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  • Animals  (21,529)
  • Elasticity
  • Fracture
  • American Association for the Advancement of Science (AAAS)  (21,566)
  • Am. Soc. Mech. Eng.
  • Institute of Physics
  • 1
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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〉Landolt, Hans-Peter -- Holst, Sebastian C -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):517-8. doi: 10.1126/science.aaf8178.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Pharmacology and Toxicology, University of Zurich, Zurich, Switzerland. Zurich Center for Interdisciplinary Sleep Research, University of Zurich, Zurich, Switzerland. landolt@pharma.uzh.ch. ; Institute of Pharmacology and Toxicology, University of Zurich, Zurich, Switzerland. Zurich Center for Interdisciplinary Sleep Research, University of Zurich, Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126024" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cations/*metabolism ; Cerebral Cortex/*physiology ; Male ; Potassium/*metabolism ; Sleep/*physiology ; Wakefulness/*physiology
    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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  • 2
    Publication Date: 2016-04-30
    Description: Sleep has been described in animals ranging from worms to humans. Yet the electrophysiological characteristics of brain sleep, such as slow-wave (SW) and rapid eye movement (REM) activities, are thought to be restricted to mammals and birds. Recording from the brain of a lizard, the Australian dragon Pogona vitticeps, we identified SW and REM sleep patterns, thus pushing back the probable evolution of these dynamics at least to the emergence of amniotes. The SW and REM sleep patterns that we observed in lizards oscillated continuously for 6 to 10 hours with a period of ~80 seconds. The networks controlling SW-REM antagonism in amniotes may thus originate from a common, ancient oscillator circuit. Lizard SW dynamics closely resemble those observed in rodent hippocampal CA1, yet they originate from a brain area, the dorsal ventricular ridge, that has no obvious hodological similarity with the mammalian hippocampus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shein-Idelson, Mark -- Ondracek, Janie M -- Liaw, Hua-Peng -- Reiter, Sam -- Laurent, Gilles -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):590-5. doi: 10.1126/science.aaf3621.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Brain Research, Frankfurt am Main, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126045" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Brain/*physiology ; CA1 Region, Hippocampal/physiology ; Lizards/*physiology ; Sleep, REM/*physiology
    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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  • 3
    Publication Date: 2016-04-30
    Description: Sahl et al in their Comment raise criticisms of our work that fall into three classes: image artifacts, resolution criteria, and comparative performance on live cells. We explore each of these in turn.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Dong -- Betzig, Eric -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):527. doi: 10.1126/science.aad8396. Epub 2016 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Laboratory of Biological Macromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, P.R. China. Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147. lidong@ibp.ac.cn betzige@janelia.hhmi.org. ; Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147. lidong@ibp.ac.cn betzige@janelia.hhmi.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126031" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytoskeleton/*ultrastructure ; *Endocytosis ; Imaging, Three-Dimensional/*methods ; Microscopy, Fluorescence/*methods ; Organelles/*ultrastructure
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2016-04-30
    Description: Recent studies in human populations and mouse models reveal notable congruences in gut microbial taxa whose abundances are partly regulated by host genotype. Host genes associating with these taxa are related to diet sensing, metabolism, and immunity. These broad patterns are further validated in similar studies of nonmammalian microbiomes. The next generation of genome-wide association studies will expand the size of the data sets and refine the microbial phenotypes to fully capture these intriguing signatures of host-microbiome coevolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodrich, Julia K -- Davenport, Emily R -- Waters, Jillian L -- Clark, Andrew G -- Ley, Ruth E -- R01 DK093595/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):532-5. doi: 10.1126/science.aad9379.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Cornell University, Ithaca NY, USA. ; Department of Molecular Biology and Genetics, Cornell University, Ithaca NY, USA. Department of Microbiome Science, Max Planck Institute for Developmental Biology, Tubingen, Germany. ; Department of Molecular Biology and Genetics, Cornell University, Ithaca NY, USA. Department of Microbiology, Cornell University, Ithaca NY, USA. Department of Microbiome Science, Max Planck Institute for Developmental Biology, Tubingen, Germany. rel222@cornell.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126034" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/*classification/genetics ; Diet ; *Genome-Wide Association Study ; Genotype ; Humans ; Mice ; Microbiota/genetics/*physiology ; Phenotype ; *Quantitative Trait Loci ; Species Specificity
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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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〉O'Neill, Scott L -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):526. doi: 10.1126/science.352.6285.526-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Eliminate Dengue Program, School of Biological Sciences, Monash University, Clayton, Victoria 3800, Australia. scott.oneill@monash.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126028" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Culicidae/*microbiology ; Dengue/*prevention & control ; Mosquito Control/*methods ; *Wolbachia
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2016-04-30
    Description: Systems in thermodynamic equilibrium are not only characterized by time-independent macroscopic properties, but also satisfy the principle of detailed balance in the transitions between microscopic configurations. Living systems function out of equilibrium and are characterized by directed fluxes through chemical states, which violate detailed balance at the molecular scale. Here we introduce a method to probe for broken detailed balance and demonstrate how such nonequilibrium dynamics are manifest at the mesosopic scale. The periodic beating of an isolated flagellum from Chlamydomonas reinhardtii exhibits probability flux in the phase space of shapes. With a model, we show how the breaking of detailed balance can also be quantified in stationary, nonequilibrium stochastic systems in the absence of periodic motion. We further demonstrate such broken detailed balance in the nonperiodic fluctuations of primary cilia of epithelial cells. Our analysis provides a general tool to identify nonequilibrium dynamics in cells and tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Battle, Christopher -- Broedersz, Chase P -- Fakhri, Nikta -- Geyer, Veikko F -- Howard, Jonathon -- Schmidt, Christoph F -- MacKintosh, Fred C -- P50GM068763/GM/NIGMS NIH HHS/ -- R13GM085967/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):604-7. doi: 10.1126/science.aac8167.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Drittes Physikalisches Institut, Georg-August-Universitat, 37077 Gottingen, Germany. The Kavli Institute for Theoretical Physics, University of California, Santa Barbara, CA 93106, USA. ; The Kavli Institute for Theoretical Physics, University of California, Santa Barbara, CA 93106, USA. Arnold-Sommerfeld-Center for Theoretical Physics and Center for NanoScience, Ludwig-Maximilians-Universitat Munchen, Theresienstrasse 37, D-80333 Munchen, Germany. Lewis-Sigler Institute for Integrative Genomics and Joseph Henry Laboratories of Physics, Princeton University, Princeton, NJ 08544, USA. ; Drittes Physikalisches Institut, Georg-August-Universitat, 37077 Gottingen, Germany. The Kavli Institute for Theoretical Physics, University of California, Santa Barbara, CA 93106, USA. Department of Physics, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT, USA. ; Drittes Physikalisches Institut, Georg-August-Universitat, 37077 Gottingen, Germany. The Kavli Institute for Theoretical Physics, University of California, Santa Barbara, CA 93106, USA. fcmack@gmail.com christoph.schmidt@phys.uni-goettingen.de. ; The Kavli Institute for Theoretical Physics, University of California, Santa Barbara, CA 93106, USA. Department of Physics and Astronomy, Vrije Universiteit, Amsterdam, Netherlands. fcmack@gmail.com christoph.schmidt@phys.uni-goettingen.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126047" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chlamydomonas reinhardtii/*physiology ; Cilia/physiology ; Dogs ; Epithelial Cells/physiology ; Flagella/*physiology ; Madin Darby Canine Kidney Cells ; Microscopy/methods ; Models, Biological ; *Motion ; Thermodynamics
