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  • Humans  (26,747)
  • Cell & Developmental Biology  (25,032)
  • Biochemistry and Biotechnology  (13,095)
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  • 1
    Publication Date: 2022-05-25
    Description: © The Author(s), 2018. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in International Journal of Environmental Research and Public Health 15 (2018): 723, doi:10.3390/ijerph15040723.
    Description: There has been a massive increase in recent years of the use of lead (Pb) isotopes in attempts to better understand sources and pathways of Pb in the environment and in man or experimental animals. Unfortunately, there have been many cases where the quality of the isotopic data, especially that obtained by quadrupole inductively coupled plasma mass spectrometry (Q-ICP-MS), are questionable, resulting in questionable identification of potential sources, which, in turn, impacts study interpretation and conclusions. We present several cases where the isotopic data have compromised interpretation because of the use of only the major isotopes 208Pb/206Pb and 207Pb/206Pb, or their graphing in other combinations. We also present some examples comparing high precision data from thermal ionization (TIMS) or multi-collector plasma mass spectrometry (MC-ICP-MS) to illustrate the deficiency in the Q-ICP-MS data. In addition, we present cases where Pb isotopic ratios measured on Q-ICP-MS are virtually impossible for terrestrial samples. We also evaluate the Pb isotopic data for rat studies, which had concluded that Pb isotopic fractionation occurs between different organs and suggest that this notion of biological fractionation of Pb as an explanation for isotopic differences is not valid. Overall, the brief review of these case studies shows that Q-ICP-MS as commonly practiced is not a suitable technique for precise and accurate Pb isotopic analysis in the environment and health fields
    Keywords: Lead isotopes ; ICP-MS ; TIMS ; MC-ICP-MS ; Environment ; Humans ; Rats ; Fractionation
    Repository Name: Woods Hole Open Access Server
    Type: Article
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haddad, Nick M -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1166-7. doi: 10.1126/science.aad5072.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Applied Ecology, North Carolina State University, Raleigh, NC 27695, USA. nick_haddad@ncsu.ed.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785459" target="_blank"〉PubMed〈/a〉
    Keywords: Brazil ; *Conservation of Natural Resources ; Humans ; *Transportation
    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: 2016-01-20
    Description: Telomeres are the protective end-complexes at the termini of eukaryotic chromosomes. Telomere attrition can lead to potentially maladaptive cellular changes, block cell division, and interfere with tissue replenishment. Recent advances in the understanding of human disease processes have clarified the roles of telomere biology, especially in diseases of human aging and in some aging-related processes. Greater overall telomere attrition predicts mortality and aging-related diseases in inherited telomere syndrome patients, and also in general human cohorts. However, genetically caused variations in telomere maintenance either raise or lower risks and progression of cancers, in a highly cancer type-specific fashion. Telomere maintenance is determined by genetic factors and is also cumulatively shaped by nongenetic influences throughout human life; both can interact. These and other recent findings highlight both causal and potentiating roles for telomere attrition in human diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blackburn, Elizabeth H -- Epel, Elissa S -- Lin, Jue -- CA096840/CA/NCI NIH HHS/ -- GM026259/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1193-8. doi: 10.1126/science.aab3389.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94143, USA. elizabeth.blackburn@ucsf.edu. ; Department of Psychiatry, University of California, San Francisco, CA 94143, USA. ; Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785477" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics ; Cell Division/genetics ; Disease/*genetics ; *Genetic Predisposition to Disease ; Humans ; Life Style ; Neoplasms/genetics ; Stress, Physiological ; Telomerase/metabolism ; Telomere/chemistry/*physiology/ultrastructure ; Telomere Homeostasis/*genetics
    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
    Publication Date: 2016-01-20
    Description: Massive open online courses (MOOCs) are often characterized as remedies to educational disparities related to social class. Using data from 68 MOOCs offered by Harvard and MIT between 2012 and 2014, we found that course participants from the United States tended to live in more-affluent and better-educated neighborhoods than the average U.S. resident. Among those who did register for courses, students with greater socioeconomic resources were more likely to earn a certificate. Furthermore, these differences in MOOC access and completion were larger for adolescents and young adults, the traditional ages where people find on-ramps into science, technology, engineering, and mathematics (STEM) coursework and careers. Our findings raise concerns that MOOCs and similar approaches to online learning can exacerbate rather than reduce disparities in educational outcomes related to socioeconomic status.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hansen, John D -- Reich, Justin -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1245-8. doi: 10.1126/science.aab3782. Epub 2015 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard Graduate School of Education, Harvard University, Cambridge, MA 02138, USA. john_hansen@mail.harvard.edu. ; Office of Digital Learning, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785488" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Career Choice ; Certification/*methods ; Education, Distance/*methods ; Engineering/education ; Humans ; Internet ; Learning ; Mathematics/education ; *Online Systems ; Science/education ; *Social Class ; Students ; Technology/education ; United States ; Young Adult
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    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: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1188-90. doi: 10.1126/science.350.6265.1188.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785475" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/blood/genetics/*physiology ; Animals ; Biological Clocks/genetics/*physiology ; Biomarkers/blood/metabolism ; DNA/genetics ; DNA Methylation ; Epigenesis, Genetic ; Humans ; Mice ; Rats ; Telomere Homeostasis
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Escobar, Herton -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1138-9. doi: 10.1126/science.350.6265.1138. Epub 2015 Dec 3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785449" target="_blank"〉PubMed〈/a〉
    Keywords: Arsenic/analysis ; Brazil ; Copper/analysis ; *Disasters ; *Environmental Restoration and Remediation ; Food Chain ; Humans ; Mercury/analysis ; Metals, Heavy/*analysis ; Rivers ; Sewage/*analysis ; Structure Collapse ; *Tsunamis
    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
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheid, Johannes F -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1175. doi: 10.1126/science.aad7133.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital, Boston, MA 02114, USA. The Rockefeller University, New York, NY 10021, USA. fscheid@partners.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785466" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/genetics/immunology/isolation & purification ; Antibodies, Neutralizing/genetics/*immunology/isolation & purification ; B-Lymphocytes/*immunology ; Cell Separation/methods ; HIV Antibodies/genetics/*immunology/isolation & purification ; HIV Infections/*blood ; Humans ; Immunologic Memory ; Mice ; env Gene Products, Human Immunodeficiency Virus/*immunology
    Print ISSN: 0036-8075
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  • 8
    Publication Date: 2016-01-20
    Description: Congenital heart disease (CHD) patients have an increased prevalence of extracardiac congenital anomalies (CAs) and risk of neurodevelopmental disabilities (NDDs). Exome sequencing of 1213 CHD parent-offspring trios identified an excess of protein-damaging de novo mutations, especially in genes highly expressed in the developing heart and brain. These mutations accounted for 20% of patients with CHD, NDD, and CA but only 2% of patients with isolated CHD. Mutations altered genes involved in morphogenesis, chromatin modification, and transcriptional regulation, including multiple mutations in RBFOX2, a regulator of mRNA splicing. Genes mutated in other cohorts examined for NDD were enriched in CHD cases, particularly those with coexisting NDD. These findings reveal shared genetic contributions to CHD, NDD, and CA and provide opportunities for improved prognostic assessment and early therapeutic intervention in CHD patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Homsy, Jason -- Zaidi, Samir -- Shen, Yufeng -- Ware, James S -- Samocha, Kaitlin E -- Karczewski, Konrad J -- DePalma, Steven R -- McKean, David -- Wakimoto, Hiroko -- Gorham, Josh -- Jin, Sheng Chih -- Deanfield, John -- Giardini, Alessandro -- Porter, George A Jr -- Kim, Richard -- Bilguvar, Kaya -- Lopez-Giraldez, Francesc -- Tikhonova, Irina -- Mane, Shrikant -- Romano-Adesman, Angela -- Qi, Hongjian -- Vardarajan, Badri -- Ma, Lijiang -- Daly, Mark -- Roberts, Amy E -- Russell, Mark W -- Mital, Seema -- Newburger, Jane W -- Gaynor, J William -- Breitbart, Roger E -- Iossifov, Ivan -- Ronemus, Michael -- Sanders, Stephan J -- Kaltman, Jonathan R -- Seidman, Jonathan G -- Brueckner, Martina -- Gelb, Bruce D -- Goldmuntz, Elizabeth -- Lifton, Richard P -- Seidman, Christine E -- Chung, Wendy K -- T32 HL007208/HL/NHLBI NIH HHS/ -- Arthritis Research UK/United Kingdom -- British Heart Foundation/United Kingdom -- Department of Health/United Kingdom -- Howard Hughes Medical Institute/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1262-6. doi: 10.1126/science.aac9396.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA, USA. Cardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA. ; Department of Genetics, Yale University School of Medicine, New Haven, CT, USA. ; Departments of Systems Biology and Biomedical Informatics, Columbia University Medical Center, New York, NY, USA. ; Department of Genetics, Harvard Medical School, Boston, MA, USA. NIHR Cardiovascular Biomedical Research Unit at Royal Brompton & Harefield NHS Foundation and Trust and Imperial College London, London, UK. National Heart & Lung Institute, Imperial College London, London, UK. ; Department of Genetics, Harvard Medical School, Boston, MA, USA. Analytical and Translational Genetics Unit, Massachusetts General Hospital and Harvard Medical School, Boston MA, USA. ; Department of Genetics, Harvard Medical School, Boston, MA, USA. Howard Hughes Medical Institute, Harvard University, Boston, MA, USA. ; Department of Genetics, Harvard Medical School, Boston, MA, USA. ; Department of Cardiology, University College London and Great Ormond Street Hospital, London, UK. ; Department of Pediatrics, University of Rochester Medical Center, The School of Medicine and Dentistry, Rochester, NY, USA. ; Section of Cardiothoracic Surgery, University of Southern California Keck School of Medicine, Los Angeles, CA, USA. ; Department of Genetics, Yale University School of Medicine, New Haven, CT, USA. Yale Center for Genome Analysis, Yale University, New Haven, CT, USA. ; Yale Center for Genome Analysis, Yale University, New Haven, CT, USA. ; Steven and Alexandra Cohen Children's Medical Center of New York, New Hyde Park, NY, USA. ; Departments of Systems Biology and Biomedical Informatics, Columbia University Medical Center, New York, NY, USA. Department of Applied Physics and Applied Mathematics, Columbia University, New York, NY, USA. ; Department of Neurology, Columbia University Medical Center, New York, NY, USA. ; Department of Pediatrics, Columbia University Medical Center, New York, NY, USA. ; Department of Cardiology, Children's Hospital Boston, Boston, MA, USA. ; Division of Pediatric Cardiology, University of Michigan, Ann Arbor, MI, USA. ; Department of Pediatrics, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada. ; Department of Cardiology, Boston Children's Hospital, Boston, MA, USA. ; Department of Pediatric Cardiac Surgery, The Children's Hospital of Philadelphia, Philadelphia, PA, USA. ; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA. ; Department of Psychiatry, University of California San Francisco, San Francisco, CA, USA. ; Heart Development and Structural Diseases Branch, Division of Cardiovascular Sciences, NHLBI/NIH, Bethesda, MD, USA. ; Department of Genetics, Yale University School of Medicine, New Haven, CT, USA. bruce.gelb@mssm.edu goldmuntz@email.chop.edu martina.brueckner@yale.edu richard.lifton@yale.edu cseidman@genetics.med.harvard.edu wkc15@cumc.columbia.edu. ; Mindich Child Health and Development Institute and Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY, USA. bruce.gelb@mssm.edu goldmuntz@email.chop.edu martina.brueckner@yale.edu richard.lifton@yale.edu cseidman@genetics.med.harvard.edu wkc15@cumc.columbia.edu. ; Department of Pediatrics, The Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Division of Cardiology, The Children's Hospital of Philadelphia, Philadelphia, PA, USA. bruce.gelb@mssm.edu goldmuntz@email.chop.edu martina.brueckner@yale.edu richard.lifton@yale.edu cseidman@genetics.med.harvard.edu wkc15@cumc.columbia.edu. ; Department of Genetics, Yale University School of Medicine, New Haven, CT, USA. Howard Hughes Medical Institute, Yale University, New Haven, CT, USA. bruce.gelb@mssm.edu goldmuntz@email.chop.edu martina.brueckner@yale.edu richard.lifton@yale.edu cseidman@genetics.med.harvard.edu wkc15@cumc.columbia.edu. ; Department of Genetics, Harvard Medical School, Boston, MA, USA. Howard Hughes Medical Institute, Harvard University, Boston, MA, USA. Cardiovascular Division, Brigham & Women's Hospital, Harvard University, Boston, MA, USA. bruce.gelb@mssm.edu goldmuntz@email.chop.edu martina.brueckner@yale.edu richard.lifton@yale.edu cseidman@genetics.med.harvard.edu wkc15@cumc.columbia.edu. ; Departments of Pediatrics and Medicine, Columbia University Medical Center, New York, NY, USA. bruce.gelb@mssm.edu goldmuntz@email.chop.edu martina.brueckner@yale.edu richard.lifton@yale.edu cseidman@genetics.med.harvard.edu wkc15@cumc.columbia.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785492" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/abnormalities/metabolism ; Child ; Congenital Abnormalities/genetics ; Exome/genetics ; Heart Defects, Congenital/*diagnosis/*genetics ; Humans ; Mutation ; Nervous System Malformations/*genetics ; Neurogenesis/*genetics ; Prognosis ; RNA Splicing/genetics ; RNA, Messenger/genetics ; RNA-Binding Proteins/genetics ; Repressor Proteins/genetics ; Transcription, Genetic
    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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  • 9
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: Nicotinamide adenine dinucleotide (NAD(+)) is a coenzyme found in all living cells. It serves both as a critical coenzyme for enzymes that fuel reduction-oxidation reactions, carrying electrons from one reaction to another, and as a cosubstrate for other enzymes such as the sirtuins and poly(adenosine diphosphate-ribose) polymerases. Cellular NAD(+) concentrations change during aging, and modulation of NAD(+) usage or production can prolong both health span and life span. Here we review factors that regulate NAD(+) and discuss how supplementation with NAD(+) precursors may represent a new therapeutic opportunity for aging and its associated disorders, particularly neurodegenerative diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Verdin, Eric -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1208-13. doi: 10.1126/science.aac4854.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institutes, Department of Medicine, University of California, San Francisco, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785480" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/drug effects/genetics/*metabolism ; Biosynthetic Pathways ; DNA Damage ; Diabetes Mellitus, Type 2/metabolism ; Fatty Liver/metabolism ; Humans ; Mitochondria/metabolism ; NAD/*metabolism ; Neurodegenerative Diseases/drug therapy/*metabolism ; Obesity/metabolism ; Oxidation-Reduction ; Poly(ADP-ribose) Polymerases/metabolism ; Sirtuins/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hurtley, Stella -- Roberts, Leslie -- Ray, L Bryan -- Purnell, Beverly A -- Ash, Caroline -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1180-1. doi: 10.1126/science.350.6265.1180.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785472" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics ; Animals ; Health ; Humans ; Mitochondria/metabolism ; Stem Cells/physiology ; Telomere/*genetics ; *Telomere Homeostasis
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ford, Adam T -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1175. doi: 10.1126/science.aad7134.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Integrative Biology at the University of Guelph, Guelph, Ontario, Canada. adamford@uoguelph.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785465" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Wild ; Antelopes ; *Dogs ; Endangered Species ; *Food Chain ; *Grassland ; *Herbivory ; Humans ; Plants
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  • 12
    Publication Date: 2016-01-20
    Description: Flow regulation and irrigation alter local freshwater conditions, but their global effects are highly uncertain. We investigated these global effects from 1901 to 2008, using hydroclimatic observations in 100 large hydrological basins. Globally, we find consistent and dominant effects of increasing relative evapotranspiration from both activities, and decreasing temporal runoff variability from flow regulation. The evapotranspiration effect increases the long-term average human consumption of fresh water by 3563 +/- 979 km(3)/year from 1901-1954 to 1955-2008. This increase raises a recent estimate of the current global water footprint of humanity by around 18%, to 10,688 +/- 979 km(3)/year. The results highlight the global impact of local water-use activities and call for their relevant account in Earth system modeling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaramillo, Fernando -- Destouni, Georgia -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1248-51. doi: 10.1126/science.aad1010.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physical Geography and Bolin Centre for Climate Research, Stockholm University, SE-106 91, Stockholm, Sweden. Department of Biological and Environmental Sciences, University of Gothenburg, 40530 Goteborg, Sweden. fernando.jaramillo@natgeo.su.se. ; Department of Physical Geography and Bolin Centre for Climate Research, Stockholm University, SE-106 91, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785489" target="_blank"〉PubMed〈/a〉
