompeu Fabra, 08003 Barcelona, Spain. ; European Molecular Biology Laboratory, 69117 Heidelberg, Germany. hentze@embl.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816364" target="_blank"〉PubMed〈/a〉
    Keywords: Genome, Human/*genetics ; Genome, Viral/*genetics ; Humans ; Protein Biosynthesis/*genetics ; RNA Caps/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 182
    Publication Date: 2016-04-30
    Description: Microbial colonization of mucosal tissues during infancy plays an instrumental role in the development and education of the host mammalian immune system. These early-life events can have long-standing consequences: facilitating tolerance to environmental exposures or contributing to the development of disease in later life, including inflammatory bowel disease, allergy, and asthma. Recent studies have begun to define a critical period during early development in which disruption of optimal host-commensal interactions can lead to persistent and in some cases irreversible defects in the development and training of specific immune subsets. Here, we discuss the role of early-life education of the immune system during this "window of opportunity," when microbial colonization has a potentially critical impact on human health and disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gensollen, Thomas -- Iyer, Shankar S -- Kasper, Dennis L -- Blumberg, Richard S -- DK0034854/DK/NIDDK NIH HHS/ -- DK44319/DK/NIDDK NIH HHS/ -- R21 AI090102/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):539-44. doi: 10.1126/science.aad9378.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Gastroenterology, Hepatology, and Endoscopy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. ; Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA, USA. ; Division of Gastroenterology, Hepatology, and Endoscopy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. rblumberg@partners.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126036" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Asthma/immunology/microbiology ; Humans ; Hypersensitivity/immunology/microbiology ; Immune System/*immunology ; Immune Tolerance ; Infant, Newborn ; Inflammatory Bowel Diseases/immunology/microbiology ; Intestinal Mucosa/*immunology/*microbiology ; Microbiota/*immunology ; Natural Killer T-Cells/immunology ; Symbiosis ; T-Lymphocyte Subsets/immunology
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  • 183
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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〉Wade, Lizzie -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):129-30. doi: 10.1126/science.352.6282.129. Epub 2016 Apr 7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124429" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Anthozoa ; Biodiversity ; Colombia ; Conservation of Natural Resources/*methods ; *Coral Reefs ; *Ships
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  • 184
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wala, Jeremiah -- Beroukhim, Rameen -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1398-9. doi: 10.1126/science.aaf5542.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Medical Oncology and Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115, USA, and Broad Institute, Cambridge, MA 02142, USA. ; Departments of Medical Oncology and Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115, USA, and Broad Institute, Cambridge, MA 02142, USA. rameen_beroukhim@dfci.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013717" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosome Aberrations ; *Gene Expression Regulation, Leukemic ; Humans ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/*genetics ; Proto-Oncogenes/*genetics ; *Sequence Deletion ; *Translocation, Genetic
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  • 185
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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〉Gibbons, Ann -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):648-9. doi: 10.1126/science.351.6274.648.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912836" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Disease/*genetics ; Humans ; Neanderthals/*genetics
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  • 186
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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〉Wade, Lizzie -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1141-3. doi: 10.1126/science.351.6278.1141.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965607" target="_blank"〉PubMed〈/a〉