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  • 9
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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〉Rupprecht, Jean-Francois -- Prost, Jacques -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):514-5. doi: 10.1126/science.aaf4611.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mechanobiology Institute, National University of Singapore, 117411 Singapore. ; Mechanobiology Institute, National University of Singapore, 117411 Singapore. Laboratoire Physico Chimie Curie, Institut Curie, PSL Research University, CNRS, 75005 Paris, France. Sorbonne Universities, UPMC Univ Paris 06, CNRS, Laboratoire Physico Chimie Curie, 75005 Paris, France. jacques.prost@curie.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126022" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chlamydomonas reinhardtii/*physiology ; Flagella/*physiology ; *Motion
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2016-04-30
    Description: Li et al (Research Articles, 28 August 2015, aab3500) purport to present solutions to long-standing challenges in live-cell microscopy, reporting relatively fast acquisition times in conjunction with improved image resolution. We question the methods' reliability to visualize specimen features at sub-100-nanometer scales, because the mandatory mathematical processing of the recorded data leads to artifacts that are either difficult or impossible to disentangle from real features. We are also concerned about the chosen approach of subjectively comparing images from different super-resolution methods, as opposed to using quantitative measures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sahl, Steffen J -- Balzarotti, Francisco -- Keller-Findeisen, Jan -- Leutenegger, Marcel -- Westphal, Volker -- Egner, Alexander -- Lavoie-Cardinal, Flavie -- Chmyrov, Andriy -- Grotjohann, Tim -- Jakobs, Stefan -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):527. doi: 10.1126/science.aad7983. Epub 2016 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Biophysical Chemistry, Department of NanoBiophotonics, Am Fassberg 11, 37077 Gottingen, Germany. ssahl@mpibpc.mpg.de fbalzar@mpibpc.mpg.de sjakobs@mpibpc.mpg.de. ; Max Planck Institute for Biophysical Chemistry, Department of NanoBiophotonics, Am Fassberg 11, 37077 Gottingen, Germany. ; Laser Laboratory Gottingen, Hans-Adolf-Krebs-Weg 1, 37077 Gottingen, Germany. ; Institut Universitaire en Sante Mentale de Quebec, Cellular and Molecular Neuroscience Research Axis, 2601 Chemin de la Canardiere, Quebec, G1J 2G3, Canada. ; Helmholtz Zentrum Munchen, Institute of Biological and Medical Imaging, Ingolstadter Landstrasse 1, 85764 Neuherberg, Germany. Technische Universitat Munchen, Chair for Biological Imaging, Ismaningerstrasse 22, 81675 Munchen, Germany. ; Max Planck Institute for Biophysical Chemistry, Department of NanoBiophotonics, Am Fassberg 11, 37077 Gottingen, Germany. University of Gottingen Medical Faculty, Department of Neurology, Robert-Koch-Str. 40, 37075 Gottingen, Germany. ssahl@mpibpc.mpg.de fbalzar@mpibpc.mpg.de sjakobs@mpibpc.mpg.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126030" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytoskeleton/*ultrastructure ; *Endocytosis ; Imaging, Three-Dimensional/*methods ; Microscopy, Fluorescence/*methods ; Organelles/*ultrastructure
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  • 11
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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〉Kupferschmidt, Kai -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):128-9. doi: 10.1126/science.352.6282.128. Epub 2016 Apr 7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124428" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/virology ; Angola/epidemiology ; Animals ; Chick Embryo ; Disease Outbreaks/*prevention & control ; Humans ; Vaccination/statistics & numerical data ; World Health Organization ; Yellow Fever/*epidemiology/*prevention & control ; Yellow Fever Vaccine/*administration & dosage
    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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  • 12
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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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〉Alley, Richard B -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):151-2. doi: 10.1126/science.aaf4837.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Geosciences and Earth and Environmental Systems Institute, Pennsylvania State University, University Park, PA, USA. rba6@psu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124443" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Migration ; Animals ; *Climate Change ; *Extinction, Biological ; Fossils ; *Greenhouse Effect ; Hot Temperature
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-29
    Description: Metastatic disease is the leading cause of cancer-related deaths and involves critical interactions between tumor cells and the microenvironment. Hypoxia is a potent microenvironmental factor promoting metastatic progression. Clinically, hypoxia and the expression of the hypoxia-inducible transcription factors HIF-1 and HIF-2 are associated with increased distant metastasis and poor survival in a variety of tumor types. Moreover, HIF signaling in malignant cells influences multiple steps within the metastatic cascade. Here we review research focused on elucidating the mechanisms by which the hypoxic tumor microenvironment promotes metastatic progression. These studies have identified potential biomarkers and therapeutic targets regulated by hypoxia that could be incorporated into strategies aimed at preventing and treating metastatic disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rankin, Erinn B -- Giaccia, Amato J -- CA-197713/CA/NCI NIH HHS/ -- CA-198291/CA/NCI NIH HHS/ -- CA-67166/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):175-80. doi: 10.1126/science.aaf4405. Epub 2016 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University Medical Center, Stanford, CA 94305-5152, USA. Department of Obstetrics and Gynecology, Stanford University Medical Center, Stanford, CA 94305-5152, USA. ; Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University Medical Center, Stanford, CA 94305-5152, USA. giaccia@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124451" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/*metabolism ; Biomarkers, Tumor/analysis/metabolism ; Cell Hypoxia ; Cell Movement ; Disease Progression ; Drug Resistance, Neoplasm ; Epithelial-Mesenchymal Transition ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism ; Neoplasm Invasiveness ; Neoplasm Metastasis/*pathology/*therapy ; Radiation Tolerance ; Signal Transduction ; *Tumor Microenvironment
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  • 16