    Keywords: *Agricultural Irrigation ; Climate Change ; *Drinking ; *Fresh Water ; Humans ; Plant Transpiration ; Water Supply/*standards
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  • 13
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: The potential for the gut microbiota to affect health has a particular relevance for older individuals. This is because the microbiota may modulate aging-related changes in innate immunity, sarcopaenia, and cognitive function, all of which are elements of frailty. Both cell culture-dependent and -independent studies show that the gut microbiota of older people differs from that of younger adults. There is no chronological threshold or age at which the composition of the microbiota suddenly alters; rather, changes occur gradually with time. Our detailed analyses have separated the microbiota into groups associated with age, long-term residential care, habitual diet, and degree of retention of a core microbiome. We are beginning to understand how these groups change with aging and how they relate to clinical phenotypes. These data provide a framework for analyzing microbiota-health associations, distinguishing correlation from causation, identifying microbiota interaction with physiological aging processes, and developing microbiota-based health surveillance for older adults.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Toole, Paul W -- Jeffery, Ian B -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1214-5. doi: 10.1126/science.aac8469.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Microbiology and APC Microbiome Institute, University College Cork, Cork T12 Y337, Ireland. pwotoole@ucc.ie. ; School of Microbiology and APC Microbiome Institute, University College Cork, Cork T12 Y337, Ireland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785481" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; *Aging ; Food Habits ; Frail Elderly ; *Gastrointestinal Microbiome ; Health ; Humans
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  • 14
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akiyama, Hiroko -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1135. doi: 10.1126/science.aad9386.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hiroko Akiyama is a professor at the Institute of Gerontology at the University of Tokyo, 7-3-1 Hongo, Bunkyoku, Tokyo, Japan. akiyama@iog.u-tokyo.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785447" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Female ; Humans ; Japan ; *Longevity ; Retirement ; Social Security
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alexandrov, Ludmil B -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1175. doi: 10.1126/science.aad7363.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Theoretical Biology and Biophysics (T-6), Los Alamos National Laboratory, Los Alamos, NM 87545, USA. lba@lanl.gov.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785464" target="_blank"〉PubMed〈/a〉
    Keywords: *Computer Simulation ; DNA Mutational Analysis ; Genomics/*methods ; Humans ; *Models, Genetic ; *Mutagenesis ; Mutation ; Neoplasms/classification/*genetics/pathology
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amigo, Ignacio -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1286. doi: 10.1126/science.350.6265.1286.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ignacio Amigo is a postdoctoral researcher in the biochemistry department of the Chemistry Institute at the University of Sao Paulo in Brazil. Send your story to SciCareerEditor@aaas.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785493" target="_blank"〉PubMed〈/a〉
    Keywords: Biochemistry ; Humans ; Molecular Biology ; Parenting/*psychology ; *Paternal Behavior
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    Publication Date: 2016-01-20
    Description: Age is the greatest risk factor for nearly every major cause of mortality in developed nations. Despite this, most biomedical research focuses on individual disease processes without much consideration for the relationships between aging and disease. Recent discoveries in the field of geroscience, which aims to explain biological mechanisms of aging, have provided insights into molecular processes that underlie biological aging and, perhaps more importantly, potential interventions to delay aging and promote healthy longevity. Here we describe some of these advances, along with efforts to move geroscience from the bench to the clinic. We also propose that greater emphasis should be placed on research into basic aging processes, because interventions that slow aging will have a greater effect on quality of life compared with disease-specific approaches.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaeberlein, Matt -- Rabinovitch, Peter S -- Martin, George M -- P30AG013280/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1191-3. doi: 10.1126/science.aad3267.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Washington, Seattle, WA 98195, USA. kaeber@uw.edu. ; Department of Pathology, University of Washington, Seattle, WA 98195, USA. ; Department of Pathology, University of Washington, Seattle, WA 98195, USA. Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785476" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Diet ; Exercise ; Geriatrics/*trends ; *Health ; Humans ; Mortality ; Preventive Medicine/*trends ; Risk Factors ; TOR Serine-Threonine Kinases/antagonists & inhibitors ; Translational Medical Research/trends
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1186-7. doi: 10.1126/science.350.6265.1186.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785474" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/genetics/physiology ; Caenorhabditis elegans Proteins/genetics/physiology ; Caloric Restriction ; Death ; Humans ; Hydra/genetics/physiology ; Longevity/genetics/*physiology ; Mice ; Mutation ; Phosphatidylinositol 3-Kinases/genetics/physiology
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: Research into stem cells and aging aims to understand how stem cells maintain tissue health, what mechanisms ultimately lead to decline in stem cell function with age, and how the regenerative capacity of somatic stem cells can be enhanced to promote healthy aging. Here, we explore the effects of aging on stem cells in different tissues. Recent research has focused on the ways that genetic mutations, epigenetic changes, and the extrinsic environmental milieu influence stem cell functionality over time. We describe each of these three factors, the ways in which they interact, and how these interactions decrease stem cell health over time. We are optimistic that a better understanding of these changes will uncover potential strategies to enhance stem cell function and increase tissue resiliency into old age.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodell, Margaret A -- Rando, Thomas A -- P01 AG036695/AG/NIA NIH HHS/ -- R01 AG047820/AG/NIA NIH HHS/ -- R01 AR062185/AR/NIAMS NIH HHS/ -- R37 AG023806/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1199-204. doi: 10.1126/science.aab3388.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cells and Regenerative Medicine Center, Center for Cell and Gene Therapy, and Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030, USA. goodell@bcm.edu rando@stanford.edu. ; Glenn Center for the Biology of Aging and Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA, and Center for Regenerative Rehabilitation, Veterans Administration Palo Alto Health Care System, Palo Alto, CA 94304, USA. goodell@bcm.edu rando@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785478" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/*physiology ; Aging/*physiology ; Animals ; Cell Aging ; Epigenesis, Genetic ; Genetic Drift ; *Health ; Humans ; Mice ; Mutation ; Organ Specificity ; Selection, Genetic
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greenbaum, Dov -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1176. doi: 10.1126/science.350.6265.1176-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Zvi Meitar Institute for Legal Implications of Emerging Technologies, Interdisciplinary Center, Herzliya Israel and Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT 10463, USA. dov.greenbaum@yale.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785467" target="_blank"〉PubMed〈/a〉
    Keywords: *Clothing ; Humans ; *Military Personnel ; *Robotics ; Walking/*physiology
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grimm, David -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1182-5. doi: 10.1126/science.350.6265.1182.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785473" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Animals ; Body Weight ; Cats ; Dogs ; Humans ; *Longevity ; Pets/*physiology
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, Ry -- Gill, Jason J -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1163-4. doi: 10.1126/science.aad6791.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Phage Technology, Texas A&M University, College Station, TX 77843, USA. Department of Biochemistry and Biophysics, Texas A&M University, College Station, TX 77843, USA. ryland@tamu.edu jason.gill@tamu.edu. ; Center for Phage Technology, Texas A&M University, College Station, TX 77843, USA. Department of Animal Science, Texas A&M University, College Station, TX 77843, USA. ryland@tamu.edu jason.gill@tamu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785457" target="_blank"〉PubMed〈/a〉
    Keywords: *Bacteriocins ; Biological Therapy/*methods ; Burns/microbiology/therapy ; *Caudovirales ; Drug Resistance, Bacterial ; Gram-Positive Bacterial Infections/*therapy ; Humans
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gura, Trisha -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1139-40. doi: 10.1126/science.350.6265.1139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785450" target="_blank"〉PubMed〈/a〉
    Keywords: Biotechnology/trends ; DNA/*genetics ; Drug Discovery/*methods ; Drug Evaluation, Preclinical/*methods ; Drug Industry/trends ; Humans ; *Small Molecule Libraries
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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
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉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
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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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    American Association for the Advancement of Science (AAAS)
    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):1136-7. doi: 10.1126/science.351.6278.1136.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965604" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; *Bacteria/classification/genetics/isolation & purification ; Biometric Identification/*methods ; Cell Phones ; Clothing ; *Forensic Medicine ; Humans ; *Microbiota ; RNA, Ribosomal, 16S/genetics/isolation & purification ; Sex Factors
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Segal, Rosalind A -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1494. doi: 10.1126/science.351.6280.1494.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rosalind A. Segal is a neurobiology professor at Harvard Medical School and co-chair of cancer biology at the Dana-Farber Cancer Institute in Boston. Send your story to SciCareerEditor@aaas.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013735" target="_blank"〉PubMed〈/a〉
    Keywords: *Career Choice ; Female ; Humans ; Neurobiology/manpower ; *Sexism ; *Women, Working
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    Publication Date: 2016-02-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Claiborne, Anne B -- English, Rebecca A -- Kahn, Jeffrey P -- 10002265/PHS HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):668-70. doi: 10.1126/science.aaf3091. Epub 2016 Feb 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Medicine, U.S. National Academies of Sciences, Engineering, and Medicine, Washington, DC 20001, USA. aclaiborne@nas.edu. ; Institute of Medicine, U.S. National Academies of Sciences, Engineering, and Medicine, Washington, DC 20001, USA. ; Johns Hopkins Berman Institute of Bioethics, Johns Hopkins University, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26842937" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Nucleus/genetics ; DNA, Mitochondrial/genetics ; Ethics, Medical ; *Government Regulation ; Humans ; Mitochondrial Diseases/genetics/*prevention & control ; Mitochondrial Replacement Therapy/*ethics/*standards ; *Oocytes ; United States ; United States Food and Drug Administration ; *Zygote
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawler, Andrew -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):280-1. doi: 10.1126/science.352.6283.280.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081048" target="_blank"〉PubMed〈/a〉
    Keywords: Archaeology ; Estonia ; History, Ancient ; Humans ; Ships ; Skeleton ; Slavery/*history ; Sweden
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Servick, Kelly -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1130-2. doi: 10.1126/science.351.6278.1130.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965601" target="_blank"〉PubMed〈/a〉
    Keywords: Bites and Stings ; Criminal Law/*statistics & numerical data ; Dermatoglyphics ; Firearms ; Forensic Sciences/legislation & jurisprudence/*statistics & numerical data/trends ; Humans ; Wounds, Gunshot
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Servick, Kelly -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):15. doi: 10.1126/science.351.6268.15.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721984" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; California ; Cell Differentiation ; Clinical Trials as Topic ; Drug Industry ; Embryonic Stem Cells/cytology/*transplantation ; Financing, Organized ; Humans ; Photoreceptor Cells/physiology ; Rats ; Regenerative Medicine/*economics/*trends ; Retina/cytology/physiology ; Stem Cell Research/*economics
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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〉Lawler, Andrew -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):501-2. doi: 10.1126/science.352.6285.501.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126014" target="_blank"〉PubMed〈/a〉
    Keywords: China/epidemiology ; DNA, Bacterial/*genetics ; Disease Outbreaks/*history ; Europe/epidemiology ; History, Medieval ; Humans ; Plague/epidemiology/*history/microbiology ; Yersinia pestis/*classification/genetics/pathogenicity
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawler, Andrew -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):111-2. doi: 10.1126/science.351.6269.111.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744387" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Drinking Water ; *Droughts ; Humans ; Indian Ocean ; Iraq ; Mesopotamia ; Salinity ; Warfare ; Water Resources/*supply & distribution ; *Wetlands
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):434. doi: 10.1126/science.351.6272.434.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823407" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-Retroviral Agents/*pharmacokinetics/therapeutic use ; *Drug Resistance, Viral ; HIV/drug effects/*genetics/physiology ; HIV Infections/blood/*drug therapy/*virology ; Humans ; Lymph Nodes/*virology ; Male ; Mutagenesis ; RNA, Viral/analysis ; Tissue Distribution ; Virus Replication
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):16-9. doi: 10.1126/science.351.6268.16.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721985" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomedical Research/*economics ; Communicable Disease Control/*economics ; Financial Management ; Humans ; National Institutes of Health (U.S.) ; United States ; Vaccines/*economics
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shanahan, Jesse -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):418. doi: 10.1126/science.351.6271.418.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jesse Shanahan is a master's student in astronomy at Wesleyan University in Middletown, Connecticut. Send your story to SciCareerEditor@aaas.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26798017" target="_blank"〉PubMed〈/a〉
    Keywords: Astronomy/*education ; *Career Mobility ; Disabled Persons/*psychology/statistics & numerical data ; Fear ; *Hostility ; Humans ; Male ; United States
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  • 38
    Publication Date: 2016-01-30
    Description: Cystic fibrosis (CF) is caused by mutations in the gene that encodes the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel. In humans and pigs, the loss of CFTR impairs respiratory host defenses, causing airway infection. But CF mice are spared. We found that in all three species, CFTR secreted bicarbonate into airway surface liquid. In humans and pigs lacking CFTR, unchecked H(+) secretion by the nongastric H(+)/K(+) adenosine triphosphatase (ATP12A) acidified airway surface liquid, which impaired airway host defenses. In contrast, mouse airways expressed little ATP12A and secreted minimal H(+); consequently, airway surface liquid in CF and non-CF mice had similar pH. Inhibiting ATP12A reversed host defense abnormalities in human and pig airways. Conversely, expressing ATP12A in CF mouse airways acidified airway surface liquid, impaired defenses, and increased airway bacteria. These findings help explain why CF mice are protected from infection and nominate ATP12A as a potential therapeutic target for CF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shah, Viral S -- Meyerholz, David K -- Tang, Xiao Xiao -- Reznikov, Leah -- Abou Alaiwa, Mahmoud -- Ernst, Sarah E -- Karp, Philip H -- Wohlford-Lenane, Christine L -- Heilmann, Kristopher P -- Leidinger, Mariah R -- Allen, Patrick D -- Zabner, Joseph -- McCray, Paul B Jr -- Ostedgaard, Lynda S -- Stoltz, David A -- Randak, Christoph O -- Welsh, Michael J -- 5T32GM007337/GM/NIGMS NIH HHS/ -- DK054759/DK/NIDDK NIH HHS/ -- F30 HL123239/HL/NHLBI NIH HHS/ -- F30HL123239/HL/NHLBI NIH HHS/ -- HL091842/HL/NHLBI NIH HHS/ -- HL117744/HL/NHLBI NIH HHS/ -- HL51670/HL/NHLBI NIH HHS/ -- K08HL097071/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):503-7. doi: 10.1126/science.aad5589.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Iowa, Iowa City, IA 52242, USA. Department of Molecular Physiology and Biophysics, Pappajohn Biomedical Institute, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA. ; Department of Pathology, University of Iowa, Iowa City, IA 52242, USA. ; Department of Medicine, University of Iowa, Iowa City, IA 52242, USA. Howard Hughes Medical Institute, University of Iowa, Iowa City, IA 52242, USA. ; Department of Medicine, University of Iowa, Iowa City, IA 52242, USA. ; Department of Pediatrics University of Iowa, Iowa City, IA 52242, USA. ; Department of Microbiology, University of Iowa, Iowa City, IA 52242, USA. ; Department of Pediatrics University of Iowa, Iowa City, IA 52242, USA. Department of Microbiology, University of Iowa, Iowa City, IA 52242, USA. ; Department of Medicine, University of Iowa, Iowa City, IA 52242, USA. Department of Molecular Physiology and Biophysics, Pappajohn Biomedical Institute, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA. Department of Biomedical Engineering, College of Engineering, University of Iowa, Iowa City, IA 52242, USA. ; Department of Medicine, University of Iowa, Iowa City, IA 52242, USA. Department of Molecular Physiology and Biophysics, Pappajohn Biomedical Institute, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA. Howard Hughes Medical Institute, University of Iowa, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823428" target="_blank"〉PubMed〈/a〉
