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  • Articles  (7)
  • Time Factors
  • 2015-2019  (7)
  • Science. 348(6231): 242-5. doi: 10.1126/science.aaa3952.  (1)
  • Science. 348(6234): 574-8. doi: 10.1126/science.aaa1511.  (1)
  • Science. 348(6235): 694-9. doi: 10.1126/science.aaa3662.  (1)
  • Science. 350(6256): 47. doi: 10.1126/science.aad3003.  (1)
  • Science. 350(6264): 1104-7. doi: 10.1126/science.aad0344.  (1)
  • Science. 351(6278): 1143. doi: 10.1126/science.351.6278.1143.  (1)
  • Science. 351(6278): 1204-8. doi: 10.1126/science.aac5610.  (1)
  • 25
  • Medicine  (7)
  • Political Science
  • Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
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  • Articles  (7)
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  • 1
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    The microbial death clock (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kupferschmidt, Kai -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1143. doi: 10.1126/science.351.6278.1143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965608" target="_blank"〉PubMed〈/a〉
    Keywords: Acinetobacter/*growth & development ; Animals ; *Death ; Humans ; Mice ; Moraxellaceae/*growth & development ; Rhizobiaceae/*growth & development ; Time Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Schedule-dependent interaction between anticancer treatments (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-03-12
    Description: The oncogene MDMX is overexpressed in many cancers, leading to suppression of the tumor suppressor p53. Inhibitors of the oncogene product MDMX therefore might help reactivate p53 and enhance the efficacy of DNA-damaging drugs. However, we currently lack a quantitative understanding of how MDMX inhibition affects the p53 signaling pathway and cell sensitivity to DNA damage. Live cell imaging showed that MDMX depletion triggered two distinct phases of p53 accumulation in single cells: an initial postmitotic pulse, followed by low-amplitude oscillations. The response to DNA damage was sharply different in these two phases; in the first phase, MDMX depletion was synergistic with DNA damage in causing cell death, whereas in the second phase, depletion of MDMX inhibited cell death. Thus a quantitative understanding of signal dynamics and cellular states is important for designing an optimal schedule of dual-drug administration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Sheng-Hong -- Forrester, William -- Lahav, Galit -- F32GM105205/GM/NIGMS NIH HHS/ -- GM083303/GM/NIGMS NIH HHS/ -- R01 GM083303/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1204-8. doi: 10.1126/science.aac5610. Epub 2016 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Systems Biology, Harvard Medical School, Boston, MA, USA. ; Developmental and Molecular Pathways, Novartis Institutes for Biomedical Research, Cambridge, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965628" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/*administration & dosage ; Apoptosis ; *DNA Damage ; Gene Knockdown Techniques ; Humans ; MCF-7 Cells ; Molecular Imaging ; Neoplasms/*drug therapy ; Proto-Oncogene Proteins c-mdm2/*antagonists & inhibitors/genetics ; RNA, Small Interfering/genetics ; Signal Transduction ; Time Factors ; Tumor Suppressor Protein p53/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Bacterial division. Mechanical crack propagation drives millisecond daughter cell separation in Staphylococcus aureus (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-05-02
    Description: When Staphylococcus aureus undergoes cytokinesis, it builds a septum, generating two hemispherical daughters whose cell walls are only connected via a narrow peripheral ring. We found that resolution of this ring occurred within milliseconds ("popping"), without detectable changes in cell volume. The likelihood of popping depended on cell-wall stress, and the separating cells split open asymmetrically, leaving the daughters connected by a hinge. An elastostatic model of the wall indicated high circumferential stress in the peripheral ring before popping. Last, we observed small perforations in the peripheral ring that are likely initial points of mechanical failure. Thus, the ultrafast daughter cell separation in S. aureus appears to be driven by accumulation of stress in the peripheral ring and exhibits hallmarks of mechanical crack propagation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Xiaoxue -- Halladin, David K -- Rojas, Enrique R -- Koslover, Elena F -- Lee, Timothy K -- Huang, Kerwyn Casey -- Theriot, Julie A -- 1S10OD01227601/OD/NIH HHS/ -- DP2OD006466/OD/NIH HHS/ -- P50-GM107615/GM/NIGMS NIH HHS/ -- R01 AI036929/AI/NIAID NIH HHS/ -- R01-AI36929/AI/NIAID NIH HHS/ -- R37 AI036929/AI/NIAID NIH HHS/ -- T32 GM007276/GM/NIGMS NIH HHS/ -- T32-GM007276/GM/NIGMS NIH HHS/ -- U54-GM072970/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 May 1;348(6234):574-8. doi: 10.1126/science.aaa1511.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Stanford University, Stanford, CA 94305, USA. Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305, USA. Howard Hughes Medical Institute (HHMI), Stanford University School of Medicine, Stanford, CA 94305, USA. ; Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305, USA. Howard Hughes Medical Institute (HHMI), Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA. ; Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305, USA. Howard Hughes Medical Institute (HHMI), Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Bioengineering, Stanford University, Stanford, CA 94305, USA. ; Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305, USA. Howard Hughes Medical Institute (HHMI), Stanford University School of Medicine, Stanford, CA 94305, USA. ; Department of Bioengineering, Stanford University, Stanford, CA 94305, USA. ; Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Bioengineering, Stanford University, Stanford, CA 94305, USA. ; Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305, USA. Howard Hughes Medical Institute (HHMI), Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA. theriot@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25931560" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Wall/physiology/ultrastructure ; *Cytokinesis ; Microscopy, Electron, Scanning ; Microscopy, Video ; Staphylococcus aureus/cytology/*physiology/ultrastructure ; Stress, Mechanical ; Time Factors
    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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  • 4
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    Long-term measles-induced immunomodulation increases overall childhood infectious disease mortality (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-05-09
    Description: Immunosuppression after measles is known to predispose people to opportunistic infections for a period of several weeks to months. Using population-level data, we show that measles has a more prolonged effect on host resistance, extending over 2 to 3 years. We find that nonmeasles infectious disease mortality in high-income countries is tightly coupled to measles incidence at this lag, in both the pre- and post-vaccine eras. We conclude that long-term immunologic sequelae of measles drive interannual fluctuations in nonmeasles deaths. This is consistent with recent experimental work that attributes the immunosuppressive effects of measles to depletion of B and T lymphocytes. Our data provide an explanation for the long-term benefits of measles vaccination in preventing all-cause infectious disease. By preventing measles-associated immune memory loss, vaccination protects polymicrobial herd immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mina, Michael J -- Metcalf, C Jessica E -- de Swart, Rik L -- Osterhaus, A D M E -- Grenfell, Bryan T -- T32 GM008169/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2015 May 8;348(6235):694-9. doi: 10.1126/science.aaa3662. Epub 2015 May 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ, USA. Medical Scientist Training Program, School of Medicine, Emory University, Atlanta, GA, USA. michael.j.mina@gmail.com. ; Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ, USA. Fogarty International Center, National Institutes of Health, Bethesda, MD, USA. ; Department of Viroscience, Erasmus University Medical Center, Rotterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25954009" target="_blank"〉PubMed〈/a〉
    Keywords: B-Lymphocytes/immunology ; Child ; *Child Mortality ; Child, Preschool ; England/epidemiology ; Female ; Humans ; Immunologic Memory ; *Immunomodulation ; Incidence ; Lymphocyte Depletion ; Male ; Measles/*epidemiology/*immunology/prevention & control ; Measles Vaccine/administration & dosage/*immunology ; Opportunistic Infections/immunology/*mortality/*prevention & control ; T-Lymphocytes/immunology ; Time Factors ; United States/epidemiology ; Vaccination ; Wales/epidemiology
    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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    Cotranslational protein folding on the ribosome monitored in real time (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-11-28
    Description: Protein domains can fold into stable tertiary structures while they are synthesized on the ribosome. We used a high-performance, reconstituted in vitro translation system to investigate the folding of a small five-helix protein domain-the N-terminal domain of Escherichia coli N5-glutamine methyltransferase HemK-in real time. Our observations show that cotranslational folding of the protein, which folds autonomously and rapidly in solution, proceeds through a compact, non-native conformation that forms within the peptide tunnel of the ribosome. The compact state rearranges into a native-like structure immediately after the full domain sequence has emerged from the ribosome. Both folding transitions are rate-limited by translation, allowing for quasi-equilibrium sampling of the conformational space restricted by the ribosome. Cotranslational folding may be typical of small, intrinsically rapidly folding protein domains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holtkamp, Wolf -- Kokic, Goran -- Jager, Marcus -- Mittelstaet, Joerg -- Komar, Anton A -- Rodnina, Marina V -- New York, N.Y. -- Science. 2015 Nov 27;350(6264):1104-7. doi: 10.1126/science.aad0344.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physical Biochemistry, Max Planck Institute for Biophysical Chemistry, 37077 Gottingen, Germany. ; Center for Gene Regulation in Health and Disease and Department of Biological, Geological and Environmental Sciences, Cleveland State University, Cleveland, OH 44115, USA. ; Department of Physical Biochemistry, Max Planck Institute for Biophysical Chemistry, 37077 Gottingen, Germany. rodnina@mpibpc.mpg.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26612953" target="_blank"〉PubMed〈/a〉