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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〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):164-6. doi: 10.1126/science.352.6282.164.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124448" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/*pathology ; Bystander Effect ; Exosomes/*pathology ; Humans ; Lung Neoplasms/secondary ; Mice ; Neoplasm Invasiveness/*pathology ; Neoplasm Metastasis/*pathology ; Skin Neoplasms/pathology
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  • 17
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-29
    Description: Despite decades of study, there are still many unanswered questions about metastasis, the process by which a localized cancer becomes a systemic disease. One of these questions is the nature of the tumor cells that give rise to metastases. Although conventional models suggest that metastases are seeded by single cells from the primary tumor, there is growing evidence that seeding requires the collective action of tumor cells traveling together in clusters. Here, we review this evidence, which comes from analysis of both experimental models and patient samples. We present a model of metastatic dissemination that highlights the activities of clusters of tumor cells that retain and require their epithelial properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheung, Kevin J -- Ewald, Andrew J -- P30 CA006973/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):167-9. doi: 10.1126/science.aaf6546.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Translational Research Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. ; Departments of Cell Biology, Oncology, and Biomedical Engineering, Johns Hopkins University School of Medicine, 855 North Wolfe Street, Baltimore, MD 21205, USA. andrew.ewald@jhmi.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124449" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Epithelial Cells/pathology ; Humans ; Mice ; *Models, Biological ; Neoplasm Metastasis/*pathology ; Neoplasm Seeding ; Neoplasms, Experimental/pathology ; Neoplastic Cells, Circulating/*pathology
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  • 18
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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〉Kupferschmidt, Kai -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):391-2. doi: 10.1126/science.352.6284.391. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102452" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Communicable Diseases/diagnosis/*epidemiology/etiology ; Echinococcosis/diagnosis/epidemiology ; Echinococcus/isolation & purification ; *Emigration and Immigration ; Europe ; Humans ; Mass Screening ; Methicillin Resistance ; Methicillin-Resistant Staphylococcus aureus/isolation & purification ; *Refugees
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  • 19
    Publication Date: 2016-04-23
    Description: Ecological character displacement is a process of morphological divergence that reduces competition for limited resources. We used genomic analysis to investigate the genetic basis of a documented character displacement event in Darwin's finches on Daphne Major in the Galapagos Islands: The medium ground finch diverged from its competitor, the large ground finch, during a severe drought. We discovered a genomic region containing the HMGA2 gene that varies systematically among Darwin's finch species with different beak sizes. Two haplotypes that diverged early in the radiation were involved in the character displacement event: Genotypes associated with large beak size were at a strong selective disadvantage in medium ground finches (selection coefficient s = 0.59). Thus, a major locus has apparently facilitated a rapid ecological diversification in the adaptive radiation of Darwin's finches.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamichhaney, Sangeet -- Han, Fan -- Berglund, Jonas -- Wang, Chao -- Almen, Markus Sallman -- Webster, Matthew T -- Grant, B Rosemary -- Grant, Peter R -- Andersson, Leif -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):470-4. doi: 10.1126/science.aad8786.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden. ; Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ, USA. ; Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden. Department of Animal Breeding and Genetics, Swedish University of Agricultural Sciences, Uppsala, Sweden. Department of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX, USA. leif.andersson@imbim.uu.se.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102486" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Beak/*anatomy & histology ; Body Size/genetics ; *Droughts ; Ecuador ; Female ; Finches/*anatomy & histology/classification/*genetics ; Genomics ; Genotype ; HMGA2 Protein/genetics ; Haplotypes ; Organ Size/genetics ; Phylogeny ; *Quantitative Trait Loci ; *Selection, Genetic
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  • 20
    Publication Date: 2016-04-23
    Description: Sauropod dinosaurs exhibit the largest ontogenetic size range among terrestrial vertebrates, but a dearth of very young individuals has hindered understanding of the beginning of their growth trajectory. A new specimen of Rapetosaurus krausei sheds light on early life in the smallest stage of one of the largest dinosaurs. Bones record rapid growth rates and hatching lines, indicating that this individual weighed ~3.4 kilograms at hatching. Just several weeks later, when it likely succumbed to starvation in a drought-stressed ecosystem, it had reached a mass of ~40 kilograms and was ~35 centimeters tall at the hip. Unexpectedly, Rapetosaurus limb bones grew isometrically throughout their development. Cortical remodeling, limb isometry, and thin calcified hypertrophic metaphyseal cartilages indicate an active, precocial growth strategy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Curry Rogers, Kristina -- Whitney, Megan -- D'Emic, Michael -- Bagley, Brian -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):450-3. doi: 10.1126/science.aaf1509. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biology and Geology Departments, Macalester College, St. Paul, MN 55105, USA. rogersk@macalester.edu. ; Department of Biology, University of Washington, Seattle, WA 98185-1800, USA. ; Biology Department, Adelphi University, Garden City, NY 11530-0701, USA. ; Department of Earth Sciences, University of Minnesota, Minneapolis, MN 55455-1333, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102482" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Weight ; *Bone Development ; Bone and Bones/*anatomy & histology ; Calcification, Physiologic ; Cartilage/anatomy & histology/growth & development ; Dinosaurs/*anatomy & histology/*growth & development ; Droughts ; Ecosystem ; Extremities/anatomy & histology/growth & development ; Madagascar ; Starvation/veterinary
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
    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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  • 22
    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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  • 23
    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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  • 24
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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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  • 25
    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
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  • 26
    Publication Date: 2016-04-23
    Description: Pershing et al (Reports, 13 November, p. 809) concluded that failure to account for temperature in the assessment and management of Gulf of Maine Atlantic cod caused overfishing. We argue that the "extra mortality" calculation driving this conclusion is an artifact. Environmental factors affect all stocks, but attribution of additional mortality to temperature alone by Pershing et al is unsupported by the data.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palmer, Michael C -- Deroba, Jonathan J -- Legault, Christopher M -- Brooks, Elizabeth N -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):423. doi: 10.1126/science.aad9674.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Northeast Fisheries Science Center, Population Dynamics Branch, 166 Water Street, Woods Hole, MA 02543, USA. michael.palmer@noaa.gov. ; Northeast Fisheries Science Center, Population Dynamics Branch, 166 Water Street, Woods Hole, MA 02543, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102473" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; *Fisheries ; Gadus morhua/*physiology ; *Global Warming