    Keywords: Acids/metabolism ; Animals ; Bicarbonates/metabolism ; Cystic Fibrosis/*metabolism/*microbiology ; H(+)-K(+)-Exchanging ATPase/genetics/*metabolism ; Humans ; Hydrogen-Ion Concentration ; Lung/*metabolism/*microbiology ; Mice ; Mice, Inbred CFTR/genetics/metabolism ; Mice, Transgenic ; Swine
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  • 39
    Publication Date: 2016-01-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- Enserink, Martin -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):12-3. doi: 10.1126/science.351.6268.12.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721981" target="_blank"〉PubMed〈/a〉
    Keywords: Africa, Western/epidemiology ; Antiviral Agents/therapeutic use ; Clinical Trials as Topic ; Cytosine/analogs & derivatives/therapeutic use ; Ebola Vaccines/therapeutic use ; Ebolavirus/drug effects ; *Epidemics ; Global Health ; Hemorrhagic Fever, Ebola/*drug therapy/*epidemiology ; Humans ; Organophosphonates/therapeutic use ; World Health Organization
    Print ISSN: 0036-8075
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  • 40
    Publication Date: 2016-03-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Collins, Francis S -- Anderson, James M -- Austin, Christopher P -- Battey, James F -- Birnbaum, Linda S -- Briggs, Josephine P -- Clayton, Janine A -- Cuthbert, Bruce -- Eisinger, Robert W -- Fauci, Anthony S -- Gallin, John I -- Gibbons, Gary H -- Glass, Roger I -- Gottesman, Michael M -- Gray, Patricia A -- Green, Eric D -- Greider, Franziska B -- Hodes, Richard -- Hudson, Kathy L -- Humphreys, Betsy -- Katz, Stephen I -- Koob, George F -- Koroshetz, Walter J -- Lauer, Michael S -- Lorsch, Jon R -- Lowy, Douglas R -- McGowan, John J -- Murray, David M -- Nakamura, Richard -- Norris, Andrea -- Perez-Stable, Eliseo J -- Pettigrew, Roderic I -- Riley, William T -- Rodgers, Griffin P -- Sieving, Paul A -- Somerman, Martha J -- Spong, Catherine Y -- Tabak, Lawrence A -- Volkow, Nora D -- Wilder, Elizabeth L -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1405. doi: 10.1126/science.351.6280.1405-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Office of the Director, NIH, Bethesda, MD 20892, USA. collinsf@mail.nih.gov. ; Division of Program Coordination, Planning, and Strategic Initiatives, NIH, Bethesda, MD 20892, USA. ; National Center for Advancing Translational Science, NIH, Rockville, MD 20850, USA. ; National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, MD 20892, USA. ; National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA. ; National Center for Complementary and Integrative Health, NIH, Bethesda, MD 20892, USA. ; Office of Research on Women's Health, NIH, Bethesda, MD 20892, USA. ; National Institute of Mental Health, NIH, Bethesda, MD 20892, USA. ; Office of AIDS Research, NIH, Bethesda, MD 20892, USA. ; National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA. ; Clinical Center, NIH, Bethesda, MD 20892, USA. ; National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892, USA. ; Fogarty International Center, NIH, Bethesda, MD 20892, USA. ; Office of Intramural Research, NIH, Bethesda, MD 20892, USA. ; National Institute of Nursing Research, NIH, Bethesda, MD 20892, USA. ; National Human Genome Research Institute, NIH, Bethesda, MD 20892, USA. ; Office of Research Infrastructure Programs, NIH, Bethesda, MD 20892, USA. ; National Institute on Aging, NIH, Bethesda, MD 20892, USA. ; Office of the Director, NIH, Bethesda, MD 20892, USA. ; National Library of Medicine, NIH, Bethesda, MD 20892, USA. ; National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, MD 20892, USA. ; National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD 20892, USA. ; NINDS, NIH, Bethesda, MD 20892, USA. ; Office of Extramural Research, NIH, Bethesda, MD 20892, USA. ; National Institute of General Medical Sciences, NIH, Bethesda, MD 20892, USA. ; National Cancer Institute, NIH, Bethesda, MD 20892, USA. ; Office of Management, NIH, Bethesda, MD 20892, USA. ; Office of Disease Prevention, NIH, Bethesda, MD 20892, USA. ; Center for Scientific Review, NIH, Bethesda, MD 20892, USA. ; Center for Information Technology, NIH, Bethesda, MD 20892, USA. ; National Institute on Minority Health and Health Disparities, NIH, Bethesda, MD 20892, USA. ; National Institute of Biomedical Imaging and Bioengineering, NIH, Bethesda, MD 20892, USA. ; Office of Behavioral and Social Sciences Research, NIH, Bethesda, MD 20892, USA. ; National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA. ; National Eye Institute, NIH, Bethesda, MD 20892, USA. ; National Institute of Dental and Craniofacial Research, NIH, Bethesda, MD 20892, USA. ; Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD 20892, USA. ; National Institute on Drug Abuse, NIH, Bethesda, MD 20892, USA. ; Office of Strategic Coordination, NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013720" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomedical Research/*economics ; Humans ; National Institutes of Health (U.S.)/*economics
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  • 41
    Publication Date: 2016-02-26
    Description: Mota and Herculano-Houzel (Reports, 3 July 2015, p. 74) assign power functions to neuroanatomical data and present a model to account for evolutionary patterns of cortical folding in the mammalian brain. We detail how the model assumptions are in conflict with experimental and observational work and show that the model itself does not accurately fit the data.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewitus, Eric -- Kelava, Iva -- Kalinka, Alex T -- Tomancak, Pavel -- Huttner, Wieland B -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):825. doi: 10.1126/science.aad2029.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Biologie, Ecole Normale Superieure, Paris, France. lewitus@biologie.ens.fr huttner@mpi-cbg.de. ; MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge Biomedical Campus, Cambridge CB2 0QH, UK. ; Institute of Population Genetics, Vetmeduni, Vienna, Austria. ; Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany. ; Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany. lewitus@biologie.ens.fr huttner@mpi-cbg.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cerebral Cortex ; Humans ; Lissencephaly/*pathology ; Neurons/*cytology
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  • 42
    Publication Date: 2016-02-26
    Description: Voltage-gated CaV1.2 channels (L-type calcium channel alpha1C subunits) are critical mediators of transcription-dependent neural plasticity. Whether these channels signal via the influx of calcium ion (Ca(2+)), voltage-dependent conformational change (VDeltaC), or a combination of the two has thus far been equivocal. We fused CaV1.2 to a ligand-gated Ca(2+)-permeable channel, enabling independent control of localized Ca(2+) and VDeltaC signals. This revealed an unexpected dual requirement: Ca(2+) must first mobilize actin-bound Ca(2+)/calmodulin-dependent protein kinase II, freeing it for subsequent VDeltaC-mediated accumulation. Neither signal alone sufficed to activate transcription. Signal order was crucial: Efficiency peaked when Ca(2+) preceded VDeltaC by 10 to 20 seconds. CaV1.2 VDeltaC synergistically augmented signaling by N-methyl-d-aspartate receptors. Furthermore, VDeltaC mistuning correlated with autistic symptoms in Timothy syndrome. Thus, nonionic VDeltaC signaling is vital to the function of CaV1.2 in synaptic and neuropsychiatric processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Boxing -- Tadross, Michael R -- Tsien, Richard W -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):863-7. doi: 10.1126/science.aad3647.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience and Physiology and New York University Neuroscience Institute, New York, NY 10016, USA. ; Department of Molecular and Cellular Physiology, Beckman Center, School of Medicine, Stanford University, Stanford, CA 94305, USA. Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147, USA. tadrossm@janelia.hhmi.org. ; Department of Neuroscience and Physiology and New York University Neuroscience Institute, New York, NY 10016, USA. Department of Molecular and Cellular Physiology, Beckman Center, School of Medicine, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912895" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/genetics/metabolism ; Calcium Channel Blockers/pharmacology ; Calcium Channels, L-Type/chemistry/*metabolism ; *Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; *Gene Expression Regulation ; HEK293 Cells ; Hippocampus/cytology ; Humans ; Long QT Syndrome/genetics/metabolism ; Neuronal Plasticity/*genetics ; Neurons/drug effects/*metabolism ; Nimodipine/pharmacology ; Protein Conformation/drug effects ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/metabolism ; Syndactyly/genetics/metabolism
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  • 43
    facet.materialart.
    Unknown
    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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  • 44
    Publication Date: 2016-02-27
    Description: Rasmussen and Svensson correctly point out that there is currently no satisfactory method to fully align the Greenland and Cariaco Basin records of climate change. However, our approach using interstadial onsets as tie-points allows direct comparison between radiocarbon dates and Greenland climate records. Crucially, both the standard Greenland and the merged Greenland-Cariaco time scales show that interstadial warming was associated with megafaunal genetic transitions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cooper, Alan -- Turney, Chris -- Hughen, Konrad -- New York, N.Y. -- Science. 2016 Feb 26;351(6276):927. doi: 10.1126/science.aad8016.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Adelaide, Australian Centre for Ancient DNA, School of Earth and Environmental Sciences, and Environment Institute, Adelaide, Australia. alan.cooper@adelaide.edu.au. ; Climate Change Research Centre, School of Biological, Earth and Environmental Sciences, University of New South Wales, Sydney, Australia. ; Department of Marine Chemistry and Geochemistry, Woods Hole Oceanographic Institution, Woods Hole, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26917762" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Extinction, Biological ; Global Warming/*history ; Humans
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  • 45
    Publication Date: 2016-04-30
    Description: Noncoding variants play a central role in the genetics of complex traits, but we still lack a full understanding of the molecular pathways through which they act. We quantified the contribution of cis-acting genetic effects at all major stages of gene regulation from chromatin to proteins, in Yoruba lymphoblastoid cell lines (LCLs). About ~65% of expression quantitative trait loci (eQTLs) have primary effects on chromatin, whereas the remaining eQTLs are enriched in transcribed regions. Using a novel method, we also detected 2893 splicing QTLs, most of which have little or no effect on gene-level expression. These splicing QTLs are major contributors to complex traits, roughly on a par with variants that affect gene expression levels. Our study provides a comprehensive view of the mechanisms linking genetic variation to variation in human gene regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Yang I -- van de Geijn, Bryce -- Raj, Anil -- Knowles, David A -- Petti, Allegra A -- Golan, David -- Gilad, Yoav -- Pritchard, Jonathan K -- R01MH084703/MH/NIMH NIH HHS/ -- R01MH101825/MH/NIMH NIH HHS/ -- U01HG007036/HG/NHGRI NIH HHS/ -- U54CA149145/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):600-4. doi: 10.1126/science.aad9417. Epub 2016 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Stanford University, Stanford, CA, USA. ; Department of Human Genetics, University of Chicago, Chicago, IL, USA. ; Department of Computer Science, Stanford University, Stanford, CA, USA. Department of Radiology, Stanford University, Stanford, CA, USA. ; Genome Institute, Washington University in St. Louis, St. Louis, MO, USA. ; Department of Human Genetics, University of Chicago, Chicago, IL, USA. gilad@uchicago.edu pritch@stanford.edu. ; Department of Genetics, Stanford University, Stanford, CA, USA. Department of Biology, Stanford University, Stanford, CA, USA. Howard Hughes Medical Institute, Stanford University, Stanford, CA, USA. gilad@uchicago.edu pritch@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126046" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chromatin/metabolism ; *Gene Expression Regulation ; *Genetic Variation ; Genome-Wide Association Study ; Humans ; Immune System Diseases/*genetics ; Lymphocytes/immunology ; Phenotype ; Polymorphism, Single Nucleotide ; *Quantitative Trait Loci ; RNA Splicing/*genetics
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  • 46
    Publication Date: 2016-04-30
    Description: Fecal microbiota transplantation (FMT) has shown efficacy in treating recurrent Clostridium difficile infection and is increasingly being applied to other gastrointestinal disorders, yet the fate of native and introduced microbial strains remains largely unknown. To quantify the extent of donor microbiota colonization, we monitored strain populations in fecal samples from a recent FMT study on metabolic syndrome patients using single-nucleotide variants in metagenomes. We found extensive coexistence of donor and recipient strains, persisting 3 months after treatment. Colonization success was greater for conspecific strains than for new species, the latter falling within fluctuation levels observed in healthy individuals over a similar time frame. Furthermore, same-donor recipients displayed varying degrees of microbiota transfer, indicating individual patterns of microbiome resistance and donor-recipient compatibilities.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Simone S -- Zhu, Ana -- Benes, Vladimir -- Costea, Paul I -- Hercog, Rajna -- Hildebrand, Falk -- Huerta-Cepas, Jaime -- Nieuwdorp, Max -- Salojarvi, Jarkko -- Voigt, Anita Y -- Zeller, Georg -- Sunagawa, Shinichi -- de Vos, Willem M -- Bork, Peer -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):586-9. doi: 10.1126/science.aad8852.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Structural and Computational Biology Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany. School of Biotechnology and Biomolecular Sciences, University of New South Wales, 2052 Sydney, Australia. ; Structural and Computational Biology Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany. ; Genomics Core Facility, European Molecular Biology Laboratory, 69117 Heidelberg, Germany. ; Department of Vascular Medicine, Academic Medical Center, 1105 AZ Amsterdam, Netherlands. Diabetes Center, Vrije University Medical Center, 1018 HV Amsterdam, Netherlands. Wallenberg Laboratory, University of Gothenburg, 41345 Gothenburg, Sweden. ; Department of Veterinary Biosciences, University of Helsinki, 00014 Helsinki, Finland. Department of Biosciences, University of Helsinki, 00014 Helsinki, Finland. ; Structural and Computational Biology Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany. Department of Applied Tumor Biology, Institute of Pathology, University Hospital Heidelberg, 69120 Heidelberg, Germany. Molecular Medicine Partnership Unit, University of Heidelberg and European Molecular Biology Laboratory, 69120 Heidelberg, Germany. ; Structural and Computational Biology Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany. bork@embl.de willem.devos@wur.nl sunagawa@embl.de. ; Department of Veterinary Biosciences, University of Helsinki, 00014 Helsinki, Finland. Laboratory of Microbiology, Wageningen University, 6703 HB Wageningen, Netherlands. Immunobiology Research Program, Department of Bacteriology and Immunology, University of Helsinki, 00014 Helsinki, Finland. bork@embl.de willem.devos@wur.nl sunagawa@embl.de. ; Structural and Computational Biology Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany. Molecular Medicine Partnership Unit, University of Heidelberg and European Molecular Biology Laboratory, 69120 Heidelberg, Germany. Max Delbruck Centre for Molecular Medicine, 13125 Berlin, Germany. Department of Bioinformatics, Biocenter, University of Wurzburg, 97074 Wurzburg, Germany. bork@embl.de willem.devos@wur.nl sunagawa@embl.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126044" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteria/classification/isolation & purification ; Clostridium Infections/microbiology/*therapy ; *Fecal Microbiota Transplantation ; Feces/microbiology ; Gastrointestinal Microbiome/*physiology ; Humans ; Symbiosis ; Tissue Donors ; Transplantation, Homologous
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  • 47
    Publication Date: 2016-04-02
    Description: The recent rapid spread of Zika virus and its unexpected linkage to birth defects and an autoimmune neurological syndrome have generated worldwide concern. Zika virus is a flavivirus like the dengue, yellow fever, and West Nile viruses. We present the 3.8 angstrom resolution structure of mature Zika virus, determined by cryo-electron microscopy (cryo-EM). The structure of Zika virus is similar to other known flavivirus structures, except for the ~10 amino acids that surround the Asn(154) glycosylation site in each of the 180 envelope glycoproteins that make up the icosahedral shell. The carbohydrate moiety associated with this residue, which is recognizable in the cryo-EM electron density, may function as an attachment site of the virus to host cells. This region varies not only among Zika virus strains but also in other flaviviruses, which suggests that differences in this region may influence virus transmission and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4845755/" 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/PMC4845755/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sirohi, Devika -- Chen, Zhenguo -- Sun, Lei -- Klose, Thomas -- Pierson, Theodore C -- Rossmann, Michael G -- Kuhn, Richard J -- R01 AI073755/AI/NIAID NIH HHS/ -- R01 AI076331/AI/NIAID NIH HHS/ -- R01AI073755/AI/NIAID NIH HHS/ -- R01AI076331/AI/NIAID NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):467-70. doi: 10.1126/science.aaf5316. Epub 2016 Mar 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Markey Center for Structural Biology and Purdue Institute for Inflammation, Immunology and Infectious Disease, Purdue University, West Lafayette, IN 47907, USA. ; Viral Pathogenesis Section, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27033547" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cryoelectron Microscopy ; Glycosylation ; Humans ; Molecular Sequence Data ; Protein Structure, Tertiary ; Viral Envelope Proteins/chemistry/ultrastructure ; Viral Matrix Proteins/chemistry/ultrastructure ; Zika Virus/*chemistry/*ultrastructure