    Keywords: *Crime ; *Fires ; *Forensic Sciences ; Humans ; Mexico ; Students ; Waste Disposal Facilities
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  • 187
    Publication Date: 2016-02-26
    Description: Monoubiquitinated histone H2B plays multiple roles in transcription activation. H2B is deubiquitinated by the Spt-Ada-Gcn5 acetyltransferase (SAGA) coactivator, which contains a four-protein subcomplex known as the deubiquitinating (DUB) module. The crystal structure of the Ubp8/Sgf11/Sus1/Sgf73 DUB module bound to a ubiquitinated nucleosome reveals that the DUB module primarily contacts H2A/H2B, with an arginine cluster on the Sgf11 zinc finger domain docking on the conserved H2A/H2B acidic patch. The Ubp8 catalytic domain mediates additional contacts with H2B, as well as with the conjugated ubiquitin. We find that the DUB module deubiquitinates H2B both in the context of the nucleosome and in H2A/H2B dimers complexed with the histone chaperone, FACT, suggesting that SAGA could target H2B at multiple stages of nucleosome disassembly and reassembly during transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morgan, Michael T -- Haj-Yahya, Mahmood -- Ringel, Alison E -- Bandi, Prasanthi -- Brik, Ashraf -- Wolberger, Cynthia -- GM-095822/GM/NIGMS NIH HHS/ -- Y1-CO-1020/CO/NCI NIH HHS/ -- Y1-GM-1104/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):725-8. doi: 10.1126/science.aac5681.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biophysics and Biophysical Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. ; Department of Chemistry, Ben-Gurion University of the Negev, Beer Sheva 8410501, Israel. ; Schulich Faculty of Chemistry, Technion-Israel Institute of Technology, Haifa 3200008, Israel. ; Department of Biophysics and Biophysical Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. cwolberg@jhmi.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912860" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catalytic Domain ; Crystallography, X-Ray ; Endopeptidases/*chemistry ; Histone Acetyltransferases/*chemistry ; Histones/*chemistry ; Nuclear Proteins/*chemistry ; Nucleosomes/enzymology ; Protein Multimerization ; Protein Structure, Secondary ; RNA-Binding Proteins/*chemistry ; Saccharomyces cerevisiae Proteins/*chemistry ; Trans-Activators/*chemistry ; Transcription Factors/*chemistry ; Transcriptional Activation ; Ubiquitin/chemistry ; *Ubiquitination ; Xenopus laevis ; Zinc Fingers
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  • 188
    Publication Date: 2016-02-26
    Description: De Lussanet claims that our model that accounts for the degree of folding of the cerebral cortex based on the product of cortical surface area and the square root of cortical thickness is better reduced to the product of gray-matter proportion and folding index. Lewitus et al., in turn, claim that the assumptions of our model are in conflict with experimental data; that the model does not accurately fit the data; and that the ancestral mammalian brain was gyrencephalic. Here, we show that both claims are inappropriate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mota, Bruno -- Herculano-Houzel, Suzana -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):826. doi: 10.1126/science.aad2346.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instituto de Fisica, Universidade Federal do Rio de Janeiro, Brasil. ; Instituto de Ciencias Biomedicas, Universidade Federal do Rio de Janeiro, Brasil. suzanahh@gmail.com.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912888" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cerebral Cortex ; Humans ; Lissencephaly/*pathology ; Neurons/*cytology
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  • 189
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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〉Gibbons, Ann -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1250-1. doi: 10.1126/science.351.6279.1250. Epub 2016 Mar 17.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989228" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asia ; Biological Evolution ; Bone and Bones ; DNA/genetics ; Europe ; Female ; Fossils ; Humans ; Male ; *Mating Preference, Animal ; Neanderthals/*genetics/*psychology ; *Sexual Behavior
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  • 190