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  • 27
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):394-5. doi: 10.1126/science.352.6284.394. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102455" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Evolution, Molecular ; Foundations ; Genes ; Genetic Research/*economics ; Great Britain ; Humans ; *Research Support as Topic ; *Selection, Genetic ; Sweden ; United States
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  • 28
    Publication Date: 2016-04-23
    Description: Palmer et al and Swain et al suggest that our "extra mortality" time series is spurious. In response, we show that including temperature-dependent mortality improves abundance estimates and that warming waters reduce growth rates in Gulf of Maine cod. Far from being spurious, temperature effects on this stock are clear, and continuing to ignore them puts the stock in jeopardy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pershing, Andrew J -- Alexander, Michael A -- Hernandez, Christina M -- Kerr, Lisa A -- Le Bris, Arnault -- Mills, Katherine E -- Nye, Janet A -- Record, Nicholas R -- Scannell, Hillary A -- Scott, James D -- Sherwood, Graham D -- Thomas, Andrew C -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):423. doi: 10.1126/science.aae0463.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gulf of Maine Research Institute, 350 Commercial Street, Portland, ME 04101, USA. apershing@gmri.org. ; National Oceanic and Atmospheric Administration (NOAA) Earth System Research Laboratory, Boulder, CO 80305, USA. ; Woods Hole Oceanographic Institution, 86 Water Street, Woods Hole, MA 02543, USA. ; Gulf of Maine Research Institute, 350 Commercial Street, Portland, ME 04101, USA. ; School of Marine and Atmospheric Sciences, Stony Brook University, Stony Brook, NY 11794, USA. ; Bigelow Laboratory for Ocean Sciences, 60 Bigelow Drive, East Boothbay, ME 04544, USA. ; University of Washington School of Oceanography, 1503 Northeast Boat Street, Seattle, WA 98105, USA. ; National Oceanic and Atmospheric Administration (NOAA) Earth System Research Laboratory, Boulder, CO 80305, USA. Cooperative Institute for Research in Environmental Sciences, University of Colorado Boulder, Boulder, CO 80309, USA. ; School of Marine Sciences, University of Maine, 5706 Aubert Hall, Orono, ME 04469, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102475" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; *Fisheries ; Gadus morhua/*physiology ; *Global Warming
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  • 29
    Publication Date: 2016-04-23
    Description: Influenza A virus (IAV) causes up to half a million deaths worldwide annually, 90% of which occur in older adults. We show that IAV-infected monocytes from older humans have impaired antiviral interferon production but retain intact inflammasome responses. To understand the in vivo consequence, we used mice expressing a functional Mx gene encoding a major interferon-induced effector against IAV in humans. In Mx1-intact mice with weakened resistance due to deficiencies in Mavs and Tlr7, we found an elevated respiratory bacterial burden. Notably, mortality in the absence of Mavs and Tlr7 was independent of viral load or MyD88-dependent signaling but dependent on bacterial burden, caspase-1/11, and neutrophil-dependent tissue damage. Therefore, in the context of weakened antiviral resistance, vulnerability to IAV disease is a function of caspase-dependent pathology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pillai, Padmini S -- Molony, Ryan D -- Martinod, Kimberly -- Dong, Huiping -- Pang, Iris K -- Tal, Michal C -- Solis, Angel G -- Bielecki, Piotr -- Mohanty, Subhasis -- Trentalange, Mark -- Homer, Robert J -- Flavell, Richard A -- Wagner, Denisa D -- Montgomery, Ruth R -- Shaw, Albert C -- Staeheli, Peter -- Iwasaki, Akiko -- 5T32HL066987-13/HL/NHLBI NIH HHS/ -- AI062428/AI/NIAID NIH HHS/ -- AI064705/AI/NIAID NIH HHS/ -- AI081884/AI/NIAID NIH HHS/ -- F31 AG039163/AG/NIA NIH HHS/ -- HHSN272201100019C/PHS HHS/ -- K24 AG02489/AG/NIA NIH HHS/ -- K24 AG042489/AG/NIA NIH HHS/ -- N01 AI500031/AI/NIAID NIH HHS/ -- P30 AG21342/AG/NIA NIH HHS/ -- R01HL102101/HL/NHLBI NIH HHS/ -- R01HL125501/HL/NHLBI NIH HHS/ -- T32 AI007019-36/AI/NIAID NIH HHS/ -- T32 AI007019-38/AI/NIAID NIH HHS/ -- T32 AI055403/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):463-6. doi: 10.1126/science.aaf3926.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Yale School of Medicine, New Haven, CT 06520, USA. ; Program in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA. ; Section of Infectious Diseases, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut, USA. ; Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut, USA. ; Department of Pathology, Yale School of Medicine, New Haven, CT 06520, USA. ; Department of Immunobiology, Yale School of Medicine, New Haven, CT 06520, USA. Howard Hughes Medical Institute, Yale School of Medicine, New Haven, CT 06520, USA. ; Section of Rheumatology, Department of Internal Medicine, Yale School of Medicine, New Haven, CT 06520, USA. ; Institut fur Medizinische Mikrobiologie und Hygiene, Institute of Virology, University Medical Center Freiburg, Hermann-Herder-Strasse 11, 79104 Freiburg, Germany. ; Department of Immunobiology, Yale School of Medicine, New Haven, CT 06520, USA. Howard Hughes Medical Institute, Yale School of Medicine, New Haven, CT 06520, USA. akiko.iwasaki@yale.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102485" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics/metabolism ; Adult ; Aged ; Aged, 80 and over ; Animals ; Bacterial Infections/etiology/*immunology ; Caspase 1/metabolism ; Caspases/metabolism ; Female ; Humans ; Immunity, Innate/genetics/*immunology ; Influenza A virus/*immunology ; Influenza, Human/complications/*immunology ; Interferon-beta/immunology ; Male ; Membrane Glycoproteins/genetics/metabolism ; Mice ; Monocytes/immunology ; Myxovirus Resistance Proteins/genetics/*physiology ; Neutrophils/immunology ; Orthomyxoviridae Infections/*immunology ; Respiratory Tract Infections/*immunology/microbiology ; Toll-Like Receptor 7/genetics/metabolism ; Viral Load ; Young Adult
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  • 30
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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〉Hulme, Philip E -- Le Roux, Johannes J -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):422. doi: 10.1126/science.352.6284.422-b. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Bio-Protection Research Centre, Lincoln University, Lincoln 7647, Canterbury, New Zealand. philip.hulme@lincoln.ac.nz. ; The Bio-Protection Research Centre, Lincoln University, Lincoln 7647, Canterbury, New Zealand. Centre for Invasion Biology, Department of Botany and Zoology, Stellenbosch University, Matieland 7602, South Africa.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Conservation of Natural Resources/*methods ; *Extinction, Biological ; Humans
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  • 31
    Publication Date: 2016-04-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joppa, L N -- O'Connor, B -- Visconti, P -- Smith, C -- Geldmann, J -- Hoffmann, M -- Watson, J E M -- Butchart, S H M -- Virah-Sawmy, M -- Halpern, B S -- Ahmed, S E -- Balmford, A -- Sutherland, W J -- Harfoot, M -- Hilton-Taylor, C -- Foden, W -- Di Minin, E -- Pagad, S -- Genovesi, P -- Hutton, J -- Burgess, N D -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):416-8. doi: 10.1126/science.aaf3565. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉See supplementary materials for complete list of author affiliations. lujoppa@microsoft.com. ; See supplementary materials for complete list of author affiliations.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102469" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; Datasets as Topic/*standards ; Endangered Species/*statistics & numerical data ; Human Activities ; Humans