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  • 48
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):440-3. doi: 10.1126/science.351.6272.440.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823410" target="_blank"〉PubMed〈/a〉
    Keywords: Child ; Child, Preschool ; DNA Mutational Analysis ; DNA Repair/genetics ; Female ; *Genes, Neoplasm ; *Genetic Predisposition to Disease ; Humans ; Male ; Mutation ; Neoplasms/*genetics/mortality ; Pedigree ; Tumor Suppressor Protein p53/genetics
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  • 49
    Publication Date: 2016-04-16
    Description: The nuclear pore complex (NPC) controls the transport of macromolecules between the nucleus and cytoplasm, but its molecular architecture has thus far remained poorly defined. We biochemically reconstituted NPC core protomers and elucidated the underlying protein-protein interaction network. Flexible linker sequences, rather than interactions between the structured core scaffold nucleoporins, mediate the assembly of the inner ring complex and its attachment to the NPC coat. X-ray crystallographic analysis of these scaffold nucleoporins revealed the molecular details of their interactions with the flexible linker sequences and enabled construction of full-length atomic structures. By docking these structures into the cryoelectron tomographic reconstruction of the intact human NPC and validating their placement with our nucleoporin interactome, we built a composite structure of the NPC symmetric core that contains ~320,000 residues and accounts for ~56 megadaltons of the NPC's structured mass. Our approach provides a paradigm for the structure determination of similarly complex macromolecular assemblies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Daniel H -- Stuwe, Tobias -- Schilbach, Sandra -- Rundlet, Emily J -- Perriches, Thibaud -- Mobbs, George -- Fan, Yanbin -- Thierbach, Karsten -- Huber, Ferdinand M -- Collins, Leslie N -- Davenport, Andrew M -- Jeon, Young E -- Hoelz, Andre -- 5 T32 GM07616/GM/NIGMS NIH HHS/ -- ACB-12002/PHS HHS/ -- AGM-12006/PHS HHS/ -- R01 GM111461/GM/NIGMS NIH HHS/ -- R01-GM111461/GM/NIGMS NIH HHS/ -- T32 GM007616/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):aaf1015. doi: 10.1126/science.aaf1015. Epub 2016 Apr 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Chemistry and Chemical Engineering, California Institute of Technology, 1200 East California Boulevard, Pasadena, CA 91125, USA. ; Division of Chemistry and Chemical Engineering, California Institute of Technology, 1200 East California Boulevard, Pasadena, CA 91125, USA. hoelz@caltech.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081075" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Amino Acid Sequence ; Cryoelectron Microscopy ; Crystallography, X-Ray ; Cytoplasm/metabolism ; Electron Microscope Tomography ; Fungal Proteins/chemistry/genetics/metabolism ; Humans ; Molecular Sequence Data ; Nuclear Pore/chemistry/*metabolism/*ultrastructure ; Nuclear Pore Complex Proteins/chemistry/genetics/*metabolism ; *Protein Interaction Maps ; Protein Structure, Tertiary ; Protein Subunits/chemistry/genetics/metabolism
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  • 50
    Publication Date: 2016-02-26
    Description: Many modern human genomes retain DNA inherited from interbreeding with archaic hominins, such as Neandertals, yet the influence of this admixture on human traits is largely unknown. We analyzed the contribution of common Neandertal variants to over 1000 electronic health record (EHR)-derived phenotypes in ~28,000 adults of European ancestry. We discovered and replicated associations of Neandertal alleles with neurological, psychiatric, immunological, and dermatological phenotypes. Neandertal alleles together explained a significant fraction of the variation in risk for depression and skin lesions resulting from sun exposure (actinic keratosis), and individual Neandertal alleles were significantly associated with specific human phenotypes, including hypercoagulation and tobacco use. Our results establish that archaic admixture influences disease risk in modern humans, provide hypotheses about the effects of hundreds of Neandertal haplotypes, and demonstrate the utility of EHR data in evolutionary analyses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simonti, Corinne N -- Vernot, Benjamin -- Bastarache, Lisa -- Bottinger, Erwin -- Carrell, David S -- Chisholm, Rex L -- Crosslin, David R -- Hebbring, Scott J -- Jarvik, Gail P -- Kullo, Iftikhar J -- Li, Rongling -- Pathak, Jyotishman -- Ritchie, Marylyn D -- Roden, Dan M -- Verma, Shefali S -- Tromp, Gerard -- Prato, Jeffrey D -- Bush, William S -- Akey, Joshua M -- Denny, Joshua C -- Capra, John A -- 1K22LM011938/LM/NLM NIH HHS/ -- 1R01GM114128/GM/NIGMS NIH HHS/ -- 5T32EY021453/EY/NEI NIH HHS/ -- R01GM110068/GM/NIGMS NIH HHS/ -- R01LM010685/LM/NLM NIH HHS/ -- U01HG004438/HG/NHGRI NIH HHS/ -- U01HG004608/HG/NHGRI NIH HHS/ -- U01HG004609/HG/NHGRI NIH HHS/ -- U01HG004610/HG/NHGRI NIH HHS/ -- U01HG006378/HG/NHGRI NIH HHS/ -- U01HG006379/HG/NHGRI NIH HHS/ -- U01HG006380/HG/NHGRI NIH HHS/ -- U01HG006382/HG/NHGRI NIH HHS/ -- U01HG006385/HG/NHGRI NIH HHS/ -- U01HG006388/HG/NHGRI NIH HHS/ -- U01HG006389/HG/NHGRI NIH HHS/ -- U01HG008657/HG/NHGRI NIH HHS/ -- U01HG04599/HG/NHGRI NIH HHS/ -- U01HG04603/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):737-41. doi: 10.1126/science.aad2149.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vanderbilt Genetics Institute, Vanderbilt University, Nashville, TN, USA. ; Department of Genome Sciences, University of Washington, Seattle, WA, USA. ; Department of Biomedical Informatics, Vanderbilt University, Nashville, TN, USA. ; Mount Sinai School of Medicine, New York, NY, USA. ; Department of Medicine (Medical Genetics), University of Washington Medical Center, Seattle, WA, USA. ; Center for Genetic Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. ; Department of Genome Sciences, University of Washington, Seattle, WA, USA. Department of Medicine (Medical Genetics), University of Washington Medical Center, Seattle, WA, USA. ; Center for Human Genetics, Marshfield Clinic, Marshfield, WI, USA. ; Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, USA. ; Division of Genomic Medicine, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA. ; Division of Health Sciences Research, Mayo Clinic, Rochester, MN, USA. ; Department of Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, PA, USA. Biomedical and Translational Informatics, Geisinger Health System, Danville, PA, USA. ; Vanderbilt Genetics Institute, Vanderbilt University, Nashville, TN, USA. Department of Biomedical Informatics, Vanderbilt University, Nashville, TN, USA. Department of Medicine, Vanderbilt University, Nashville, TN, USA. Department of Pharmacology, Vanderbilt University, Nashville, TN, USA. ; Department of Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, PA, USA. ; Weis Center for Research, Geisinger Health System, Danville, PA, USA. Division of Molecular Biology and Human Genetics, Department of Biomedical Sciences, Faculty of Health Science, Stellenbosch University, Tygerberg, South Africa. ; Department of Epidemiology and Biostatistics, Case Western Reserve University, Cleveland, OH, USA. ; Vanderbilt Genetics Institute, Vanderbilt University, Nashville, TN, USA. Department of Biomedical Informatics, Vanderbilt University, Nashville, TN, USA. Department of Medicine, Vanderbilt University, Nashville, TN, USA. ; Vanderbilt Genetics Institute, Vanderbilt University, Nashville, TN, USA. Department of Biomedical Informatics, Vanderbilt University, Nashville, TN, USA. Department of Biological Sciences, Vanderbilt University, Nashville, TN, USA. Center for Quantitative Sciences, Vanderbilt University, Nashville, TN, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912863" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Depression/genetics ; Disease/*genetics ; European Continental Ancestry Group/genetics ; Evolution, Molecular ; Genetic Variation ; Genome, Human ; Haplotypes ; Humans ; Keratosis, Actinic/genetics ; Neanderthals/*genetics ; Phenotype
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  • 51
    Publication Date: 2016-02-27
    Description: Ebola virus disease in humans is highly lethal, with case fatality rates ranging from 25 to 90%. There is no licensed treatment or vaccine against the virus, underscoring the need for efficacious countermeasures. We ascertained that a human survivor of the 1995 Kikwit Ebola virus disease outbreak maintained circulating antibodies against the Ebola virus surface glycoprotein for more than a decade after infection. From this survivor we isolated monoclonal antibodies (mAbs) that neutralize recent and previous outbreak variants of Ebola virus and mediate antibody-dependent cell-mediated cytotoxicity in vitro. Strikingly, monotherapy with mAb114 protected macaques when given as late as 5 days after challenge. Treatment with a single human mAb suggests that a simplified therapeutic strategy for human Ebola infection may be possible.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corti, Davide -- Misasi, John -- Mulangu, Sabue -- Stanley, Daphne A -- Kanekiyo, Masaru -- Wollen, Suzanne -- Ploquin, Aurelie -- Doria-Rose, Nicole A -- Staupe, Ryan P -- Bailey, Michael -- Shi, Wei -- Choe, Misook -- Marcus, Hadar -- Thompson, Emily A -- Cagigi, Alberto -- Silacci, Chiara -- Fernandez-Rodriguez, Blanca -- Perez, Laurent -- Sallusto, Federica -- Vanzetta, Fabrizia -- Agatic, Gloria -- Cameroni, Elisabetta -- Kisalu, Neville -- Gordon, Ingelise -- Ledgerwood, Julie E -- Mascola, John R -- Graham, Barney S -- Muyembe-Tamfun, Jean-Jacques -- Trefry, John C -- Lanzavecchia, Antonio -- Sullivan, Nancy J -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1339-42. doi: 10.1126/science.aad5224. Epub 2016 Feb 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Research in Biomedicine, Universita della Svizzera Italiana, CH-6500 Bellinzona, Switzerland. Humabs BioMed SA, 6500 Bellinzona, Switzerland. ; Vaccine Research Center, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. ; U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, MD 21702, USA. ; Institute for Research in Biomedicine, Universita della Svizzera Italiana, CH-6500 Bellinzona, Switzerland. ; Humabs BioMed SA, 6500 Bellinzona, Switzerland. ; National Institute for Biomedical Research, National Laboratory of Public Health, Kinshasa B.P. 1197, Democratic Republic of the Congo. ; Institute for Research in Biomedicine, Universita della Svizzera Italiana, CH-6500 Bellinzona, Switzerland. Institute of Microbiology, ETH Zurich, CH-8093 Zurich, Switzerland. ; Vaccine Research Center, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. njsull@mail.nih.gov.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26917593" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Antibodies, Monoclonal/*administration & dosage/immunology/isolation & ; purification ; Antibodies, Neutralizing/*administration & dosage/immunology/isolation & ; purification ; Antibodies, Viral/*administration & dosage/immunology/isolation & purification ; Clinical Trials as Topic ; Disease Outbreaks ; Ebolavirus/*immunology ; Female ; Hemorrhagic Fever, Ebola/epidemiology/*prevention & control ; Humans ; Macaca ; Male ; Molecular Sequence Data ; Survivors
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  • 52
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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〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):284-7. doi: 10.1126/science.352.6283.284.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081051" target="_blank"〉PubMed〈/a〉
    Keywords: Clinical Trials as Topic ; Female ; Fetal Diseases/*prevention & control ; Humans ; Osteogenesis Imperfecta/*prevention & control ; Pregnancy ; *Stem Cell Transplantation ; *Stem Cells
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  • 53
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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〉Sommer, Morten O A -- Suess, Beatrix -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):144-5. doi: 10.1126/science.aaf6189.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Novo Nordisk Foundation Center for Biosustainability, Technical University of Denmark, DK-2970 Horsholm, Denmark. msom@bio.dtu.dk. ; Technische Universitat Darmstadt, 64287 Darmstadt, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124438" target="_blank"〉PubMed〈/a〉
    Keywords: Drug Resistance, Bacterial/*genetics ; *Gene Expression Regulation, Bacterial ; Genome-Wide Association Study/*methods ; High-Throughput Nucleotide Sequencing/*methods ; Humans ; Riboswitch/*genetics ; *Transcription Termination, Genetic
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  • 54
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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〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):286. doi: 10.1126/science.352.6283.286.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081052" target="_blank"〉PubMed〈/a〉
    Keywords: Clinical Trials as Topic ; Female ; Fetal Growth Retardation/*therapy ; Gene Transfer Techniques ; Genetic Therapy/*methods ; Humans ; Placenta ; Pregnancy ; Uterine Artery ; Vascular Endothelial Growth Factor A/*genetics
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1126. doi: 10.1126/science.351.6278.1126.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965598" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cholesterol, HDL/*blood ; Coronary Disease/*blood/*genetics ; Female ; Humans ; Male ; Scavenger Receptors, Class B/*genetics
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  • 56
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sood, Prashant -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):825. doi: 10.1126/science.351.6275.825-c.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Medical Sciences, University of Aberdeen, Aberdeen City, AB25 2ZD, UK. drprashantsood@gmail.com.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912887" target="_blank"〉PubMed〈/a〉
    Keywords: *Cartoons as Topic ; Humans ; India ; *Physician-Patient Relations ; Students, Medical ; *Trust ; Vaccination/psychology
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  • 57
    Publication Date: 2016-01-30
    Description: Translated regions distinct from annotated coding sequences have emerged as essential elements of the proteome. This includes upstream open reading frames (uORFs) present in mRNAs controlled by the integrated stress response (ISR) that show "privileged" translation despite inhibited eukaryotic initiation factor 2-guanosine triphosphate-initiator methionyl transfer RNA (eIF2.GTP.Met-tRNA(i )(Met)). We developed tracing translation by T cells to directly measure the translation products of uORFs during the ISR. We identified signature translation events from uORFs in the 5' untranslated region of binding immunoglobulin protein (BiP) mRNA (also called heat shock 70-kilodalton protein 5 mRNA) that were not initiated at the start codon AUG. BiP expression during the ISR required both the alternative initiation factor eIF2A and non-AUG-initiated uORFs. We propose that persistent uORF translation, for a variety of chaperones, shelters select mRNAs from the ISR, while simultaneously generating peptides that could serve as major histocompatibility complex class I ligands, marking cells for recognition by the adaptive immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Starck, Shelley R -- Tsai, Jordan C -- Chen, Keling -- Shodiya, Michael -- Wang, Lei -- Yahiro, Kinnosuke -- Martins-Green, Manuela -- Shastri, Nilabh -- Walter, Peter -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):aad3867. doi: 10.1126/science.aad3867.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, Howard Hughes Medical Institute, University of California, San Francisco, CA 94143, USA. Division of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA. shelley@walterlab.ucsf.edu nshastri@berkeley.edu peter@walterlab.ucsf.edu. ; Department of Biochemistry and Biophysics, Howard Hughes Medical Institute, University of California, San Francisco, CA 94143, USA. ; Division of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA. ; Department of Cell Biology and Neuroscience, University of California, Riverside, CA 92521, USA. ; Departments of Molecular Infectiology, Graduate School of Medicine, Chiba University, Chiba, Japan. ; Division of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA. shelley@walterlab.ucsf.edu nshastri@berkeley.edu peter@walterlab.ucsf.edu. ; Department of Biochemistry and Biophysics, Howard Hughes Medical Institute, University of California, San Francisco, CA 94143, USA. shelley@walterlab.ucsf.edu nshastri@berkeley.edu peter@walterlab.ucsf.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823435" target="_blank"〉PubMed〈/a〉
    Keywords: 5' Untranslated Regions/*genetics ; Cell Tracking ; Codon, Initiator/genetics ; Eukaryotic Initiation Factor-2/metabolism ; Heat-Shock Proteins/*biosynthesis/genetics ; Humans ; Open Reading Frames/genetics ; Protein Biosynthesis/*genetics ; RNA, Messenger/*genetics ; Stress, Physiological/*genetics ; T-Lymphocytes/metabolism/microbiology/physiology
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Curry, Andrew -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1384-9. doi: 10.1126/science.351.6280.1384.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013711" target="_blank"〉PubMed〈/a〉
    Keywords: Bone and Bones/*injuries ; Germany ; History, Ancient ; Humans ; Military Personnel/*history ; Oceans and Seas ; Rivers ; Skull/injuries ; Violence/*history ; *Warfare ; Weapons/*history