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- Culotta, Elizabeth -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):503-4. doi: 10.1126/science.352.6285.503.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126016" target="_blank"〉PubMed〈/a〉
    Keywords: Anthropology ; Congresses as Topic ; Female ; Humans ; Male ; Research Personnel ; Sexual Harassment/*prevention & control
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 191
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nathanson, Neal -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):133. doi: 10.1126/science.351.6269.133.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emeritus Professor, Department of Microbiology, University of Pennsylvania, Philadelphia, PA 19104, USA. nathansn@upenn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744400" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*economics/*mortality ; Biomedical Research/*economics ; *Cost of Illness ; Humans
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  • 192
    Publication Date: 2016-04-02
    Description: Until recently, programmed cell death was conceived of as a single set of molecular pathways. We now know of several distinct sets of death-inducing mechanisms that lead to differing cell-death processes. In one of them--apoptosis--the dying cell affects others minimally. In contrast, programmed necrotic cell death causes release of immunostimulatory intracellular components after cell-membrane rupture. Defining the in vivo relevance of necrotic death is hampered because the molecules initiating it [such as receptor-interacting protein kinase-1 (RIPK1), RIPK3, or caspase-1] also serve other functions. Proteins that participate in late events in two forms of programmed necrosis [mixed lineage kinase domain-like protein (MLKL) in necroptosis and gasdermin-D in pyroptosis] were recently discovered, bringing us closer to identifying molecules that strictly serve in death mediation, thereby providing probes for better assessing its role in inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wallach, David -- Kang, Tae-Bong -- Dillon, Christopher P -- Green, Douglas R -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):aaf2154. doi: 10.1126/science.aaf2154.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomolecular Sciences, The Weizmann Institute of Science, 76100 Rehovot, Israel. d.wallach@weizmann.ac.il douglas.green@stjude.org. ; Department of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chung-Ju 380-701, Korea. ; Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. ; Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. d.wallach@weizmann.ac.il douglas.green@stjude.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034377" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caspase 1/metabolism ; Cytokines/metabolism ; Humans ; Inflammation/*metabolism/*pathology ; Necrosis/pathology ; Neoplasm Proteins/metabolism ; Protein Kinases/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism
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  • 193
    Publication Date: 2016-03-05
    Description: Examining complete gene knockouts within a viable organism can inform on gene function. We sequenced the exomes of 3222 British adults of Pakistani heritage with high parental relatedness, discovering 1111 rare-variant homozygous genotypes with predicted loss of function (knockouts) in 781 genes. We observed 13.7% fewer homozygous knockout genotypes than we expected, implying an average load of 1.6 recessive-lethal-equivalent loss-of-function (LOF) variants per adult. When genetic data were linked to the individuals' lifelong health records, we observed no significant relationship between gene knockouts and clinical consultation or prescription rate. In this data set, we identified a healthy PRDM9-knockout mother and performed phased genome sequencing on her, her child, and control individuals. Our results show that meiotic recombination sites are localized away from PRDM9-dependent hotspots. Thus, natural LOF variants inform on essential genetic loci and demonstrate PRDM9 redundancy in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Narasimhan, Vagheesh M -- Hunt, Karen A -- Mason, Dan -- Baker, Christopher L -- Karczewski, Konrad J -- Barnes, Michael R -- Barnett, Anthony H -- Bates, Chris -- Bellary, Srikanth -- Bockett, Nicholas A -- Giorda, Kristina -- Griffiths, Christopher J -- Hemingway, Harry -- Jia, Zhilong -- Kelly, M Ann -- Khawaja, Hajrah A -- Lek, Monkol -- McCarthy, Shane -- McEachan, Rosie -- O'Donnell-Luria, Anne -- Paigen, Kenneth -- Parisinos, Constantinos A -- Sheridan, Eamonn -- Southgate, Laura -- Tee, Louise -- Thomas, Mark -- Xue, Yali -- Schnall-Levin, Michael -- Petkov, Petko M -- Tyler-Smith, Chris -- Maher, Eamonn R -- Trembath, Richard C -- MacArthur, Daniel G -- Wright, John -- Durbin, Richard -- van Heel, David A -- GM 099640/GM/NIGMS NIH HHS/ -- MR/M009017/1/Medical Research Council/United Kingdom -- R01 GM104371/GM/NIGMS NIH HHS/ -- R01GM104371/GM/NIGMS NIH HHS/ -- WT098051/Wellcome Trust/United Kingdom -- WT099769/Wellcome Trust/United Kingdom -- WT101597/Wellcome Trust/United Kingdom -- WT102627/Wellcome Trust/United Kingdom -- British Heart Foundation/United Kingdom -- Arthritis Research UK/United Kingdom -- Cancer Research UK/United Kingdom -- Department of Health/United Kingdom -- Chief Scientist Office/United Kingdom -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):474-7. doi: 10.1126/science.aac8624. Epub 2016 Mar 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK. ; Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK. ; Bradford Institute for Health Research, Bradford Teaching Hospitals National Health Service (NHS) Foundation Trust, Bradford BD9 6RJ, UK. ; Center for Genome Dynamics, The Jackson Laboratory, Bar Harbor, ME 04609, USA. ; Analytic and Translational Genetics Unit, Massachusetts General Hospital, Boston, MA 02114, USA. Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK. ; Diabetes and Endocrine Centre, Heart of England NHS Foundation Trust and University of Birmingham, Birmingham B9 5SS, UK. ; TPP, Mill House, Troy Road, Leeds LS18 5TN, UK. ; Aston Research Centre for Healthy Ageing, Aston University, Birmingham B4 7ET, UK. ; 10X Genomics, 7068 Koll Center Parkway, Suite 415, Pleasanton, CA 94566, USA. ; Farr Institute of Health Informatics Research, London NW1 2DA, UK. Institute of Health Informatics, University College London, London NW1 2DA, UK. ; School of Clinical and Experimental Medicine, University of Birmingham, Birmingham B15 2TT, UK. ; Department of Medical Genetics, University of Cambridge and National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre, Box 238, Cambridge Biomedical Campus, Cambridge CB2 0QQ, UK. Cambridge University Hospitals NHS Foundation Trust, Cambridge Biomedical Campus, Cambridge CB2 0QQ, UK. ; Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK. Faculty of Life Sciences and Medicine, King's College London, London SE1 1UL, UK. ; Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK. rd@sanger.ac.uk d.vanheel@qmul.ac.uk. ; Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK. rd@sanger.ac.uk d.vanheel@qmul.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26940866" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Consanguinity ; DNA Mutational Analysis ; Drug Prescriptions ; Exome/genetics ; Female ; Fertility ; Gene Knockout Techniques ; Genes, Lethal ; Genetic Loci ; Genome, Human ; Great Britain ; *Health ; Histone-Lysine N-Methyltransferase/*genetics ; Homologous Recombination ; Homozygote ; Humans ; Male ; Mothers ; Pakistan/ethnology ; Phenotype
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  • 194
    Publication Date: 2016-01-28
    Description: Muscle contraction depends on release of Ca(2+) from the sarcoplasmic reticulum (SR) and reuptake by the Ca(2+)adenosine triphosphatase SERCA. We discovered a putative muscle-specific long noncoding RNA that encodes a peptide of 34 amino acids and that we named dwarf open reading frame (DWORF). DWORF localizes to the SR membrane, where it enhances SERCA activity by displacing the SERCA inhibitors, phospholamban, sarcolipin, and myoregulin. In mice, overexpression of DWORF in cardiomyocytes increases peak Ca(2+) transient amplitude and SR Ca(2+) load while reducing the time constant of cytosolic Ca(2+) decay during each cycle of contraction-relaxation. Conversely, slow skeletal muscle lacking DWORF exhibits delayed Ca(2+) clearance and relaxation and reduced SERCA activity. DWORF is the only endogenous peptide known to activate the SERCA pump by physical interaction and provides a means for enhancing muscle contractility.