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  • 32
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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〉Roberts, Leslie -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):403. doi: 10.1126/science.352.6284.403. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102460" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimalarials/pharmacology/*therapeutic use ; Artemisinins/pharmacology/*therapeutic use ; Drug Resistance/*genetics ; Humans ; Malaria, Falciparum/*drug therapy/epidemiology/*parasitology ; Mutation ; Myanmar/epidemiology ; Plasmodium falciparum/*drug effects/genetics
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  • 33
    Publication Date: 2016-04-23
    Description: The microtubule (MT) cytoskeleton can transmit mechanical signals and resist compression in contracting cardiomyocytes. How MTs perform these roles remains unclear because of difficulties in observing MTs during the rapid contractile cycle. Here, we used high spatial and temporal resolution imaging to characterize MT behavior in beating mouse myocytes. MTs deformed under contractile load into sinusoidal buckles, a behavior dependent on posttranslational "detyrosination" of alpha-tubulin. Detyrosinated MTs associated with desmin at force-generating sarcomeres. When detyrosination was reduced, MTs uncoupled from sarcomeres and buckled less during contraction, which allowed sarcomeres to shorten and stretch with less resistance. Conversely, increased detyrosination promoted MT buckling, stiffened the myocyte, and correlated with impaired function in cardiomyopathy. Thus, detyrosinated MTs represent tunable, compression-resistant elements that may impair cardiac function in disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robison, Patrick -- Caporizzo, Matthew A -- Ahmadzadeh, Hossein -- Bogush, Alexey I -- Chen, Christina Yingxian -- Margulies, Kenneth B -- Shenoy, Vivek B -- Prosser, Benjamin L -- HL089847/HL/NHLBI NIH HHS/ -- HL105993/HL/NHLBI NIH HHS/ -- R00-HL114879/HL/NHLBI NIH HHS/ -- R01EB017753/EB/NIBIB NIH HHS/ -- T32AR053461-09/AR/NIAMS NIH HHS/ -- T32HL007954/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):aaf0659. doi: 10.1126/science.aaf0659.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Pennsylvania Muscle Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. ; Department of Materials Science and Engineering, University of Pennsylvania School of Engineering and Applied Science, Philadelphia, PA 19104, USA. ; Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. ; Department of Physiology, Pennsylvania Muscle Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. bpros@mail.med.upenn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Desmin/metabolism ; Elasticity ; Heart Failure/metabolism/physiopathology ; Humans ; Male ; Mice ; Microtubules/*metabolism ; Models, Biological ; *Myocardial Contraction ; Myocytes, Cardiac/metabolism/*physiology ; Peptide Synthases/genetics/metabolism ; *Protein Processing, Post-Translational ; RNA, Small Interfering/genetics ; Rats ; Rats, Sprague-Dawley ; Sarcomeres/metabolism ; Tubulin/*metabolism ; Tyrosine/*metabolism
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sarrazin, Francois -- Lecomte, Jane -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):422-3. doi: 10.1126/science.352.6284.422-c. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sorbonne Universites, UPMC Univ. Paris 06, Museum National d'Histoire Naturelle, CNRS, CESCO, UMR 7204, 75005 Paris, France. sarrazin@mnhn.fr. ; Ecologie Systematique Evolution, Univ. Paris-Sud, CNRS, AgroParisTech, Universite Paris-Saclay, 91400 Orsay, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102472" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Conservation of Natural Resources/*methods ; *Extinction, Biological ; Humans
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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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  • 36
    Publication Date: 2016-04-16
    Description: Drug resistance compromises control of malaria. Here, we show that resistance to a commonly used antimalarial medication, atovaquone, is apparently unable to spread. Atovaquone pressure selects parasites with mutations in cytochrome b, a respiratory protein with low but essential activity in the mammalian blood phase of the parasite life cycle. Resistance mutations rescue parasites from the drug but later prove lethal in the mosquito phase, where parasites require full respiration. Unable to respire efficiently, resistant parasites fail to complete mosquito development, arresting their life cycle. Because cytochrome b is encoded by the maternally inherited parasite mitochondrion, even outcrossing with wild-type strains cannot facilitate spread of resistance. Lack of transmission suggests that resistance will be unable to spread in the field, greatly enhancing the utility of atovaquone in malaria control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodman, Christopher D -- Siregar, Josephine E -- Mollard, Vanessa -- Vega-Rodriguez, Joel -- Syafruddin, Din -- Matsuoka, Hiroyuki -- Matsuzaki, Motomichi -- Toyama, Tomoko -- Sturm, Angelika -- Cozijnsen, Anton -- Jacobs-Lorena, Marcelo -- Kita, Kiyoshi -- Marzuki, Sangkot -- McFadden, Geoffrey I -- AI031478/AI/NIAID NIH HHS/ -- RR00052/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):349-53. doi: 10.1126/science.aad9279.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of BioSciences, University of Melbourne, Melbourne, VIC 3010, Australia. gim@unimelb.edu.au deang@unimelb.edu.au. ; School of BioSciences, University of Melbourne, Melbourne, VIC 3010, Australia. Eijkman Institute for Molecular Biology, JI Diponegoro no. 69, Jakarta, 10430, Indonesia. Department of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. ; School of BioSciences, University of Melbourne, Melbourne, VIC 3010, Australia. ; Johns Hopkins University Bloomberg School of Public Health, Department of Molecular Microbiology and Immunology, Malaria Research Institute, Baltimore, MD 21205, USA. ; Eijkman Institute for Molecular Biology, JI Diponegoro no. 69, Jakarta, 10430, Indonesia. Department of Parasitology, Faculty of Medicine, Hasanuddin University, Jalan Perintis Kemerdekaan Km10, Makassar 90245, Indonesia. ; Division of Medical Zoology, Jichi Medical University, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan. ; Department of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. ; Department of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. School of Tropical Medicine and Global Health, Nagasaki University, Sakamoto, Nagasaki 852-8523, Japan. ; Eijkman Institute for Molecular Biology, JI Diponegoro no. 69, Jakarta, 10430, Indonesia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anopheles/*parasitology ; Antimalarials/*pharmacology/therapeutic use ; Atovaquone/*pharmacology/therapeutic use ; Cell Line ; Cytochromes b/*genetics ; Drug Resistance/*genetics ; Genes, Mitochondrial/genetics ; Humans ; Life Cycle Stages/drug effects/genetics ; Malaria/drug therapy/*parasitology/transmission ; Male ; Mice ; Mitochondria/*genetics ; Mutation ; Plasmodium berghei/*drug effects/genetics/growth & development ; Selection, Genetic
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  • 37
    Publication Date: 2016-04-16