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Currie, Janet -- Grenfell, Bryan -- Farrar, Jeremy -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):815-6. doi: 10.1126/science.aad8521.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Princeton University, Woodrow Wilson School, Princeton, NJ 08540, USA. jcurrie@princeton.edu. ; Princeton University, Woodrow Wilson School, Princeton, NJ 08540, USA. ; Wellcome Trust, 215 Euston Road, London NW1 2BE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912880" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Communicable Disease Control/*methods/*organization & administration ; Delivery of Health Care ; Disease Reservoirs ; Epidemics/*prevention & control ; *Global Health ; Hemorrhagic Fever, Ebola/epidemiology/prevention & control ; Humans ; International Cooperation ; Zika Virus Infection/epidemiology/prevention & control ; Zoonoses/prevention & control/transmission
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Starr, Douglas -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1133-6. doi: 10.1126/science.351.6278.1133.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965602" target="_blank"〉PubMed〈/a〉
    Keywords: *Criminal Law ; DNA/genetics ; DNA Fingerprinting/*legislation & jurisprudence ; False Positive Reactions ; Genetic Testing/*legislation & jurisprudence ; Humans ; Prisons ; Sequence Analysis, DNA/*standards
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  • 61
    Publication Date: 2016-01-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Da Cruz, Sandrine -- Cleveland, Don W -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):125-6. doi: 10.1126/science.aad9872.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research, University of California at San Diego, La Jolla, CA 92093, USA. ; Ludwig Institute for Cancer Research, University of California at San Diego, La Jolla, CA 92093, USA. Department of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, CA 92093, USA. dcleveland@ucsd.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744395" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Nucleus/*metabolism ; Cytoplasm/*metabolism ; DNA-Binding Proteins/*metabolism ; Humans ; Nerve Tissue Proteins/*metabolism ; Neurodegenerative Diseases/*metabolism ; *Protein Aggregates ; RNA, Messenger/*metabolism
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  • 62
    Publication Date: 2016-04-28
    Description: Riboswitches and attenuators are cis-regulatory RNA elements, most of which control bacterial gene expression via metabolite-mediated, premature transcription termination. We developed an unbiased experimental approach for genome-wide discovery of such ribo-regulators in bacteria. We also devised an experimental platform that quantitatively measures the in vivo activity of all such regulators in parallel and enables rapid screening for ribo-regulators that respond to metabolites of choice. Using this approach, we detected numerous antibiotic-responsive ribo-regulators that control antibiotic resistance genes in pathogens and in the human microbiome. Studying one such regulator in Listeria monocytogenes revealed an attenuation mechanism mediated by antibiotic-stalled ribosomes. Our results expose broad roles for conditional termination in regulating antibiotic resistance and provide a tool for discovering riboswitches and attenuators that respond to previously unknown ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dar, Daniel -- Shamir, Maya -- Mellin, J R -- Koutero, Mikael -- Stern-Ginossar, Noam -- Cossart, Pascale -- Sorek, Rotem -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):aad9822. doi: 10.1126/science.aad9822.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel. ; Institut Pasteur, Unite des Interactions Bacteries-Cellules, Paris, F-75015 France. INSERM, U604, Paris, F-75015 France. Institut National de la Recherche Agronomique, USC2020, Paris, F-75015 France. ; Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel. rotem.sorek@weizmann.ac.il.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27120414" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/genetics ; Anti-Bacterial Agents/pharmacology ; Bacillus subtilis/drug effects/genetics ; Drug Resistance, Bacterial/*genetics ; Enterococcus faecalis/drug effects ; Gastrointestinal Microbiome/drug effects/genetics ; *Gene Expression Regulation, Bacterial ; Genome, Bacterial/genetics ; Genome-Wide Association Study/*methods ; High-Throughput Nucleotide Sequencing/*methods ; Humans ; Listeria monocytogenes/drug effects/genetics ; Ribosomes/metabolism ; Riboswitch/*genetics ; Sequence Analysis, RNA/methods ; *Transcription Termination, Genetic
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ma, Eric H -- Jones, Russell G -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):670-1. doi: 10.1126/science.aaf1929.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Goodman Cancer Research Centre, Department of Physiology, McGill University, Montreal, QC, H3A 1A3, Canada. Department of Physiology, McGill University, Montreal, QC, H3G 1Y6, Canada. ; Goodman Cancer Research Centre, Department of Physiology, McGill University, Montreal, QC, H3A 1A3, Canada. Department of Physiology, McGill University, Montreal, QC, H3G 1Y6, Canada. russell.jones@mcgill.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Mitochondria/*metabolism ; Multiprotein Complexes/*metabolism ; Purines/*biosynthesis/*metabolism ; TOR Serine-Threonine Kinases/*metabolism ; Tetrahydrofolates/*metabolism
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  • 64
    Publication Date: 2016-02-26
    Description: The cerebrum of large mammals is convoluted, whereas that of small mammals is smooth. Mota and Herculano-Houzel (Reports, 3 July 2015, p. 74) inspired a model on an old theory that proposed a fractal geometry. I show that their model reduces to the product of gray-matter proportion times the folding index. This proportional relation describes the available data even better than the fractal model.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Lussanet, Marc H E -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):825. doi: 10.1126/science.aad0127.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Sports Science, University of Munster, Horstmarer Landweg 62b, D-48149 Munster, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912885" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cerebral Cortex ; Humans ; Lissencephaly/*pathology ; Neurons/*cytology
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  • 65
    Publication Date: 2016-03-19
    Description: Sanchez et al.'s textbook k-anonymization example does not prove, or even suggest, that location and other big-data data sets can be anonymized and of general use. The synthetic data set that they "successfully anonymize" bears no resemblance to modern high-dimensional data sets on which their methods fail. Moving forward, deidentification should not be considered a useful basis for policy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Montjoye, Yves-Alexandre -- Pentland, Alex Sandy -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1274. doi: 10.1126/science.aaf1578.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Harvard University, Institute for Quantitative Social Science, Cambridge, MA 02138, USA. yvesalexandre@demontjoye.com. ; Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989244" target="_blank"〉PubMed〈/a〉
    Keywords: *Commerce ; *Data Collection ; Female ; Humans ; *Information Dissemination ; Male ; *Privacy
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 66
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, Richard -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1138-40. doi: 10.1126/science.351.6278.1138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965605" target="_blank"〉PubMed〈/a〉
    Keywords: Computer Simulation ; *Explosions ; *Forensic Sciences ; Humans ; *Nuclear Weapons ; United States
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  • 67
    Publication Date: 2016-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dejana, Elisabetta -- Betsholtz, Christer -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):341-2. doi: 10.1126/science.aaf1139.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden. FIRC Institute of Molecular Oncology, Milan, Italy. Department of Oncology and Hemato-Oncology, Milan University, Milan, Italy. elisabetta.dejana@igp.uu.se christer.betsholtz@igp.uu.se. ; Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden. Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden. elisabetta.dejana@igp.uu.se christer.betsholtz@igp.uu.se.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26798001" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Movement ; Cerebral Cortex/*embryology ; Humans ; Neural Stem Cells/*physiology ; *Neurogenesis ; Oligodendroglia/*physiology ; *Organogenesis ; Spinal Cord/*embryology
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  • 68
    Publication Date: 2016-01-09
    Description: The stomach bacterium Helicobacter pylori is one of the most prevalent human pathogens. It has dispersed globally with its human host, resulting in a distinct phylogeographic pattern that can be used to reconstruct both recent and ancient human migrations. The extant European population of H. pylori is known to be a hybrid between Asian and African bacteria, but there exist different hypotheses about when and where the hybridization took place, reflecting the complex demographic history of Europeans. Here, we present a 5300-year-old H. pylori genome from a European Copper Age glacier mummy. The "Iceman" H. pylori is a nearly pure representative of the bacterial population of Asian origin that existed in Europe before hybridization, suggesting that the African population arrived in Europe within the past few thousand years.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4775254/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4775254/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maixner, Frank -- Krause-Kyora, Ben -- Turaev, Dmitrij -- Herbig, Alexander -- Hoopmann, Michael R -- Hallows, Janice L -- Kusebauch, Ulrike -- Vigl, Eduard Egarter -- Malfertheiner, Peter -- Megraud, Francis -- O'Sullivan, Niall -- Cipollini, Giovanna -- Coia, Valentina -- Samadelli, Marco -- Engstrand, Lars -- Linz, Bodo -- Moritz, Robert L -- Grimm, Rudolf -- Krause, Johannes -- Nebel, Almut -- Moodley, Yoshan -- Rattei, Thomas -- Zink, Albert -- 2P50 GM076547/GM/NIGMS NIH HHS/ -- P50 GM076547/GM/NIGMS NIH HHS/ -- R01 GM087221/GM/NIGMS NIH HHS/ -- S10 RR027584/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):162-5. doi: 10.1126/science.aad2545.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Mummies and the Iceman, European Academy of Bozen/Bolzano (EURAC), Viale Druso 1, 39100 Bolzano, Italy. frank.maixner@eurac.edu albert.zink@eurac.edu. ; Institute of Clinical Molecular Biology, Kiel University, Schittenhelmstrasse 12, 24105 Kiel, Germany. ; CUBE-Division of Computational Systems Biology, Department of Microbiology and Ecosystem Science, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria. ; Institute for Archaeological Sciences, University of Tubingen, Rumelinstrasse 23, 72072 Tubingen, Germany. Max Planck Institute for the Science of Human History, Kahlaische Strasse 10, 07745 Jena, Germany. ; Institute for Systems Biology, 401 Terry Avenue North, Seattle, WA 98109, USA. ; Scuola Superiore Sanitaria Provinciale "Claudiana," Via Lorenz Bohler 13, 39100 Bolzano, Italy. ; Department of Gastroenterology, Hepatology, and Infectious Diseases, Otto-von-Guericke University, Leipziger Strasse 44, 39120 Magdeburg, Germany. ; Universite de Bordeaux, Centre National de Reference des Helicobacters et Campylobacters and INSERM U853, 146 rue Leo Saignat, 33076 Bordeaux, France. ; Institute for Mummies and the Iceman, European Academy of Bozen/Bolzano (EURAC), Viale Druso 1, 39100 Bolzano, Italy. ; Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 141 83 Stockholm, Sweden. ; Department of Veterinary and Biomedical Sciences, Pennsylvania State University, University Park, PA 16802, USA. ; Robert Mondavi Institute for Food Science, University of California, Davis, CA 95616, USA. ; Department of Zoology, University of Venda, Private Bag X5050, Thohoyandou 0950, Republic of South Africa. Department of Integrative Biology and Evolution, Konrad Lorenz Institute for Ethology, University of Veterinary Medicine Vienna, Savoyenstrasse 1a, 1160 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744403" target="_blank"〉PubMed〈/a〉
    Keywords: Asia ; Chromosome Mapping ; DNA, Bacterial/genetics/isolation & purification ; Europe ; Genome, Bacterial/*genetics ; Helicobacter Infections/*microbiology ; Helicobacter pylori/*genetics/isolation & purification ; Human Migration ; Humans ; *Hybridization, Genetic ; Ice Cover/microbiology ; Mummies/microbiology ; Phylogeny ; Phylogeography ; Sequence Analysis, DNA ; Stomach/*microbiology
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  • 69
    Publication Date: 2016-03-26
    Description: During cancer metastasis, tumor cells penetrate tissues through tight interstitial spaces, which requires extensive deformation of the cell and its nucleus. Here, we investigated mammalian tumor cell migration in confining microenvironments in vitro and in vivo. Nuclear deformation caused localized loss of nuclear envelope (NE) integrity, which led to the uncontrolled exchange of nucleo-cytoplasmic content, herniation of chromatin across the NE, and DNA damage. The incidence of NE rupture increased with cell confinement and with depletion of nuclear lamins, NE proteins that structurally support the nucleus. Cells restored NE integrity using components of the endosomal sorting complexes required for transport III (ESCRT III) machinery. Our findings indicate that cell migration incurs substantial physical stress on the NE and its content and requires efficient NE and DNA damage repair for cell survival.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4833568/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4833568/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Denais, Celine M -- Gilbert, Rachel M -- Isermann, Philipp -- McGregor, Alexandra L -- te Lindert, Mariska -- Weigelin, Bettina -- Davidson, Patricia M -- Friedl, Peter -- Wolf, Katarina -- Lammerding, Jan -- R01 HL082792/HL/NHLBI NIH HHS/ -- R01 NS059348/NS/NINDS NIH HHS/ -- S10OD018516/OD/NIH HHS/ -- U54 CA143876/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):353-8. doi: 10.1126/science.aad7297. Epub 2016 Mar 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nancy E. and Peter C. Meinig School of Biomedical Engineering and Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA. ; Department of Cell Biology, Radboud University Medical Center, Nijmegen, Netherlands. ; Department of Cell Biology, Radboud University Medical Center, Nijmegen, Netherlands. Department of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Cancer Genomics Center, Netherlands (CGC.nl). ; Nancy E. and Peter C. Meinig School of Biomedical Engineering and Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, USA. jan.lammerding@cornell.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013428" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; *Cell Movement ; Chromatin/metabolism ; Cytoplasm/metabolism ; DNA Damage ; Endosomal Sorting Complexes Required for Transport/metabolism ; Humans ; Lamins/deficiency ; Neoplasms/metabolism/*pathology ; Nuclear Envelope/metabolism/*pathology ; Stress, Mechanical ; *Tumor Microenvironment
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  • 70
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-05-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takamura, Noboru -- Orita, Makiko -- Yamashita, Shunichi -- Chhem, Rethy -- New York, N.Y. -- Science. 2016 May 6;352(6286):666. doi: 10.1126/science.352.6286.666-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, 852-8523 Japan. takamura@nagasaki-u.ac.jp. ; Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, 852-8523 Japan. ; Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, 852-8523 Japan. Cambodia Development Resource Institute, Phnom Penh 622, Cambodia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27151855" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Radiation-Induced/*epidemiology ; *Disasters ; *Epidemics ; Female ; *Fukushima Nuclear Accident ; Humans ; Radiation Exposure/*adverse effects ; Thyroid Gland/*abnormalities/*pathology ; Thyroid Neoplasms/*epidemiology
    Print ISSN: 0036-8075
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  • 71
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Devkota, Suzanne -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):452-3. doi: 10.1126/science.aaf1353.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA. suzanne.devkota@cshs.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823414" target="_blank"〉PubMed〈/a〉
    Keywords: Diabetes Mellitus, Type 2/*microbiology ; Female ; Gastrointestinal Microbiome/*drug effects/*physiology ; Humans ; Male ; Metformin/*pharmacology
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  • 72
    Publication Date: 2016-01-28
    Description: Genes encoding human beta-type globin undergo a developmental switch from embryonic to fetal to adult-type expression. Mutations in the adult form cause inherited hemoglobinopathies or globin disorders, including sickle cell disease and thalassemia. Some experimental results have suggested that these diseases could be treated by induction of fetal-type hemoglobin (HbF). However, the mechanisms that repress HbF in adults remain unclear. We found that the LRF/ZBTB7A transcription factor occupies fetal gamma-globin genes and maintains the nucleosome density necessary for gamma-globin gene silencing in adults, and that LRF confers its repressive activity through a NuRD repressor complex independent of the fetal globin repressor BCL11A. Our study may provide additional opportunities for therapeutic targeting in the treatment of hemoglobinopathies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4778394/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4778394/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Masuda, Takeshi -- Wang, Xin -- Maeda, Manami -- Canver, Matthew C -- Sher, Falak -- Funnell, Alister P W -- Fisher, Chris -- Suciu, Maria -- Martyn, Gabriella E -- Norton, Laura J -- Zhu, Catherine -- Kurita, Ryo -- Nakamura, Yukio -- Xu, Jian -- Higgs, Douglas R -- Crossley, Merlin -- Bauer, Daniel E -- Orkin, Stuart H -- Kharchenko, Peter V -- Maeda, Takahiro -- R01 AI084905/AI/NIAID NIH HHS/ -- R01 HL032259/HL/NHLBI NIH HHS/ -- R56 DK105001/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):285-9. doi: 10.1126/science.aad3312.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; Department of Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA. ; Division of Hematology/Oncology, Boston Children's Hospital, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. ; School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW 2052, Australia. ; Medical Research Council, Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, Oxford University, Oxford, UK. ; Cell Engineering Division, RIKEN BioResource Center, Tsukuba, Ibaraki, Japan. ; Cell Engineering Division, RIKEN BioResource Center, Tsukuba, Ibaraki, Japan. Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan. ; Division of Hematology/Oncology, Boston Children's Hospital, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Children's Research Institute, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Division of Hematology/Oncology, Boston Children's Hospital, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Howard Hughes Medical Institute, Boston, MA 02115, USA. ; Department of Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA. peter.kharchenko@post.harvard.edu tmaeda@partners.org. ; Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. peter.kharchenko@post.harvard.edu tmaeda@partners.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816381" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/genetics ; Animals ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Chromatin/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Erythroblasts/cytology ; Erythropoiesis/genetics ; Fetal Hemoglobin/*genetics ; *Gene Silencing ; Humans ; Mice ; Mice, Knockout ; Nuclear Proteins/genetics/*metabolism ; Repressor Proteins/genetics/*metabolism ; Sequence Deletion ; Thalassemia/genetics ; Transcription Factors/genetics/*metabolism ; gamma-Globins/*genetics