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, Benjamin R -- Makarewich, Catherine A -- Anderson, Douglas M -- Winders, Benjamin R -- Troupes, Constantine D -- Wu, Fenfen -- Reese, Austin L -- McAnally, John R -- Chen, Xiongwen -- Kavalali, Ege T -- Cannon, Stephen C -- Houser, Steven R -- Bassel-Duby, Rhonda -- Olson, Eric N -- AR-063182/AR/NIAMS NIH HHS/ -- DK-099653/DK/NIDDK NIH HHS/ -- F30AR 067094/AR/NIAMS NIH HHS/ -- HL-077439,/HL/NHLBI NIH HHS/ -- HL-093039/HL/NHLBI NIH HHS/ -- HL-111665/HL/NHLBI NIH HHS/ -- R01 AR063182/AR/NIAMS NIH HHS/ -- U01-HL-100401/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):271-5. doi: 10.1126/science.aad4076.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Physiology, Temple University School of Medicine, Philadelphia, PA 19140, USA. Department of Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA 19140, USA. ; Department of Neurology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Department of Physiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. eric.olson@utsouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816378" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Binding Proteins/metabolism ; Humans ; Mice ; Mice, Knockout ; *Muscle Contraction ; Muscle Proteins/metabolism ; Muscle, Skeletal/*metabolism ; Myocardial Contraction ; Myocytes, Cardiac/*metabolism ; Peptides/genetics/*metabolism ; Proteolipids/metabolism ; RNA, Long Noncoding/genetics/metabolism ; Sarcoplasmic Reticulum/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/*metabolism ; Transcription, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 195
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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〉Waqas, Ahmed -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1358. doi: 10.1126/science.351.6279.1358.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ahmed Waqas is in the final year of his Bachelor of Medicine and Bachelor of Surgery degree at the CMH Lahore Medical College and Institute of Dentistry in Pakistan. Send your story to SciCareerEditor@aaas.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989255" target="_blank"〉PubMed〈/a〉
    Keywords: *Career Choice ; Humans ; Mental Health ; *Mentors ; Neurosurgery/education ; Pakistan ; Psychiatry/*education ; Students, Medical/*psychology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 196
    Publication Date: 2016-04-23
    Description: The general view that only adaptive immunity can build immunological memory has recently been challenged. In organisms lacking adaptive immunity, as well as in mammals, the innate immune system can mount resistance to reinfection, a phenomenon termed "trained immunity" or "innate immune memory." Trained immunity is orchestrated by epigenetic reprogramming, broadly defined as sustained changes in gene expression and cell physiology that do not involve permanent genetic changes such as mutations and recombination, which are essential for adaptive immunity. The discovery of trained immunity may open the door for novel vaccine approaches, new therapeutic strategies for the treatment of immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Netea, Mihai G -- Joosten, Leo A B -- Latz, Eicke -- Mills, Kingston H G -- Natoli, Gioacchino -- Stunnenberg, Hendrik G -- O'Neill, Luke A J -- Xavier, Ramnik J -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):aaf1098. doi: 10.1126/science.aaf1098. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, Netherlands. mihai.netea@radboudumc.nl. ; Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, Netherlands. ; Institute of Innate Immunity, Bonn University, Bonn, Germany. Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA. German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany. ; School of Biochemistry and Immunology, Trinity College, Dublin, Ireland. ; Department of Experimental Oncology, European Institute of Oncology, Milan, Italy. ; Department of Molecular Biology, Faculties of Science and Medicine, Radboud Institute of Molecular Life Sciences, Radboud University, Nijmegen, Netherlands. ; The Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Center for Computational and Integrative Biology and Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102489" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Methylation ; Epigenesis, Genetic ; Histones/metabolism ; Humans ; Immunity, Innate/genetics/*immunology ; Immunologic Memory/genetics/*immunology ; Infection/*immunology ; Inflammation/immunology ; Invertebrates/immunology ; Plants/immunology ; Transcription, Genetic ; Vaccination ; Vaccines/*immunology
    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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  • 197
    Publication Date: 2016-01-09