    Description: Coral bleaching events threaten the sustainability of the Great Barrier Reef (GBR). Here we show that bleaching events of the past three decades have been mitigated by induced thermal tolerance of reef-building corals, and this protective mechanism is likely to be lost under near-future climate change scenarios. We show that 75% of past thermal stress events have been characterized by a temperature trajectory that subjects corals to a protective, sub-bleaching stress, before reaching temperatures that cause bleaching. Such conditions confer thermal tolerance, decreasing coral cell mortality and symbiont loss during bleaching by over 50%. We find that near-future increases in local temperature of as little as 0.5 degrees C result in this protective mechanism being lost, which may increase the rate of degradation of the GBR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ainsworth, Tracy D -- Heron, Scott F -- Ortiz, Juan Carlos -- Mumby, Peter J -- Grech, Alana -- Ogawa, Daisie -- Eakin, C Mark -- Leggat, William -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):338-42. doi: 10.1126/science.aac7125.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Australian Research Council Centre of Excellence for Coral Reef Studies, James Cook University, Townsville 4810, Australia. ; Coral Reef Watch, U.S. National Oceanic and Atmospheric Administration (NOAA), College Park, MD 20740, USA. Marine Geophysical Laboratory, College of Science, Technology and Engineering, James Cook University, Townsville 4811, Australia. ; Marine Spatial Ecology Lab, School of Biological Sciences, University of Queensland, Brisbane 4072, Australia. Australian Research Council Centre of Excellence for Coral Reef Studies, University of Queensland, Brisbane 4072, Australia. ; Department of Environmental Sciences, Macquarie University, Sydney 2109, Australia. ; Australian Research Council Centre of Excellence for Coral Reef Studies, James Cook University, Townsville 4810, Australia. The College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville 4810, Australia. ; Coral Reef Watch, U.S. National Oceanic and Atmospheric Administration (NOAA), College Park, MD 20740, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081069" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthozoa/cytology/*physiology ; Cell Count ; Cell Death ; *Climate Change ; *Coral Reefs ; Dinoflagellida/cytology/physiology ; *Heat-Shock Response ; Hot Temperature ; Photosynthesis ; Pigments, Biological/*physiology ; Symbiosis
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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〉Badylak, Stephen F -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):298. doi: 10.1126/science.aaf7587.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA, USA. Department of Surgery, University of Pittsburgh, PA, USA. Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA, USA. badylaks@upmc.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081059" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biocompatible Materials ; Muscle, Skeletal/*injuries/*physiology ; *Tissue Scaffolds ; Wound Healing/*immunology
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  • 39
    Publication Date: 2016-04-16
    Description: Increasing incidence of inflammatory bowel diseases, such as Crohn's disease, in developed nations is associated with changes to the microbial environment, such as decreased prevalence of helminth colonization and alterations to the gut microbiota. We find that helminth infection protects mice deficient in the Crohn's disease susceptibility gene Nod2 from intestinal abnormalities by inhibiting colonization by an inflammatory Bacteroides species. Resistance to Bacteroides colonization was dependent on type 2 immunity, which promoted the establishment of a protective microbiota enriched in Clostridiales. Additionally, we show that individuals from helminth-endemic regions harbor a similar protective microbiota and that deworming treatment reduced levels of Clostridiales and increased Bacteroidales. These results support a model of the hygiene hypothesis in which certain individuals are genetically susceptible to the consequences of a changing microbial environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramanan, Deepshika -- Bowcutt, Rowann -- Lee, Soo Ching -- Tang, Mei San -- Kurtz, Zachary D -- Ding, Yi -- Honda, Kenya -- Gause, William C -- Blaser, Martin J -- Bonneau, Richard A -- Lim, Yvonne A L -- Loke, P'ng -- Cadwell, Ken -- AI007180/AI/NIAID NIH HHS/ -- AI093811/AI/NIAID NIH HHS/ -- AI107588/AI/NIAID NIH HHS/ -- DK090989/DK/NIDDK NIH HHS/ -- DK093668/DK/NIDDK NIH HHS/ -- DK103788/DK/NIDDK NIH HHS/ -- HL123340/HL/NHLBI NIH HHS/ -- P30CA016087/CA/NCI NIH HHS/ -- UL1 TR000038/TR/NCATS NIH HHS/ -- UL1 TR00038/TR/NCATS NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):608-12. doi: 10.1126/science.aaf3229. Epub 2016 Apr 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kimmel Center for Biology and Medicine at the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA. Sackler Institute of Graduate Biomedical Sciences, New York University School of Medicine, New York, NY 10016, USA. ; Departments of Microbiology and Medicine, New York University School of Medicine, New York, NY 10016, USA. ; Department of Parasitology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. ; Sackler Institute of Graduate Biomedical Sciences, New York University School of Medicine, New York, NY 10016, USA. Departments of Microbiology and Medicine, New York University School of Medicine, New York, NY 10016, USA. ; Department of Pathology, New York University Langone Medical Center, New York, NY 10016, USA. ; RIKEN Center for Integrative Medical Sciences (IMS), Yokohama, Kanagawa 230-0045, Japan. Japan Agency for Medical Research and Development (AMED)-Core Research for Evolutional Science and Technology (CREST), Tokyo 100-0004, Japan. ; Center for Immunity and Inflammation, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ 07101, USA. ; Department of Biology, Center for Genomics and Systems Biology, New York University, New York, NY 10003, USA. Courant Institute of Mathematical Sciences, New York University, New York, NY 10012, USA. Simons Center for Data Analysis, Simons Foundation, New York, NY 10011, USA. ; Department of Parasitology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. ken.cadwell@med.nyu.edu png.loke@nyumc.org limailian@um.edu.my. ; Departments of Microbiology and Medicine, New York University School of Medicine, New York, NY 10016, USA. ken.cadwell@med.nyu.edu png.loke@nyumc.org limailian@um.edu.my. ; Kimmel Center for Biology and Medicine at the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA. Departments of Microbiology and Medicine, New York University School of Medicine, New York, NY 10016, USA. ken.cadwell@med.nyu.edu png.loke@nyumc.org limailian@um.edu.my.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27080105" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteroides/*immunology ; Bacteroides Infections/*immunology ; Clostridiales/immunology ; Clostridium Infections/immunology ; Crohn Disease/*genetics/immunology ; Gastrointestinal Microbiome/*immunology ; Genetic Predisposition to Disease ; Hygiene Hypothesis ; Intestines/*immunology/microbiology/parasitology ; Mice ; Mice, Mutant Strains ; Nod2 Signaling Adaptor Protein/*genetics ; Trichuriasis/*immunology ; Trichuris/*immunology
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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〉Burke, Brian -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):295-6. doi: 10.1126/science.aaf7735.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Medical Biology, 8A Biomedical Grove, 06-06 Immunos, 138648 Singapore. brian.burke@imb.a-star.edu.sg.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081057" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Movement ; *DNA Breaks, Double-Stranded ; Endosomal Sorting Complexes Required for Transport/*metabolism ; Humans ; Neoplasms/*pathology ; Nuclear Envelope/*pathology/*ultrastructure ; *Tumor Microenvironment
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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〉Kintisch, Eli -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):278. doi: 10.1126/science.352.6283.278.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081046" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arctic Regions ; *Conservation of Natural Resources ; *Euphausiacea ; *Fisheries ; *Fishes
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 42
    Publication Date: 2016-04-16