    Keywords: Escherichia coli Proteins/biosynthesis/chemistry ; Fluorescence Resonance Energy Transfer/*methods ; Peptides/chemistry ; *Protein Biosynthesis ; *Protein Folding ; Protein Methyltransferases/biosynthesis/chemistry ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Proteolysis ; Ribosomes/chemistry/*metabolism ; Time Factors
    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
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    Dopamine and serotonin signals for reward across time scales (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-10-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jeremiah Y -- New York, N.Y. -- Science. 2015 Oct 2;350(6256):47. doi: 10.1126/science.aad3003.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon H. Snyder Department of Neuroscience, Brain Science Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. jeremiah.cohen@jhmi.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26430113" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Dopamine/*metabolism ; Dopaminergic Neurons/*metabolism ; Electric Stimulation ; Humans ; Mice ; Neurophysiology/trends ; *Reward ; Serotonin/*metabolism ; Signal Transduction ; Time Factors ; Ventral Tegmental Area/*cytology
    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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  • 7
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    Mountain gorilla genomes reveal the impact of long-term population decline and inbreeding (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-04-11
    Description: Mountain gorillas are an endangered great ape subspecies and a prominent focus for conservation, yet we know little about their genomic diversity and evolutionary past. We sequenced whole genomes from multiple wild individuals and compared the genomes of all four Gorilla subspecies. We found that the two eastern subspecies have experienced a prolonged population decline over the past 100,000 years, resulting in very low genetic diversity and an increased overall burden of deleterious variation. A further recent decline in the mountain gorilla population has led to extensive inbreeding, such that individuals are typically homozygous at 34% of their sequence, leading to the purging of severely deleterious recessive mutations from the population. We discuss the causes of their decline and the consequences for their future survival.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4668944/" 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/PMC4668944/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xue, Yali -- Prado-Martinez, Javier -- Sudmant, Peter H -- Narasimhan, Vagheesh -- Ayub, Qasim -- Szpak, Michal -- Frandsen, Peter -- Chen, Yuan -- Yngvadottir, Bryndis -- Cooper, David N -- de Manuel, Marc -- Hernandez-Rodriguez, Jessica -- Lobon, Irene -- Siegismund, Hans R -- Pagani, Luca -- Quail, Michael A -- Hvilsom, Christina -- Mudakikwa, Antoine -- Eichler, Evan E -- Cranfield, Michael R -- Marques-Bonet, Tomas -- Tyler-Smith, Chris -- Scally, Aylwyn -- 098051/Wellcome Trust/United Kingdom -- 099769/Z/12/Z/Wellcome Trust/United Kingdom -- 260372/European Research Council/International -- HG002385/HG/NHGRI NIH HHS/ -- R01 HG002385/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Apr 10;348(6231):242-5. doi: 10.1126/science.aaa3952. Epub 2015 Apr 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK. ; Institut de Biologia Evolutiva (CSIC/UPF), Parque de Investigacion Biomedica de Barcelona (PRBB), Barcelona, Catalonia 08003, Spain. ; Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA. ; Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK. Department of Applied Mathematics and Theoretical Physics, University of Cambridge, Cambridge CB3 0WA, UK. ; Department of Biology, University of Copenhagen, DK-2200 Copenhagen N, Denmark. ; Institute of Medical Genetics, Cardiff University, Cardiff CF14 4XN, UK. ; Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK. Department of Biological, Geological and Environmental Sciences, University of Bologna, 40134 Bologna, Italy. ; Research and Conservation, Copenhagen Zoo, DK-2000 Frederiksberg, Denmark. ; Rwanda Development Board, KG 9 Avenue, Kigali, Rwanda. ; Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA. Howard Hughes Medical Institute, Seattle, WA 91895, USA. ; Gorilla Doctors, Karen C. Drayer Wildlife Health Center, University of California, Davis, CA 95616, USA. ; Institut de Biologia Evolutiva (CSIC/UPF), Parque de Investigacion Biomedica de Barcelona (PRBB), Barcelona, Catalonia 08003, Spain. Centro Nacional de Analisis Genomico (Parc Cientific de Barcelona), Baldiri Reixac 4, 08028 Barcelona, Spain. ; Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK. cts@sanger.ac.uk aos21@cam.ac.uk. ; Department of Genetics, University of Cambridge, Cambridge CB2 3EH, UK. cts@sanger.ac.uk aos21@cam.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25859046" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; Biological Evolution ; DNA Copy Number Variations ; Democratic Republic of the Congo ; Endangered Species ; Female ; *Genetic Variation ; *Genome ; Gorilla gorilla/classification/*genetics/physiology ; Homozygote ; *Inbreeding ; Linkage Disequilibrium ; Male ; Mutation ; Population Dynamics ; Rwanda ; Selection, Genetic ; Sequence Analysis, DNA ; Species Specificity ; Time Factors
    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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