    Description: Human activity is leaving a pervasive and persistent signature on Earth. Vigorous debate continues about whether this warrants recognition as a new geologic time unit known as the Anthropocene. We review anthropogenic markers of functional changes in the Earth system through the stratigraphic record. The appearance of manufactured materials in sediments, including aluminum, plastics, and concrete, coincides with global spikes in fallout radionuclides and particulates from fossil fuel combustion. Carbon, nitrogen, and phosphorus cycles have been substantially modified over the past century. Rates of sea-level rise and the extent of human perturbation of the climate system exceed Late Holocene changes. Biotic changes include species invasions worldwide and accelerating rates of extinction. These combined signals render the Anthropocene stratigraphically distinct from the Holocene and earlier epochs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waters, Colin N -- Zalasiewicz, Jan -- Summerhayes, Colin -- Barnosky, Anthony D -- Poirier, Clement -- Galuszka, Agnieszka -- Cearreta, Alejandro -- Edgeworth, Matt -- Ellis, Erle C -- Ellis, Michael -- Jeandel, Catherine -- Leinfelder, Reinhold -- McNeill, J R -- Richter, Daniel deB -- Steffen, Will -- Syvitski, James -- Vidas, Davor -- Wagreich, Michael -- Williams, Mark -- Zhisheng, An -- Grinevald, Jacques -- Odada, Eric -- Oreskes, Naomi -- Wolfe, Alexander P -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):aad2622. doi: 10.1126/science.aad2622.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉British Geological Survey, Keyworth, Nottingham NG12 5GG, UK. ; Department of Geology, University of Leicester, University Road, Leicester LE1 7RH, UK. ; Scott Polar Research Institute, Cambridge University, Lensfield Road, Cambridge CB2 1ER, UK. ; Department of Integrative Biology, Museum of Paleontology, and Museum of Vertebrate Zoology, University of California-Berkeley, Berkeley, CA 94720, USA. ; Morphodynamique Continentale et Cotiere, Universite de Caen Normandie, Centre National de la Recherche Scientifique (CNRS), 24 Rue des Tilleuls, F-14000 Caen, France. ; Geochemistry and the Environment Division, Institute of Chemistry, Jan Kochanowski University, 15G Swietokrzyska Street, 25-406 Kielce, Poland. ; Departamento de Estratigrafia y Paleontologia, Facultad de Ciencia y Tecnologia, Universidad del Pais Vasco/Euskal Herriko Unibertsitatea, Apartado 644, 48080 Bilbao, Spain. ; School of Archaeology and Ancient History, University of Leicester, University Road, Leicester LE1 7RH, UK. ; Department of Geography and Environmental Systems, University of Maryland-Baltimore County, Baltimore, MD 21250, USA. ; Laboratoire d'Etudes en Geophysique et Oceanographie Spatiales (CNRS, Centre National d'Etudes Spatiales, Institut de Recherche pour le Developpement, Universite Paul Sabatier), 14 Avenue Edouard Belin, 31400 Toulouse, France. ; Department of Geological Sciences, Freie Universitat Berlin, Malteserstrasse 74-100/D, 12249 Berlin, Germany. ; Georgetown University, Washington, DC, USA. ; Nicholas School of the Environment, Duke University, Box 90233, Durham, NC 27516, USA. ; The Australian National University, Canberra, Australian Capital Territory 0200, Australia. ; Department of Geological Sciences, University of Colorado-Boulder, Box 545, Boulder, CO 80309-0545, USA. ; Marine Affairs and Law of the Sea Programme, The Fridtjof Nansen Institute, Lysaker, Norway. ; Department of Geodynamics and Sedimentology, University of Vienna, A-1090 Vienna, Austria. ; State Key Laboratory of Loess and Quaternary Geology, Institute of Earth Environment, Chinese Academy of Sciences, Xi'an 710061, Beijing Normal University, Beijing 100875, China. ; Institut de Hautes Etudes Internationales et du Developpement, Chemin Eugene Rigot 2, 1211 Geneve 11, Switzerland. ; Department of Geology, University of Nairobi, Nairobi, Kenya. ; Department of the History of Science, Harvard University, Cambridge, MA 02138, USA. ; Department of Biological Sciences, University of Alberta, Edmonton, Alberta T6G 2E9, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744408" target="_blank"〉PubMed〈/a〉
    Keywords: Aluminum/analysis ; *Biota ; Carbon Cycle ; Climate ; Construction Materials/analysis ; *Earth (Planet) ; Fossil Fuels/adverse effects ; Geologic Sediments/*chemistry ; *Human Activities ; Humans ; Ice/analysis ; Introduced Species ; Plastics/analysis ; Radioactive Fallout/analysis ; Radioisotopes/analysis