    Description: Immune-mediated tissue regeneration driven by a biomaterial scaffold is emerging as an innovative regenerative strategy to repair damaged tissues. We investigated how biomaterial scaffolds shape the immune microenvironment in traumatic muscle wounds to improve tissue regeneration. The scaffolds induced a pro-regenerative response, characterized by an mTOR/Rictor-dependent T helper 2 pathway that guides interleukin-4-dependent macrophage polarization, which is critical for functional muscle recovery. Manipulating the adaptive immune system using biomaterials engineering may support the development of therapies that promote both systemic and local pro-regenerative immune responses, ultimately stimulating tissue repair.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4866509/" 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/PMC4866509/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sadtler, Kaitlyn -- Estrellas, Kenneth -- Allen, Brian W -- Wolf, Matthew T -- Fan, Hongni -- Tam, Ada J -- Patel, Chirag H -- Luber, Brandon S -- Wang, Hao -- Wagner, Kathryn R -- Powell, Jonathan D -- Housseau, Franck -- Pardoll, Drew M -- Elisseeff, Jennifer H -- P30 CA006973/CA/NCI NIH HHS/ -- P30CA006973/CA/NCI NIH HHS/ -- R01AI077610/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):366-70. doi: 10.1126/science.aad9272.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Translational Tissue Engineering Center, Wilmer Eye Institute and Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21287, USA. Bloomberg-Kimmel Institute for Cancer Immunotherapy, Johns Hopkins University School of Medicine, Baltimore, MD, USA. ; Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Bloomberg-Kimmel Institute for Cancer Immunotherapy, Johns Hopkins University School of Medicine, Baltimore, MD, USA. ; Division of Biostatistics and Bioinformatics, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Bloomberg-Kimmel Institute for Cancer Immunotherapy, Johns Hopkins University School of Medicine, Baltimore, MD, USA. ; Hugo W. Moser Research Institute at Kennedy Krieger Institute, Baltimore, MD 21205, USA, and Departments of Neurology and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081073" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Animals ; *Biocompatible Materials ; Carrier Proteins/genetics/metabolism ; Disease Models, Animal ; Homeostasis/immunology ; Interleukin-4/genetics/immunology ; Macrophages/immunology ; Mice, Inbred C57BL ; Muscle, Skeletal/*injuries/*physiology ; TOR Serine-Threonine Kinases/genetics/metabolism ; Th2 Cells/immunology ; Tissue Engineering ; *Tissue Scaffolds ; Wound Healing/*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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  • 43
    Publication Date: 2016-04-02
    Description: When animals encounter conflict they initiate and escalate aggression to establish and maintain a social hierarchy. The neural mechanisms by which animals resolve fighting behaviors to determine such social hierarchies remain unknown. We identified two subregions of the dorsal habenula (dHb) in zebrafish that antagonistically regulate the outcome of conflict. The losing experience reduced neural transmission in the lateral subregion of dHb (dHbL)-dorsal/intermediate interpeduncular nucleus (d/iIPN) circuit. Silencing of the dHbL or medial subregion of dHb (dHbM) caused a stronger predisposition to lose or win a fight, respectively. These results demonstrate that the dHbL and dHbM comprise a dual control system for conflict resolution of social aggression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chou, Ming-Yi -- Amo, Ryunosuke -- Kinoshita, Masae -- Cherng, Bor-Wei -- Shimazaki, Hideaki -- Agetsuma, Masakazu -- Shiraki, Toshiyuki -- Aoki, Tazu -- Takahoko, Mikako -- Yamazaki, Masako -- Higashijima, Shin-ichi -- Okamoto, Hitoshi -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):87-90. doi: 10.1126/science.aac9508.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Developmental Gene Regulation, RIKEN Brain Science Institute, Saitama 351-0198, Japan. ; Laboratory for Developmental Gene Regulation, RIKEN Brain Science Institute, Saitama 351-0198, Japan. Department of Life Sciences, Graduate School of Arts and Sciences, University of Tokyo, Tokyo 153-8902, Japan. ; Laboratory for Neural Computation and Adaptation, RIKEN Brain Science Institute, Saitama 351-0198, Japan. ; National Institutes of Natural Sciences, Okazaki Institute for Integrative Bioscience, National Institute for Physiological Sciences, Aichi 444-8787, Japan. ; Laboratory for Developmental Gene Regulation, RIKEN Brain Science Institute, Saitama 351-0198, Japan. Department of Life Sciences, Graduate School of Arts and Sciences, University of Tokyo, Tokyo 153-8902, Japan. Laboratory for Molecular Brain Science, Department of Life Science and Medical Bioscience, Waseda University, Tokyo 162-8430, Japan. hitoshi@brain.riken.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034372" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression/*physiology ; Animals ; *Conflict (Psychology) ; Habenula/*physiology ; Hierarchy, Social ; Interpeduncular Nucleus/physiology ; *Negotiating ; Synaptic Transmission ; Zebrafish
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  • 44
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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〉Shoubridge, Eric A -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):31-2. doi: 10.1126/science.aaf5248. Epub 2016 Mar 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Montreal Neurological Institute, Department of Human Genetics, McGill University, Montreal, Quebec, Canada. eric@ericpc.mni.mcgill.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034357" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Leigh Disease/*genetics/*therapy ; Mitochondria/*metabolism ; Oxygen/*metabolism ; Von Hippel-Lindau Tumor Suppressor Protein/*genetics
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  • 45
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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〉Leslie, Mitch -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):21-3. doi: 10.1126/science.352.6281.21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034353" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Diabetes Mellitus, Type 1/immunology ; Infection/*immunology ; Inflammation/*immunology ; Lymph Nodes/cytology/*immunology ; Mice ; Pancreas/immunology ; T-Lymphocytes/*immunology
    Print ISSN: 0036-8075
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  • 46
    Publication Date: 2016-04-02
    Description: Global climate change is a major threat to biodiversity. Large-scale analyses have generally focused on the impacts of climate change on the geographic ranges of species and on phenology, the timing of ecological phenomena. We used long-term monitoring of the abundance of breeding birds across Europe and the United States to produce, for both regions, composite population indices for two groups of species: those for which climate suitability has been either improving or declining since 1980. The ratio of these composite indices, the climate impact indicator (CII), reflects the divergent fates of species favored or disadvantaged by climate change. The trend in CII is positive and similar in the two regions. On both continents, interspecific and spatial variation in population abundance trends are well predicted by climate suitability trends.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stephens, Philip A -- Mason, Lucy R -- Green, Rhys E -- Gregory, Richard D -- Sauer, John R -- Alison, Jamie -- Aunins, Ainars -- Brotons, Lluis -- Butchart, Stuart H M -- Campedelli, Tommaso -- Chodkiewicz, Tomasz -- Chylarecki, Przemyslaw -- Crowe, Olivia -- Elts, Jaanus -- Escandell, Virginia -- Foppen, Ruud P B -- Heldbjerg, Henning -- Herrando, Sergi -- Husby, Magne -- Jiguet, Frederic -- Lehikoinen, Aleksi -- Lindstrom, Ake -- Noble, David G -- Paquet, Jean-Yves -- Reif, Jiri -- Sattler, Thomas -- Szep, Tibor -- Teufelbauer, Norbert -- Trautmann, Sven -- van Strien, Arco J -- van Turnhout, Chris A M -- Vorisek, Petr -- Willis, Stephen G -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):84-7. doi: 10.1126/science.aac4858.