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  • 73
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matacic, Catherine -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):392-3. doi: 10.1126/science.352.6284.392. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102453" target="_blank"〉PubMed〈/a〉
    Keywords: Facial Expression ; Hand ; Head ; Humans ; Israel ; Linguistics/*trends ; Persons With Hearing Impairments/*rehabilitation ; *Sign Language ; Torso
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  • 74
    Publication Date: 2016-04-09
    Description: Activation of various cell surface receptors triggers the reorganization of downstream signaling molecules into micrometer- or submicrometer-sized clusters. However, the functional consequences of such clustering have been unclear. We biochemically reconstituted a 12-component signaling pathway on model membranes, beginning with T cell receptor (TCR) activation and ending with actin assembly. When TCR phosphorylation was triggered, downstream signaling proteins spontaneously separated into liquid-like clusters that promoted signaling outputs both in vitro and in human Jurkat T cells. Reconstituted clusters were enriched in kinases but excluded phosphatases and enhanced actin filament assembly by recruiting and organizing actin regulators. These results demonstrate that protein phase separation can create a distinct physical and biochemical compartment that facilitates signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, Xiaolei -- Ditlev, Jonathon A -- Hui, Enfu -- Xing, Wenmin -- Banjade, Sudeep -- Okrut, Julia -- King, David S -- Taunton, Jack -- Rosen, Michael K -- Vale, Ronald D -- 5-F32-DK101188/DK/NIDDK NIH HHS/ -- F32 DK101188/DK/NIDDK NIH HHS/ -- R01 GM056322/GM/NIGMS NIH HHS/ -- R01-GM56322/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):595-9. doi: 10.1126/science.aad9964. Epub 2016 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute (HHMI) Summer Institute, Marine Biological Laboratory, Woods Hole, MA 02543, USA. Department of Cellular and Molecular Pharmacology and Howard Hughes Medical Institute, University of California, San Francisco, CA 94158, USA. ; Howard Hughes Medical Institute (HHMI) Summer Institute, Marine Biological Laboratory, Woods Hole, MA 02543, USA. Department of Biophysics and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; HHMI Mass Spectrometry Laboratory and Department of Molecular and Cellular Biology, University of California, Berkeley, CA 94720, USA. ; Howard Hughes Medical Institute (HHMI) Summer Institute, Marine Biological Laboratory, Woods Hole, MA 02543, USA. Department of Biophysics and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ron.vale@ucsf.edu michael.rosen@utsouthwestern.edu. ; Howard Hughes Medical Institute (HHMI) Summer Institute, Marine Biological Laboratory, Woods Hole, MA 02543, USA. Department of Cellular and Molecular Pharmacology and Howard Hughes Medical Institute, University of California, San Francisco, CA 94158, USA. ron.vale@ucsf.edu michael.rosen@utsouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27056844" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*metabolism ; Adaptor Proteins, Signal Transducing/*metabolism ; Fluorescence Recovery After Photobleaching ; Humans ; Jurkat Cells ; Membrane Proteins/*metabolism ; Mitogen-Activated Protein Kinase Kinases ; Phosphorylation ; Polymerization ; Receptors, Antigen, T-Cell/*agonists ; Signal Transduction ; T-Lymphocytes/*metabolism
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  • 75
    Publication Date: 2016-04-29
    Description: When asked to perform the same task, different individuals exhibit markedly different patterns of brain activity. This variability is often attributed to volatile factors, such as task strategy or compliance. We propose that individual differences in brain responses are, to a large degree, inherent to the brain and can be predicted from task-independent measurements collected at rest. Using a large set of task conditions, spanning several behavioral domains, we train a simple model that relates task-independent measurements to task activity and evaluate the model by predicting task activation maps for unseen subjects using magnetic resonance imaging. Our model can accurately predict individual differences in brain activity and highlights a coupling between brain connectivity and function that can be captured at the level of individual subjects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tavor, I -- Parker Jones, O -- Mars, R B -- Smith, S M -- Behrens, T E -- Jbabdi, S -- 098369/Z/12/Z/Wellcome Trust/United Kingdom -- 1U54MH091657/MH/NIMH NIH HHS/ -- MR/L009013/1/Medical Research Council/United Kingdom -- WT104765MA/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):216-20. doi: 10.1126/science.aad8127. Epub 2016 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Oxford Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB), Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford OX3 9DU, UK. Department of Diagnostic Imaging, Sheba Medical Center, Tel Hashomer, 52621, Israel. ; Oxford Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB), Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford OX3 9DU, UK. ; Oxford Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB), Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford OX3 9DU, UK. Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen, 6525 EZ Nijmegen, Netherlands. ; Oxford Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB), Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford OX3 9DU, UK. Wellcome Trust Centre for Neuroimaging, University College London, London, WC1N 3BG, UK. ; Oxford Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB), Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford OX3 9DU, UK. saad@fmrib.ox.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124457" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/*physiology ; Brain Mapping/*methods ; Humans ; Individuality ; Language ; Magnetic Resonance Imaging/*methods ; *Task Performance and Analysis
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  • 76
    Publication Date: 2016-03-26
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4838154/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4838154/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dove, Edward S -- Townend, David -- Meslin, Eric M -- Bobrow, Martin -- Littler, Katherine -- Nicol, Dianne -- de Vries, Jantina -- Junker, Anne -- Garattini, Chiara -- Bovenberg, Jasper -- Shabani, Mahsa -- Levesque, Emmanuelle -- Knoppers, Bartha M -- 099313/Wellcome Trust/United Kingdom -- 103360/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1399-400. doi: 10.1126/science.aad5269.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉J. Kenyon Mason Institute for Medicine, Life Sciences and the Law, School of Law, University of Edinburgh, UK. edward.dove@ed.ac.uk. ; Department of Health, Ethics & Society, CAPHRI Research School, Maastricht University, The Netherlands. ; Indiana University Center for Bioethics, Indiana University School of Medicine, Indianapolis, Indiana, USA. ; Honorary Faculty, Wellcome Trust Sanger Institute, Hinxton, UK. Department of Medical Genetics, University of Cambridge, UK. ; Wellcome Trust, London, UK. ; Centre for Law and Genetics, Faculty of Law, University of Tasmania, Australia. ; Department of Medicine, Faculty of Health Sciences, University of Cape Town, South Africa. ; Department of Pediatrics, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada. ; Intel Corporation, Health and Life Sciences, London, UK. ; Legal Pathways, Aerdenhout, The Netherlands. ; Centre for Biomedical Ethics and Law, KU Leuven, Leuven, Belgium. ; Centre of Genomics and Policy, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013718" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/*ethics ; Datasets as Topic/ethics ; Ethical Review/*standards ; Genetics, Medical ; Genome, Human ; Humans ; Information Dissemination/*ethics ; Internationality ; Neoplasms
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  • 77
    Publication Date: 2016-03-19
    Description: Systemic inflammation, which results from the massive release of proinflammatory molecules into the circulatory system, is a major risk factor for severe illness, but the precise mechanisms underlying its control are not fully understood. We observed that prostaglandin E2 (PGE2), through its receptor EP4, is down-regulated in human systemic inflammatory disease. Mice with reduced PGE2 synthesis develop systemic inflammation, associated with translocation of gut bacteria, which can be prevented by treatment with EP4 agonists. Mechanistically, we demonstrate that PGE2-EP4 signaling acts directly on type 3 innate lymphoid cells (ILCs), promoting their homeostasis and driving them to produce interleukin-22 (IL-22). Disruption of the ILC-IL-22 axis impairs PGE2-mediated inhibition of systemic inflammation. Hence, the ILC-IL-22 axis is essential in protecting against gut barrier dysfunction, enabling PGE2-EP4 signaling to impede systemic inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841390/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841390/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duffin, Rodger -- O'Connor, Richard A -- Crittenden, Siobhan -- Forster, Thorsten -- Yu, Cunjing -- Zheng, Xiaozhong -- Smyth, Danielle -- Robb, Calum T -- Rossi, Fiona -- Skouras, Christos -- Tang, Shaohui -- Richards, James -- Pellicoro, Antonella -- Weller, Richard B -- Breyer, Richard M -- Mole, Damian J -- Iredale, John P -- Anderton, Stephen M -- Narumiya, Shuh -- Maizels, Rick M -- Ghazal, Peter -- Howie, Sarah E -- Rossi, Adriano G -- Yao, Chengcan -- 106122/Wellcome Trust/United Kingdom -- BB/K091121/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- DK37097/DK/NIDDK NIH HHS/ -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1333-8. doi: 10.1126/science.aad9903.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh EH16 4TJ, UK. ; Division of Pathway Medicine, Edinburgh Infectious Diseases, The University of Edinburgh, Edinburgh EH16 4SB, UK. ; Institute for Immunology and Infection Research, The University of Edinburgh, Edinburgh EH9 3JT, UK. ; MRC Centre for Regenerative Medicine, The University of Edinburgh, Edinburgh EH16 4UU, UK. ; Department of Gastroenterology, First Affiliated Hospital of Jinan University, Guangzhou 510630, China. ; Department of Veterans Affairs, Tennessee Valley Health Authority, Nashville, TN 37212, USA. Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA. ; Center for Innovation in Immunoregulative Technology and Therapeutics (AK Project), Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan. Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST), Tokyo 102-0075, Japan. ; Division of Pathway Medicine, Edinburgh Infectious Diseases, The University of Edinburgh, Edinburgh EH16 4SB, UK. Centre for Synthetic and Systems Biology (SynthSys), The University of Edinburgh, Edinburgh EH9 3JD, UK. ; Medical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh EH16 4TJ, UK. chengcan.yao@ed.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Infections/genetics/immunology ; Dinoprostone/*immunology ; Gene Expression ; Humans ; Immunity, Innate ; Inflammation/drug therapy/*immunology/microbiology ; Interleukins/*immunology ; Intestines/*immunology/microbiology ; Lymphocytes/*immunology ; Mice ; Receptors, Prostaglandin E, EP4 Subtype/antagonists & ; inhibitors/genetics/*immunology ; Signal Transduction
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  • 78
    Publication Date: 2016-02-26
    Description: 5-Methylthioadenosine phosphorylase (MTAP) is a key enzyme in the methionine salvage pathway. The MTAP gene is frequently deleted in human cancers because of its chromosomal proximity to the tumor suppressor gene CDKN2A. By interrogating data from a large-scale short hairpin RNA-mediated screen across 390 cancer cell line models, we found that the viability of MTAP-deficient cancer cells is impaired by depletion of the protein arginine methyltransferase PRMT5. MTAP-deleted cells accumulate the metabolite methylthioadenosine (MTA), which we found to inhibit PRMT5 methyltransferase activity. Deletion of MTAP in MTAP-proficient cells rendered them sensitive to PRMT5 depletion. Conversely, reconstitution of MTAP in an MTAP-deficient cell line rescued PRMT5 dependence. Thus, MTA accumulation in MTAP-deleted cancers creates a hypomorphic PRMT5 state that is selectively sensitized toward further PRMT5 inhibition. Inhibitors of PRMT5 that leverage this dysregulated metabolic state merit further investigation as a potential therapy for MTAP/CDKN2A-deleted tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mavrakis, Konstantinos J -- McDonald, E Robert 3rd -- Schlabach, Michael R -- Billy, Eric -- Hoffman, Gregory R -- deWeck, Antoine -- Ruddy, David A -- Venkatesan, Kavitha -- Yu, Jianjun -- McAllister, Gregg -- Stump, Mark -- deBeaumont, Rosalie -- Ho, Samuel -- Yue, Yingzi -- Liu, Yue -- Yan-Neale, Yan -- Yang, Guizhi -- Lin, Fallon -- Yin, Hong -- Gao, Hui -- Kipp, D Randal -- Zhao, Songping -- McNamara, Joshua T -- Sprague, Elizabeth R -- Zheng, Bing -- Lin, Ying -- Cho, Young Shin -- Gu, Justin -- Crawford, Kenneth -- Ciccone, David -- Vitari, Alberto C -- Lai, Albert -- Capka, Vladimir -- Hurov, Kristen -- Porter, Jeffery A -- Tallarico, John -- Mickanin, Craig -- Lees, Emma -- Pagliarini, Raymond -- Keen, Nicholas -- Schmelzle, Tobias -- Hofmann, Francesco -- Stegmeier, Frank -- Sellers, William R -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1208-13. doi: 10.1126/science.aad5944. Epub 2016 Feb 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Novartis Institutes for Biomedical Research, Cambridge, MA 02139, USA. ; Novartis Institutes for Biomedical Research, Basel CH-4002, Switzerland. ; Novartis Institutes for Biomedical Research, Emeryville, CA 94608, USA. ; China Novartis Institutes for Biomedical Research, Shanghai 201203, China. ; Novartis Institutes for Biomedical Research, Cambridge, MA 02139, USA. william.sellers@novartis.com fstegmeier@ksqtx.com.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912361" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; Cell Survival ; Cyclin-Dependent Kinase Inhibitor p16/genetics/*metabolism ; Deoxyadenosines/metabolism ; Gene Deletion ; Humans ; Methionine/*metabolism ; Neoplasms/drug therapy/genetics/*metabolism ; Protein-Arginine N-Methyltransferases/genetics/*metabolism ; Purine-Nucleoside Phosphorylase/genetics/*metabolism ; RNA, Small Interfering/genetics ; Thionucleosides/metabolism
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  • 79
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McLaughlin, Kathleen -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):506. doi: 10.1126/science.352.6285.506.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126018" target="_blank"〉PubMed〈/a〉
    Keywords: Child, Preschool ; China ; *Counterfeit Drugs ; *Drug Industry ; Hand, Foot and Mouth Disease/prevention & control ; Hepatitis B/prevention & control ; Humans ; Rabies/virology ; *Viral Vaccines
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  • 80
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dustin, Michael L -- Muller, James -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):516-7. doi: 10.1126/science.aaf8179.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kennedy Institute of Rheumatology, The University of Oxford, Oxford, UK. Skirball Institute, New York University School of Medicine, New York, NY, USA. michael.dustin@kennedy.ox.ac.uk. ; Skirball Institute, New York University School of Medicine, New York, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126023" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*metabolism ; Adaptor Proteins, Signal Transducing/*metabolism ; Humans ; Membrane Proteins/*metabolism ; Receptors, Antigen, T-Cell/*agonists ; T-Lymphocytes/*metabolism
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  • 81
    Publication Date: 2016-03-05