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  • 198
    Publication Date: 2016-01-02
    Description: Duchenne muscular dystrophy (DMD) is a devastating disease affecting about 1 out of 5000 male births and caused by mutations in the dystrophin gene. Genome editing has the potential to restore expression of a modified dystrophin gene from the native locus to modulate disease progression. In this study, adeno-associated virus was used to deliver the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 system to the mdx mouse model of DMD to remove the mutated exon 23 from the dystrophin gene. This includes local and systemic delivery to adult mice and systemic delivery to neonatal mice. Exon 23 deletion by CRISPR-Cas9 resulted in expression of the modified dystrophin gene, partial recovery of functional dystrophin protein in skeletal myofibers and cardiac muscle, improvement of muscle biochemistry, and significant enhancement of muscle force. This work establishes CRISPR-Cas9-based genome editing as a potential therapy to treat DMD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, Christopher E -- Hakim, Chady H -- Ousterout, David G -- Thakore, Pratiksha I -- Moreb, Eirik A -- Castellanos Rivera, Ruth M -- Madhavan, Sarina -- Pan, Xiufang -- Ran, F Ann -- Yan, Winston X -- Asokan, Aravind -- Zhang, Feng -- Duan, Dongsheng -- Gersbach, Charles A -- DP1-MH100706/DP/NCCDPHP CDC HHS/ -- DP2-OD008586/OD/NIH HHS/ -- P01HL112761/HL/NHLBI NIH HHS/ -- R01DK097768/DK/NIDDK NIH HHS/ -- R01HL089221/HL/NHLBI NIH HHS/ -- R01NS90634/NS/NINDS NIH HHS/ -- T32GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):403-7. doi: 10.1126/science.aad5143. Epub 2015 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Engineering, Duke University, Durham, NC, USA. Center for Genomic and Computational Biology, Duke University, Durham, NC, USA. ; Department of Molecular Microbiology and Immunology, University of Missouri, Columbia, MO, USA. ; Gene Therapy Center, Departments of Genetics, Biochemistry and Biophysics, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. Society of Fellows, Harvard University, Cambridge, MA, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. Graduate Program in Biophysics, Harvard Medical School, Boston, MA, USA. Harvard-MIT Division of Health Sciences and Technology, Harvard Medical School, Boston, MA, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. McGovern Institute for Brain Research, Massachusetts Institute of Technology, Cambridge, MA, USA. Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA. Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA. ; Department of Molecular Microbiology and Immunology, University of Missouri, Columbia, MO, USA. Department of Neurology, University of Missouri, Columbia, MO, USA. ; Department of Biomedical Engineering, Duke University, Durham, NC, USA. Center for Genomic and Computational Biology, Duke University, Durham, NC, USA. Department of Orthopaedic Surgery, Duke University Medical Center, Durham, NC, USA. charles.gersbach@duke.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721684" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *CRISPR-Cas Systems ; Clustered Regularly Interspaced Short Palindromic Repeats ; Dependovirus ; Disease Models, Animal ; Dystrophin/*genetics ; Exons/*genetics ; Genetic Therapy/*methods ; Male ; Mice ; Mice, Inbred mdx ; Muscle, Skeletal/*metabolism ; Muscular Dystrophy, Duchenne/genetics/*therapy ; Sequence Deletion
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  • 199
    Publication Date: 2016-03-19
    Description: Postnatal colonization of the body with microbes is assumed to be the main stimulus to postnatal immune development. By transiently colonizing pregnant female mice, we show that the maternal microbiota shapes the immune system of the offspring. Gestational colonization increases intestinal group 3 innate lymphoid cells and F4/80(+)CD11c(+) mononuclear cells in the pups. Maternal colonization reprograms intestinal transcriptional profiles of the offspring, including increased expression of genes encoding epithelial antibacterial peptides and metabolism of microbial molecules. Some of these effects are dependent on maternal antibodies that potentially retain microbial molecules and transmit them to the offspring during pregnancy and in milk. Pups born to mothers transiently colonized in pregnancy are better able to avoid inflammatory responses to microbial molecules and penetration of intestinal microbes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gomez de Aguero, Mercedes -- Ganal-Vonarburg, Stephanie C -- Fuhrer, Tobias -- Rupp, Sandra -- Uchimura, Yasuhiro -- Li, Hai -- Steinert, Anna -- Heikenwalder, Mathias -- Hapfelmeier, Siegfried -- Sauer, Uwe -- McCoy, Kathy D -- Macpherson, Andrew J -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1296-302. doi: 10.1126/science.aad2571.