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Conservation Ecology Group, School of Biological and Biomedical Sciences, Durham University, South Road, Durham DH1 3LE, UK. ; Royal Society for the Protection of Birds, Centre for Conservation Science, The Lodge, Sandy, Bedfordshire SG19 2DL, UK. ; Royal Society for the Protection of Birds, Centre for Conservation Science, The Lodge, Sandy, Bedfordshire SG19 2DL, UK. Conservation Science Group, Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, UK. ; United States Geological Survey, Patuxent Wildlife Research Center, 12100 Beech Forest Road, Laurel, MD 20708, USA. ; Institute of Integrative Biology, University of Liverpool, Crown Street, Liverpool L69 3BX, UK. ; Faculty of Biology, University of Latvia, Jelgavas iela 1, Riga, LV-1004, Latvia. ; Center for Mediterranean Forest Research, Centre Tecnologic Forestal de Catalunya, InForest JRU, Solsona 25280, Spain. REAF, Cerdanyola del Valles 08193, Catalonia, Spain. CSIC, Cerdanyola del Valles 08193, Catalonia, Spain. ; Conservation Science Group, Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, UK. BirdLife International, The David Attenborough Building, Pembroke Street, Cambridge CB2 3QZ, UK. ; MITO2000 National Committee; c/o Dream Italia, Via Garibaldi 3, 52015, Pratovecchio-Stia, Arezzo, Italy. ; Ogolnopolskie Towarzystwo Ochrony Ptakow, Odrowaza 24,05-270 Marki, Poland. ; Museum and Institute of Zoology, Polish Academy of Sciences, Wilcza 64, 00-679 Warszawa, Poland. ; BirdWatch Ireland, Unit 20 Block D Bullford Business Campus, Kilcoole, County Wicklow, Ireland. ; Institute of Ecology and Earth Sciences, University of Tartu, Vanemuise Street 46, 51014 Tartu, Estonia. Estonian Ornithological Society, Veski 4, 51005 Tartu, Estonia. ; Sociedad Espanola de Ornitologia/BirdLife Melquiades Biencinto, 34, 28053 Madrid. Spain. ; European Bird Census Council, Post Office Box 6521, 6503 GA Nijmegen, Netherlands. Sovon Dutch Centre for Field Ornithology, Post Office Box 6521, 6503 GA Nijmegen, Netherlands. Department of Animal Ecology and Ecophysiology, Institute for Water and Wetland Research, Radboud University, Post Office Box 9010, 6500 GL Nijmegen, Netherlands. ; Dansk Ornitologisk Forening-BirdLife Denmark and University of Aarhus, Vesterbrogade 140, 1620 Kobenhavn V, Denmark. ; European Bird Census Council-Catalan Ornithological Institute, Natural History Museum of Barcelona, Placa Leonardo da Vinci 4-5, 08019 Barcelona, Catalonia, Spain. ; Section for Science, Nord University, 7600 Levanger, Norway. ; UMR7204 Sorbonne Universites-MNHN-CNRS-UPMC, CESCO, CRBPO, CP 135, 43 Rue Buffon, 75005 Paris, France. ; The Helsinki Lab of Ornithology, Finnish Museum of Natural History, Post Office Box 17, 00014 University of Helsinki, Finland. ; Biodiversity Unit, Department of Biology, Lund University, Ecology Building, S-223 62 Lund, Sweden. ; The British Trust for Ornithology, The Nunnery, Thetford, Norfolk IP24 2PU, UK. ; Natagora, Departement Etudes, Rue Nanon 98, B-5000 Namur, Belgium. ; Institute for Environmental Studies, Faculty of Science, Charles University in Prague, Czech Republic. Department of Zoology and Laboratory of Ornithology, Faculty of Science, Palacky University Olomouc, 17 Listopadu 50, 771 43 Olomouc, Czech Republic. ; Swiss Ornithological Institute, Seerose 1, 6204 Sempach, Switzerland. ; Institute of Environmental Sciences, University of Nyiregyhaza, Sostoi ut 31/b, 4400 Nyiregyhaza, Hungary. ; BirdLife Austria, Museumsplatz 1/10/8, A-1070 Vienna, Austria. ; Dachverband Deutscher Avifaunisten e.V. (Federation of German Avifaunists), An den Speichern 6, D-48157 Munster, Germany. ; Statistics Netherlands, Post Office Box 24500, 2490 HA The Hague, Netherlands. ; Sovon Dutch Centre for Field Ornithology, Post Office Box 6521, 6503 GA Nijmegen, Netherlands. Department of Animal Ecology and Ecophysiology, Institute for Water and Wetland Research, Radboud University, Post Office Box 9010, 6500 GL Nijmegen, Netherlands. ; Department of Zoology and Laboratory of Ornithology, Faculty of Science, Palacky University Olomouc, 17 Listopadu 50, 771 43 Olomouc, Czech Republic. Pan-European Common Bird Monitoring Scheme, Czech Society for Ornithology, Na Belidle 252/34, CZ-15000 Prague 5, Czech Republic.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034371" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Migration ; Animals ; Biodiversity ; *Birds ; Breeding ; *Climate Change ; Ecological Parameter Monitoring ; Europe ; Population Dynamics ; United States
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  • 47
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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〉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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  • 48
    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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  • 49
    Publication Date: 2016-04-02
    Description: Accurate sequence and assembly of genomes is a critical first step for studies of genetic variation. We generated a high-quality assembly of the gorilla genome using single-molecule, real-time sequence technology and a string graph de novo assembly algorithm. The new assembly improves contiguity by two to three orders of magnitude with respect to previously released assemblies, recovering 87% of missing reference exons and incomplete gene models. Although regions of large, high-identity segmental duplications remain largely unresolved, this comprehensive assembly provides new biological insight into genetic diversity, structural variation, gene loss, and representation of repeat structures within the gorilla genome. The approach provides a path forward for the routine assembly of mammalian genomes at a level approaching that of the current quality of the human genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gordon, David -- Huddleston, John -- Chaisson, Mark J P -- Hill, Christopher M -- Kronenberg, Zev N -- Munson, Katherine M -- Malig, Maika -- Raja, Archana -- Fiddes, Ian -- Hillier, LaDeana W -- Dunn, Christopher -- Baker, Carl -- Armstrong, Joel -- Diekhans, Mark -- Paten, Benedict -- Shendure, Jay -- Wilson, Richard K -- Haussler, David -- Chin, Chen-Shan -- Eichler, Evan E -- HG002385/HG/NHGRI NIH HHS/ -- HG003079/HG/NHGRI NIH HHS/ -- HG007234/HG/NHGRI NIH HHS/ -- HG007635/HG/NHGRI NIH HHS/ -- HG007990/HG/NHGRI NIH HHS/ -- R01 HG002385/HG/NHGRI NIH HHS/ -- U41 HG007635/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):aae0344. doi: 10.1126/science.aae0344.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA 98195, USA. Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA. ; Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA 98195, USA. ; Genomics Institute, University of California Santa Cruz and Howard Hughes Medical Institute, Santa Cruz, CA 95064, USA. ; McDonnell Genome Institute, Department of Medicine, Department of Genetics, Washington University School of Medicine, St. Louis, MO 63108, USA. ; Pacific Biosciences of California, Menlo Park, CA 94025, USA. ; Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA 98195, USA. Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA. eee@gs.washington.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Contig Mapping ; Evolution, Molecular ; Expressed Sequence Tags ; Female ; Genetic Variation ; Genome, Human ; Genomics ; Gorilla gorilla/*genetics ; Humans ; Sequence Alignment ; Sequence Analysis, DNA/*methods
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  • 50
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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〉Pepling, Melissa E -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):35-6. doi: 10.1126/science.aaf4943.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Syracuse University, 107 College Place, Syracuse, NY 13244, USA. mepeplin@syr.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034359" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Giant Cells/*cytology ; Oocytes/*cytology ; *Oogenesis ; Organelles/*physiology
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