    Description: As tumors grow, they acquire mutations, some of which create neoantigens that influence the response of patients to immune checkpoint inhibitors. We explored the impact of neoantigen intratumor heterogeneity (ITH) on antitumor immunity. Through integrated analysis of ITH and neoantigen burden, we demonstrate a relationship between clonal neoantigen burden and overall survival in primary lung adenocarcinomas. CD8(+)tumor-infiltrating lymphocytes reactive to clonal neoantigens were identified in early-stage non-small cell lung cancer and expressed high levels of PD-1. Sensitivity to PD-1 and CTLA-4 blockade in patients with advanced NSCLC and melanoma was enhanced in tumors enriched for clonal neoantigens. T cells recognizing clonal neoantigens were detectable in patients with durable clinical benefit. Cytotoxic chemotherapy-induced subclonal neoantigens, contributing to an increased mutational load, were enriched in certain poor responders. These data suggest that neoantigen heterogeneity may influence immune surveillance and support therapeutic developments targeting clonal neoantigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGranahan, Nicholas -- Furness, Andrew J S -- Rosenthal, Rachel -- Ramskov, Sofie -- Lyngaa, Rikke -- Saini, Sunil Kumar -- Jamal-Hanjani, Mariam -- Wilson, Gareth A -- Birkbak, Nicolai J -- Hiley, Crispin T -- Watkins, Thomas B K -- Shafi, Seema -- Murugaesu, Nirupa -- Mitter, Richard -- Akarca, Ayse U -- Linares, Joseph -- Marafioti, Teresa -- Henry, Jake Y -- Van Allen, Eliezer M -- Miao, Diana -- Schilling, Bastian -- Schadendorf, Dirk -- Garraway, Levi A -- Makarov, Vladimir -- Rizvi, Naiyer A -- Snyder, Alexandra -- Hellmann, Matthew D -- Merghoub, Taha -- Wolchok, Jedd D -- Shukla, Sachet A -- Wu, Catherine J -- Peggs, Karl S -- Chan, Timothy A -- Hadrup, Sine R -- Quezada, Sergio A -- Swanton, Charles -- 12100/Cancer Research UK/United Kingdom -- 1R01CA155010-02/CA/NCI NIH HHS/ -- 1R01CA182461-01/CA/NCI NIH HHS/ -- 1R01CA184922-01/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1463-9. doi: 10.1126/science.aaf1490. Epub 2016 Mar 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Francis Crick Institute, London WC2A 3LY, UK. Centre for Mathematics and Physics in the Life Sciences and Experimental Biology (CoMPLEX), University College London (UCL), London WC1E 6BT, UK. Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. ; Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. Cancer Immunology Unit, UCL Cancer Institute, UCL, London WC1E 6BT, UK. ; Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. ; Section for Immunology and Vaccinology, National Veterinary Institute, Technical University of Denmark, 1970 Frederiksberg C, Denmark. ; The Francis Crick Institute, London WC2A 3LY, UK. Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. ; The Francis Crick Institute, London WC2A 3LY, UK. ; Cancer Immunology Unit, UCL Cancer Institute, UCL, London WC1E 6BT, UK. Department of Cellular Pathology, UCL, London WC1E 6BT, UK. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Center for Cancer Precision Medicine, Dana-Farber Cancer Institute, Boston, MA 02215, USA. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Department of Dermatology, University Hospital, University Duisburg-Essen, 45147 Essen, Germany. German Cancer Consortium (DKTK), 69121 Heidelberg, Germany. ; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Hematology/Oncology Division, 177 Fort Washington Avenue, Columbia University, New York, NY 10032, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Weill Cornell Medical College, New York, NY 10065, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Ludwig Collaborative Laboratory, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Weill Cornell Medical College, New York, NY 10065, USA. Ludwig Collaborative Laboratory, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Department of Medicine, Harvard Medical School, Boston, MA 02115, USA. Department of Internal Medicine, Brigham and Woman's Hospital, Boston, MA 02115, USA. ; Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. Cancer Immunology Unit, UCL Cancer Institute, UCL, London WC1E 6BT, UK. s.quezada@ucl.ac.uk charles.swanton@crick.ac.uk. ; The Francis Crick Institute, London WC2A 3LY, UK. Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. s.quezada@ucl.ac.uk charles.swanton@crick.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26940869" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/drug therapy/genetics/*immunology ; Aged ; Aged, 80 and over ; Antigens, Neoplasm/genetics/*immunology ; Antineoplastic Agents/therapeutic use ; CD4-Positive T-Lymphocytes/*immunology ; CTLA-4 Antigen/immunology ; Carcinoma, Non-Small-Cell Lung/genetics/immunology ; Cell Cycle Checkpoints/immunology ; Female ; Humans ; *Immunologic Surveillance ; Lung Neoplasms/drug therapy/genetics/*immunology ; Lymphocytes, Tumor-Infiltrating/immunology ; Male ; Melanoma/immunology ; Middle Aged ; Mutation ; Programmed Cell Death 1 Receptor/immunology ; Skin Neoplasms/immunology
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  • 82
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edwards, Marc -- Bernstein, Rachel -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1230. doi: 10.1126/science.351.6278.1230.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rachel Bernstein is the editor of Science Careers. Send your story to SciCareerEditor@aaas.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965630" target="_blank"〉PubMed〈/a〉
    Keywords: Drinking Water/*analysis ; Humans ; Lead/*analysis ; Michigan ; *Water Purification
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  • 83
    Publication Date: 2016-04-29
    Description: A decline in electron transport chain (ETC) activity is associated with many human diseases. Although diminished mitochondrial adenosine triphosphate production is recognized as a source of pathology, the contribution of the associated reduction in the ratio of the amount of oxidized nicotinamide adenine dinucleotide (NAD(+)) to that of its reduced form (NADH) is less clear. We used a water-forming NADH oxidase from Lactobacillus brevis (LbNOX) as a genetic tool for inducing a compartment-specific increase of the NAD(+)/NADH ratio in human cells. We used LbNOX to demonstrate the dependence of key metabolic fluxes, gluconeogenesis, and signaling on the cytosolic or mitochondrial NAD(+)/NADH ratios. Expression of LbNOX in the cytosol or mitochondria ameliorated proliferative and metabolic defects caused by an impaired ETC. The results underscore the role of reductive stress in mitochondrial pathogenesis and demonstrate the utility of targeted LbNOX for direct, compartment-specific manipulation of redox state.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850741/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850741/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Titov, Denis V -- Cracan, Valentin -- Goodman, Russell P -- Peng, Jun -- Grabarek, Zenon -- Mootha, Vamsi K -- R01 GM099683/GM/NIGMS NIH HHS/ -- R01GM099683/GM/NIGMS NIH HHS/ -- T32 DK007191/DK/NIDDK NIH HHS/ -- T32DK007191/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):231-5. doi: 10.1126/science.aad4017. Epub 2016 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA. Department of Systems Biology, Harvard Medical School, Boston, MA, USA. Broad Institute, Cambridge, MA, USA. ; Howard Hughes Medical Institute and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA. Division of Gastroenterology, Massachusetts General Hospital, Boston, MA, USA. ; Howard Hughes Medical Institute and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA. ; Howard Hughes Medical Institute and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA. Broad Institute, Cambridge, MA, USA. ; Howard Hughes Medical Institute and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA. Department of Systems Biology, Harvard Medical School, Boston, MA, USA. Broad Institute, Cambridge, MA, USA. vamsi@hms.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124460" target="_blank"〉PubMed〈/a〉
    Keywords: Catalysis ; Cytosol/enzymology ; Electron Transport ; Electron Transport Chain Complex Proteins/genetics/*metabolism ; Genetic Complementation Test ; Gluconeogenesis/*genetics ; HeLa Cells ; Humans ; Lactobacillus brevis/enzymology/genetics ; Mitochondria/*metabolism ; Mitochondrial Diseases/enzymology/genetics ; Multienzyme Complexes/genetics/*metabolism ; NAD/*metabolism ; NADH, NADPH Oxidoreductases/genetics/*metabolism ; Oxidation-Reduction
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  • 84
    Publication Date: 2016-04-29
    Description: To explore the distinct genotypic and phenotypic states of melanoma tumors, we applied single-cell RNA sequencing (RNA-seq) to 4645 single cells isolated from 19 patients, profiling malignant, immune, stromal, and endothelial cells. Malignant cells within the same tumor displayed transcriptional heterogeneity associated with the cell cycle, spatial context, and a drug-resistance program. In particular, all tumors harbored malignant cells from two distinct transcriptional cell states, such that tumors characterized by high levels of the MITF transcription factor also contained cells with low MITF and elevated levels of the AXL kinase. Single-cell analyses suggested distinct tumor microenvironmental patterns, including cell-to-cell interactions. Analysis of tumor-infiltrating T cells revealed exhaustion programs, their connection to T cell activation and clonal expansion, and their variability across patients. Overall, we begin to unravel the cellular ecosystem of tumors and how single-cell genomics offers insights with implications for both targeted and immune therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tirosh, Itay -- Izar, Benjamin -- Prakadan, Sanjay M -- Wadsworth, Marc H 2nd -- Treacy, Daniel -- Trombetta, John J -- Rotem, Asaf -- Rodman, Christopher -- Lian, Christine -- Murphy, George -- Fallahi-Sichani, Mohammad -- Dutton-Regester, Ken -- Lin, Jia-Ren -- Cohen, Ofir -- Shah, Parin -- Lu, Diana -- Genshaft, Alex S -- Hughes, Travis K -- Ziegler, Carly G K -- Kazer, Samuel W -- Gaillard, Aleth -- Kolb, Kellie E -- Villani, Alexandra-Chloe -- Johannessen, Cory M -- Andreev, Aleksandr Y -- Van Allen, Eliezer M -- Bertagnolli, Monica -- Sorger, Peter K -- Sullivan, Ryan J -- Flaherty, Keith T -- Frederick, Dennie T -- Jane-Valbuena, Judit -- Yoon, Charles H -- Rozenblatt-Rosen, Orit -- Shalek, Alex K -- Regev, Aviv -- Garraway, Levi A -- 1U24CA180922/CA/NCI NIH HHS/ -- DP2 OD020839/OD/NIH HHS/ -- K99 CA194163/CA/NCI NIH HHS/ -- K99CA194163/CA/NCI NIH HHS/ -- P01CA163222/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- P50GM107618/GM/NIGMS NIH HHS/ -- R35CA197737/CA/NCI NIH HHS/ -- U54CA112962/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):189-96. doi: 10.1126/science.aad0501.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. Center for Cancer Precision Medicine, Dana-Farber Cancer Institute, Boston, MA 02215, USA. bizar@partners.org aregev@broadinstitute.org levi_garraway@dfci.harvard.edu. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Institute for Medical Engineering and Science, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA. Department of Chemistry, MIT, Cambridge, MA 02142, USA. Ragon Institute of Massachusetts General Hospital, MIT and Harvard University, Cambridge, MA 02139, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. Center for Cancer Precision Medicine, Dana-Farber Cancer Institute, Boston, MA 02215, USA. ; Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; Program in Therapeutic Sciences, Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia. ; HMS LINCS Center and Laboratory of Systems Pharmacology, Harvard Medical School, Boston, MA 02115, USA. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Institute for Medical Engineering and Science, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA. Ragon Institute of Massachusetts General Hospital, MIT and Harvard University, Cambridge, MA 02139, USA. Division of Health Sciences and Technology, Harvard Medical School, Boston, MA 02115, USA. ; Department of Surgical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. Department of Surgical Oncology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; Program in Therapeutic Sciences, Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA. HMS LINCS Center and Laboratory of Systems Pharmacology, Harvard Medical School, Boston, MA 02115, USA. Ludwig Center at Harvard, Boston, MA 02215, USA. ; Division of Medical Oncology, Massachusetts General Hospital Cancer Center, Boston, MA 02114, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Institute for Medical Engineering and Science, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA. Department of Chemistry, MIT, Cambridge, MA 02142, USA. Ragon Institute of Massachusetts General Hospital, MIT and Harvard University, Cambridge, MA 02139, USA. Division of Health Sciences and Technology, Harvard Medical School, Boston, MA 02115, USA. Department of Immunology, Massachusetts General Hospital, Boston, MA 02114, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Department of Biology and Koch Institute, MIT, Boston, MA 02142, USA. Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. bizar@partners.org aregev@broadinstitute.org levi_garraway@dfci.harvard.edu. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. bizar@partners.org aregev@broadinstitute.org levi_garraway@dfci.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124452" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Communication ; Cell Cycle ; Drug Resistance, Neoplasm/genetics ; Endothelial Cells/pathology ; Genomics ; Humans ; Immunotherapy ; Lymphocyte Activation ; Melanoma/*genetics/*secondary/therapy ; Microphthalmia-Associated Transcription Factor/metabolism ; Neoplasm Metastasis ; RNA/genetics ; Sequence Analysis, RNA ; Single-Cell Analysis ; Skin Neoplasms/*pathology ; Stromal Cells/pathology ; T-Lymphocytes/immunology/pathology ; Transcriptome ; *Tumor Microenvironment
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  • 85
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1128-9. doi: 10.1126/science.351.6278.1128.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965600" target="_blank"〉PubMed〈/a〉
    Keywords: Blood Stains ; *Criminal Law ; DNA Fingerprinting/standards ; Evidence-Based Medicine/*legislation & jurisprudence/*trends ; Forensic Medicine/*legislation & jurisprudence/*trends ; Humans
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  • 86
    Publication Date: 2016-01-28
    Description: Mitochondria undergo fragmentation in response to electron transport chain (ETC) poisons and mitochondrial DNA-linked disease mutations, yet how these stimuli mechanistically connect to the mitochondrial fission and fusion machinery is poorly understood. We found that the energy-sensing adenosine monophosphate (AMP)-activated protein kinase (AMPK) is genetically required for cells to undergo rapid mitochondrial fragmentation after treatment with ETC inhibitors. Moreover, direct pharmacological activation of AMPK was sufficient to rapidly promote mitochondrial fragmentation even in the absence of mitochondrial stress. A screen for substrates of AMPK identified mitochondrial fission factor (MFF), a mitochondrial outer-membrane receptor for DRP1, the cytoplasmic guanosine triphosphatase that catalyzes mitochondrial fission. Nonphosphorylatable and phosphomimetic alleles of the AMPK sites in MFF revealed that it is a key effector of AMPK-mediated mitochondrial fission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Toyama, Erin Quan -- Herzig, Sebastien -- Courchet, Julien -- Lewis, Tommy L Jr -- Loson, Oliver C -- Hellberg, Kristina -- Young, Nathan P -- Chen, Hsiuchen -- Polleux, Franck -- Chan, David C -- Shaw, Reuben J -- K99 NS091526/NS/NINDS NIH HHS/ -- K99NS091526/NS/NINDS NIH HHS/ -- P01 CA120964/CA/NCI NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- R01CA172229/CA/NCI NIH HHS/ -- R01DK080425/DK/NIDDK NIH HHS/ -- R01GM062967/GM/NIGMS NIH HHS/ -- R01GM110039/GM/NIGMS NIH HHS/ -- R01NS089456/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):275-81. doi: 10.1126/science.aab4138.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cell Biology Laboratory and Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, CA 92037, USA. ; Department of Neuroscience, Zuckerman Mind Brain Behavior Institute and Kavli Institute for Brain Science, Columbia University, New York, NY 10032, USA. ; Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA. ; Molecular and Cell Biology Laboratory and Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, CA 92037, USA. shaw@salk.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816379" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/chemistry/genetics/*metabolism ; Adenosine Monophosphate/metabolism ; Amino Acid Motifs ; Cell Line, Tumor ; Cytoplasm/enzymology ; Dactinomycin/analogs & derivatives/pharmacology ; *Energy Metabolism ; Enzyme Activation ; GTP Phosphohydrolases/genetics/metabolism ; Humans ; Microtubule-Associated Proteins/genetics/metabolism ; Mitochondria/drug effects/enzymology/*physiology ; *Mitochondrial Dynamics ; Mitochondrial Proteins/genetics/metabolism ; Molecular Sequence Data ; Rotenone/pharmacology ; *Stress, Physiological
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  • 87
    Publication Date: 2016-02-26
    Description: Transposable elements (TEs) are both a boon and a bane to eukaryotic organisms, depending on where they integrate into the genome and how their sequences function once integrated. We focus on two types of TEs: long interspersed elements (LINEs) and short interspersed elements (SINEs). LINEs and SINEs are retrotransposons; that is, they transpose via an RNA intermediate. We discuss how LINEs and SINEs have expanded in eukaryotic genomes and contribute to genome evolution. An emerging body of evidence indicates that LINEs and SINEs function to regulate gene expression by affecting chromatin structure, gene transcription, pre-mRNA processing, or aspects of mRNA metabolism. We also describe how adenosine-to-inosine editing influences SINE function and how ongoing retrotransposition is countered by the body's defense mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elbarbary, Reyad A -- Lucas, Bronwyn A -- Maquat, Lynne E -- P30 AR061307/AR/NIAMS NIH HHS/ -- R37 GM074593/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):aac7247. doi: 10.1126/science.aac7247. Epub 2016 Feb 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA. Center for RNA Biology, University of Rochester, Rochester, NY, USA. ; Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA. Center for RNA Biology, University of Rochester, Rochester, NY, USA. Department of Oncology, Wilmot Cancer Institute, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA. lynne_maquat@urmc.rochester.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912865" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/ultrastructure ; Disease/genetics ; Evolution, Molecular ; *Gene Expression Regulation ; Humans ; Long Interspersed Nucleotide Elements/genetics/*physiology ; Mice ; Protein Biosynthesis ; RNA Precursors/metabolism ; RNA Processing, Post-Transcriptional ; RNA Stability ; RNA, Messenger/metabolism ; Short Interspersed Nucleotide Elements/genetics/*physiology ; Transcription, Genetic
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  • 88
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McLaughlin, Kathleen -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):283. doi: 10.1126/science.352.6283.283.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kathleen McLaughlin is a writer in Beijing.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081050" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Aging ; China/epidemiology ; *Family Relations ; Female ; Human Migration ; Humans ; Male ; Rural Population/*statistics & numerical data ; Sociology ; Suicide/*statistics & numerical data
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  • 89
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McNutt, Marcia -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):791. doi: 10.1126/science.aaf4216.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Marcia McNutt Editor-in Chief Science Journals.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912866" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Leadership ; Male ; Policy ; Sexual Harassment/*prevention & control ; Societies ; Students ; Women
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  • 90
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McNutt, Marcia -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):641. doi: 10.1126/science.aaf4014. Epub 2016 Feb 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Marcia McNutt Editor-in-Chief Science Journals.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912832" target="_blank"〉PubMed〈/a〉