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Maurice Muller Laboratories (DKF), Universitatsklinik fur Viszerale Chirurgie und Medizin Inselspital, Murtenstrasse 35, University of Bern, 3010 Bern, Switzerland. ; Institute of Molecular Systems Biology, Swiss Federal Institute of Technology (ETH) Zurich, 8093 Zurich, Switzerland. ; Division of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Heidelberg, Germany. ; Institute for Infectious Diseases, University of Bern, 3010 Bern, Switzerland. ; Maurice Muller Laboratories (DKF), Universitatsklinik fur Viszerale Chirurgie und Medizin Inselspital, Murtenstrasse 35, University of Bern, 3010 Bern, Switzerland. andrew.macpherson@insel.ch.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989247" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; Escherichia coli/immunology ; Female ; Gastrointestinal Microbiome/*immunology ; Germ-Free Life ; Immune System/*growth & development/*microbiology ; Immunity, Innate/genetics/*immunology ; Immunity, Maternally-Acquired/genetics/*immunology ; Intestines/*immunology ; Lymphocytes/immunology ; Mice ; Mice, Inbred C57BL ; Pregnancy ; Symbiosis ; Transcription, Genetic
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  • 200
    Publication Date: 2016-01-28
    Description: To investigate gene specificity at the level of translation in both the human genome and viruses, we devised a high-throughput bicistronic assay to quantify cap-independent translation. We uncovered thousands of novel cap-independent translation sequences, and we provide insights on the landscape of translational regulation in both humans and viruses. We find extensive translational elements in the 3' untranslated region of human transcripts and the polyprotein region of uncapped RNA viruses. Through the characterization of regulatory elements underlying cap-independent translation activity, we identify potential mechanisms of secondary structure, short sequence motif, and base pairing with the 18S ribosomal RNA (rRNA). Furthermore, we systematically map the 18S rRNA regions for which reverse complementarity enhances translation. Thus, we make available insights into the mechanisms of translational control in humans and viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weingarten-Gabbay, Shira -- Elias-Kirma, Shani -- Nir, Ronit -- Gritsenko, Alexey A -- Stern-Ginossar, Noam -- Yakhini, Zohar -- Weinberger, Adina -- Segal, Eran -- New York, N.Y. -- Science. 2016 Jan 15;351(6270). pii: aad4939. doi: 10.1126/science.aad4939. Epub 2016 Jan 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Computer Science and Applied Mathematics, Weizmann Institute of Science, Rehovot 76100, Israel. Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel. ; The Delft Bioinformatics Laboratory, Department of Intelligent Systems, Delft University of Technology, Delft, Netherlands. Platform Green Synthetic Biology, Delft, Netherlands. Kluyver Centre for Genomics of Industrial Fermentation, Delft, Netherlands. ; Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel. ; Department of Computer Science, Technion, Haifa, Israel. Agilent Laboratories, Tel-Aviv, Israel. ; Department of Computer Science and Applied Mathematics, Weizmann Institute of Science, Rehovot 76100, Israel. Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel. eran.segal@weizmann.ac.il.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816383" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/genetics ; 5' Untranslated Regions/genetics ; Base Pairing ; Gene Expression Regulation, Viral ; Genome, Human/*genetics ; Genome, Viral/*genetics ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Internal Ribosome Entry Sites/genetics ; Mutagenesis ; Oligonucleotides/chemistry/genetics ; Protein Biosynthesis/*genetics ; RNA Caps/*genetics ; RNA Viruses/genetics ; RNA, Ribosomal, 18S/genetics/metabolism ; Sequence Analysis, DNA/methods ; Sequence Analysis, RNA/methods
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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