    Keywords: Corrosion ; Federal Government ; Humans ; Michigan ; *Public Health ; Safety/*economics ; Trust ; United States ; United States Environmental Protection Agency ; Water Supply/*economics
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  • 91
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Escobar, Herton -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):18. doi: 10.1126/science.352.6281.18.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034350" target="_blank"〉PubMed〈/a〉
    Keywords: *Antineoplastic Agents/chemical synthesis/chemistry/therapeutic use ; Brazil ; Clinical Trials as Topic ; Dosage Forms ; *Drug Approval ; Ethanolamines/chemical synthesis/chemistry/*therapeutic use ; Federal Government ; Humans ; Neoplasms/*drug therapy
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  • 92
    Publication Date: 2016-01-23
    Description: Oligodendrocytes myelinate axons in the central nervous system and develop from oligodendrocyte precursor cells (OPCs) that must first migrate extensively during brain and spinal cord development. We show that OPCs require the vasculature as a physical substrate for migration. We observed that OPCs of the embryonic mouse brain and spinal cord, as well as the human cortex, emerge from progenitor domains and associate with the abluminal endothelial surface of nearby blood vessels. Migrating OPCs crawl along and jump between vessels. OPC migration in vivo was disrupted in mice with defective vascular architecture but was normal in mice lacking pericytes. Thus, physical interactions with the vascular endothelium are required for OPC migration. We identify Wnt-Cxcr4 (chemokine receptor 4) signaling in regulation of OPC-endothelial interactions and propose that this signaling coordinates OPC migration with differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Hui-Hsin -- Niu, Jianqin -- Munji, Roeben -- Davalos, Dimitrios -- Chang, Junlei -- Zhang, Haijing -- Tien, An-Chi -- Kuo, Calvin J -- Chan, Jonah R -- Daneman, Richard -- Fancy, Stephen P J -- 1P01 NS083513/NS/NINDS NIH HHS/ -- 1R01NS064517/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):379-84. doi: 10.1126/science.aad3839.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of California at San Francisco (UCSF), San Francisco, CA 94158, USA. ; Departments of Pharmacology and Neuroscience, University of California at San Diego (UCSD), San Diego, CA 92093, USA. ; Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA. ; Division of Hematology, Department of Medicine, Stanford University, Stanford, CA 94305, USA. ; Division of Hematology, Department of Medicine, Stanford University, Stanford, CA 94305, USA. Department of Urology, Cleveland Clinic Foundation, Cleveland, OH 44195, USA. Howard Hughes Medical Institute (HHMI), Chevy Chase, MD 20815, USA. Duke University School of Medicine, Durham, NC 27710, USA. ; Department of Neurology, UCSF, San Francisco, CA 94158, USA. ; Department of Pediatrics, University of California at San Francisco (UCSF), San Francisco, CA 94158, USA. Department of Neurology, UCSF, San Francisco, CA 94158, USA. Division of Neonatology, UCSF, San Francisco, CA 94158, USA. Newborn Brain Research Institute, UCSF, San Francisco, CA 94158, USA. stephen.fancy@ucsf.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26798014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/cytology/embryology ; *Cell Movement ; Cerebral Cortex/blood supply/*embryology ; Endothelium, Vascular/cytology ; Humans ; Mice ; Neural Stem Cells/cytology/*physiology ; *Neurogenesis ; Oligodendroglia/cytology/*physiology ; *Organogenesis ; Pericytes/cytology/physiology ; Receptors, CXCR4/metabolism ; Signal Transduction ; Spinal Cord/blood supply/cytology/*embryology ; Wnt Proteins/metabolism
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  • 93
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fahlgren, Noah -- Bart, Rebecca -- Herrera-Estrella, Luis -- Rellan-Alvarez, Ruben -- Chitwood, Daniel H -- Dinneny, Jose R -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):824. doi: 10.1126/science.351.6275.824-a. Epub 2016 Feb 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Donald Danforth Plant Science Center, St. Louis, MO 63132, USA. ; Nacional de Genomica para la Biodiversidad, Irapuato, 36821, Mexico. ; Donald Danforth Plant Science Center, St. Louis, MO 63132, USA. jdinneny@carnegiescience.edu dchitwood@danforthcenter.org. ; Carnegie Institution for Science, Stanford, CA 94305, USA. jdinneny@carnegiescience.edu dchitwood@danforthcenter.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912883" target="_blank"〉PubMed〈/a〉
    Keywords: China ; Food, Genetically Modified/*adverse effects ; Genetic Engineering/*utilization ; Health ; Humans ; Plants, Genetically Modified/*adverse effects/genetics ; United States ; Zea mays/genetics
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  • 94
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-29
    Description: Therapeutic advances in oncology have not fully translated to the treatment of metastatic disease, which remains largely incurable. Metastatic subclones can emerge both early and late in the life of the primary tumor. A better understanding of the genetic evolution of metastatic disease has the potential to reveal differences in the therapeutic vulnerabilities of primary and metastatic tumors, shed light on the temporal patterns of and routes to metastatic colonization, and provide insight into the biology of the metastatic process. Here we review recent comparative studies of primary and metastatic tumors, including data suggesting that macroevolutionary shifts (the onset of chromosomal instability) contribute to the evolution of metastatic disease. We also discuss the practical challenges associated with these studies and how they might be overcome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turajlic, Samra -- Swanton, Charles -- C50947/A18176/Cancer Research UK/United Kingdom -- Department of Health/United Kingdom -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):169-75. doi: 10.1126/science.aaf2784.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY2, UK. Renal and Skin Units, The Royal Marsden Hospital, London SW3 6JJ, UK. ; The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY2, UK. University College London Hospitals and Cancer Institute, Cancer Research UK Lung Cancer Centre of Excellence, Huntley Street, London WC1, UK. charles.swanton@crick.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124450" target="_blank"〉PubMed〈/a〉
    Keywords: Clone Cells/pathology ; *Evolution, Molecular ; Genetic Variation ; Humans ; Neoplasm Metastasis/*genetics/*pathology ; Neoplasms/classification/genetics/pathology ; Phylogeny
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  • 95
    Publication Date: 2016-04-30
    Description: Fecal microbiome variation in the average, healthy population has remained under-investigated. Here, we analyzed two independent, extensively phenotyped cohorts: the Belgian Flemish Gut Flora Project (FGFP; discovery cohort; N = 1106) and the Dutch LifeLines-DEEP study (LLDeep; replication; N = 1135). Integration with global data sets (N combined = 3948) revealed a 14-genera core microbiota, but the 664 identified genera still underexplore total gut diversity. Sixty-nine clinical and questionnaire-based covariates were found associated to microbiota compositional variation with a 92% replication rate. Stool consistency showed the largest effect size, whereas medication explained largest total variance and interacted with other covariate-microbiota associations. Early-life events such as birth mode were not reflected in adult microbiota composition. Finally, we found that proposed disease marker genera associated to host covariates, urging inclusion of the latter in study design.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Falony, Gwen -- Joossens, Marie -- Vieira-Silva, Sara -- Wang, Jun -- Darzi, Youssef -- Faust, Karoline -- Kurilshikov, Alexander -- Bonder, Marc Jan -- Valles-Colomer, Mireia -- Vandeputte, Doris -- Tito, Raul Y -- Chaffron, Samuel -- Rymenans, Leen -- Verspecht, Chloe -- De Sutter, Lise -- Lima-Mendez, Gipsi -- D'hoe, Kevin -- Jonckheere, Karl -- Homola, Daniel -- Garcia, Roberto -- Tigchelaar, Ettje F -- Eeckhaudt, Linda -- Fu, Jingyuan -- Henckaerts, Liesbet -- Zhernakova, Alexandra -- Wijmenga, Cisca -- Raes, Jeroen -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):560-4. doi: 10.1126/science.aad3503. Epub 2016 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉KU Leuven-University of Leuven, Department of Microbiology and Immunology, Leuven, Belgium. VIB, Center for the Biology of Disease, Leuven, Belgium. ; KU Leuven-University of Leuven, Department of Microbiology and Immunology, Leuven, Belgium. VIB, Center for the Biology of Disease, Leuven, Belgium. Vrije Universiteit Brussel, Faculty of Sciences and Bioengineering Sciences, Microbiology Unit, Brussels, Belgium. ; Institute of Chemical Biology and Fundamental Medicine SB RAS, Novosibirsk, Russia. Novosibirsk State University, Novosibirsk, Russia. ; University of Groningen, University Medical Center Groningen, Department of Genetics, 9700 RB Groningen, Netherlands. ; VIB, Center for the Biology of Disease, Leuven, Belgium. Vrije Universiteit Brussel, Faculty of Sciences and Bioengineering Sciences, Microbiology Unit, Brussels, Belgium. ; University of Groningen, University Medical Center Groningen, Department of Genetics, 9700 RB Groningen, Netherlands. Top Institute Food and Nutrition, Wageningen, Netherlands. ; University of Groningen, University Medical Center Groningen, Department of Genetics, 9700 RB Groningen, Netherlands. University of Groningen, University Medical Center Groningen, Department of Pediatrics, 9700 RB Groningen, Netherlands. ; KU Leuven-University of Leuven, Department of Microbiology and Immunology, Leuven, Belgium. KU Leuven-University Hospitals Leuven, Department of General Internal Medicine, Leuven, Belgium. ; KU Leuven-University of Leuven, Department of Microbiology and Immunology, Leuven, Belgium. VIB, Center for the Biology of Disease, Leuven, Belgium. Vrije Universiteit Brussel, Faculty of Sciences and Bioengineering Sciences, Microbiology Unit, Brussels, Belgium. jeroen.raes@kuleuven.be.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126039" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteria/*classification/genetics/isolation & purification ; Belgium ; Cohort Studies ; Drug Interactions ; Feces/microbiology ; *Gastrointestinal Microbiome ; Humans
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    Electronic ISSN: 1095-9203
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  • 96
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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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    Electronic ISSN: 1095-9203
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  • 97
    Publication Date: 2016-03-26
    Description: Brazil has experienced an unprecedented epidemic of Zika virus (ZIKV), with ~30,000 cases reported to date. ZIKV was first detected in Brazil in May 2015, and cases of microcephaly potentially associated with ZIKV infection were identified in November 2015. We performed next-generation sequencing to generate seven Brazilian ZIKV genomes sampled from four self-limited cases, one blood donor, one fatal adult case, and one newborn with microcephaly and congenital malformations. Results of phylogenetic and molecular clock analyses show a single introduction of ZIKV into the Americas, which we estimated to have occurred between May and December 2013, more than 12 months before the detection of ZIKV in Brazil. The estimated date of origin coincides with an increase in air passengers to Brazil from ZIKV-endemic areas, as well as with reported outbreaks in the Pacific Islands. ZIKV genomes from Brazil are phylogenetically interspersed with those from other South American and Caribbean countries. Mapping mutations onto existing structural models revealed the context of viral amino acid changes present in the outbreak lineage; however, no shared amino acid changes were found among the three currently available virus genomes from microcephaly cases. Municipality-level incidence data indicate that reports of suspected microcephaly in Brazil best correlate with ZIKV incidence around week 17 of pregnancy, although this correlation does not demonstrate causation. Our genetic description and analysis of ZIKV isolates in Brazil provide a baseline for future studies of the evolution and molecular epidemiology of this emerging virus in the Americas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faria, Nuno Rodrigues -- Azevedo, Raimunda do Socorro da Silva -- Kraemer, Moritz U G -- Souza, Renato -- Cunha, Mariana Sequetin -- Hill, Sarah C -- Theze, Julien -- Bonsall, Michael B -- Bowden, Thomas A -- Rissanen, Ilona -- Rocco, Iray Maria -- Nogueira, Juliana Silva -- Maeda, Adriana Yurika -- Vasami, Fernanda Giseli da Silva -- Macedo, Fernando Luiz de Lima -- Suzuki, Akemi -- Rodrigues, Sueli Guerreiro -- Cruz, Ana Cecilia Ribeiro -- Nunes, Bruno Tardeli -- Medeiros, Daniele Barbosa de Almeida -- Rodrigues, Daniela Sueli Guerreiro -- Nunes Queiroz, Alice Louize -- da Silva, Eliana Vieira Pinto -- Henriques, Daniele Freitas -- Travassos da Rosa, Elisabeth Salbe -- de Oliveira, Consuelo Silva -- Martins, Livia Caricio -- Vasconcelos, Helena Baldez -- Casseb, Livia Medeiros Neves -- Simith, Darlene de Brito -- Messina, Jane P -- Abade, Leandro -- Lourenco, Jose -- Carlos Junior Alcantara, Luiz -- de Lima, Maricelia Maia -- Giovanetti, Marta -- Hay, Simon I -- de Oliveira, Rodrigo Santos -- Lemos, Poliana da Silva -- de Oliveira, Layanna Freitas -- de Lima, Clayton Pereira Silva -- da Silva, Sandro Patroca -- de Vasconcelos, Janaina Mota -- Franco, Luciano -- Cardoso, Jedson Ferreira -- Vianez-Junior, Joao Lidio da Silva Goncalves -- Mir, Daiana -- Bello, Gonzalo -- Delatorre, Edson -- Khan, Kamran -- Creatore, Marisa -- Coelho, Giovanini Evelim -- de Oliveira, Wanderson Kleber -- Tesh, Robert -- Pybus, Oliver G -- Nunes, Marcio R T -- Vasconcelos, Pedro F C -- 090532/Z/09/Z/Wellcome Trust/United Kingdom -- 095066/Wellcome Trust/United Kingdom -- 102427/Wellcome Trust/United Kingdom -- MR/L009528/1/Medical Research Council/United Kingdom -- R24 AT 120942/AT/NCCIH NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):345-9. doi: 10.1126/science.aaf5036. Epub 2016 Mar 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Technological Innovation, Evandro Chagas Institute, Ministry of Health, Ananindeua, PA 67030-000, Brazil. Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. ; Department of Arbovirology and Hemorrhagic Fevers, Evandro Chagas Institute, Ministry of Health, Ananindeua, Para State, Brazil. ; Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. ; Instituto Adolfo Lutz, University of Sao Paulo, Sao Paulo, Brazil. ; Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK. ; Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. Metabiota, San Francisco, CA 94104, USA. ; Oswaldo Cruz Foundation (FIOCRUZ), Salvador, Bahia, Brazil. ; Centre of Post Graduation in Collective Health, Department of Health, Universidade Estadual de Feira de Santana, Feira de Santana, Bahia, Brazil. ; Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA 98121, USA. Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK. ; Center for Technological Innovation, Evandro Chagas Institute, Ministry of Health, Ananindeua, PA 67030-000, Brazil. ; Laboratorio de AIDS and Imunologia Molecular, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil. ; Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada. Department of Medicine, Division of Infectious Diseases, University of Toronto, Toronto, Ontario, Canada. ; Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada. ; Brazilian Ministry of Health, Brasilia, Brazil. ; Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA. ; Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. Metabiota, San Francisco, CA 94104, USA. oliver.pybus@zoo.ox.ac.uk marcionunesbrasil@yahoo.com.br pedrovasconcelos@iec.pa.gov.br. ; Center for Technological Innovation, Evandro Chagas Institute, Ministry of Health, Ananindeua, PA 67030-000, Brazil. Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA. oliver.pybus@zoo.ox.ac.uk marcionunesbrasil@yahoo.com.br pedrovasconcelos@iec.pa.gov.br. ; Department of Arbovirology and Hemorrhagic Fevers, Evandro Chagas Institute, Ministry of Health, Ananindeua, Para State, Brazil. oliver.pybus@zoo.ox.ac.uk marcionunesbrasil@yahoo.com.br pedrovasconcelos@iec.pa.gov.br.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013429" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/virology ; Americas/epidemiology ; Animals ; *Disease Outbreaks ; Female ; Genome, Viral/genetics ; Humans ; Incidence ; Insect Vectors/virology ; Microcephaly/*epidemiology/virology ; Molecular Epidemiology ; Molecular Sequence Data ; Mutation ; Pacific Islands/epidemiology ; Phylogeny ; Pregnancy ; RNA, Viral/genetics ; Sequence Analysis, RNA ; Travel ; Zika Virus/classification/*genetics/isolation & purification ; Zika Virus Infection/*epidemiology/transmission/*virology
    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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  • 98
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):212-3. doi: 10.1126/science.351.6270.212.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816355" target="_blank"〉PubMed〈/a〉
    Keywords: Advertising as Topic/legislation & jurisprudence ; Brain/*physiology ; Cognition ; Humans ; *Learning ; Neuronal Plasticity ; Neurosciences/*legislation & jurisprudence ; Simulation Training/*legislation & jurisprudence ; Software/*legislation & jurisprudence ; Video Games/*legislation & jurisprudence
    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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  • 99
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):116-9. doi: 10.1126/science.351.6269.116.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744391" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies/*therapeutic use ; Clinical Trials as Topic ; *Cortical Spreading Depression/drug effects/immunology/physiology ; Drug Design ; Drug Industry ; Female ; Humans ; Male ; Migraine Disorders/*immunology/physiopathology/*therapy ; Receptors, Calcitonin Gene-Related Peptide/*antagonists & inhibitors/immunology ; Sex Ratio
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):397. doi: 10.1126/science.352.6284.397.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102458" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/*physiology ; Cadaver ; Humans ; Neurosciences/*trends ; *Transcranial Direct Current Stimulation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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