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  • Articles  (1,449)
  • Animals  (1,449)
  • Chemical Engineering
  • 2010-2014  (1,449)
  • 2013  (1,449)
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  • Articles  (1,449)
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  • 2010-2014  (1,449)
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  • 1
    Publication Date: 2013-12-10
    Description: Evolution drives, and is driven by, demography. A genotype moulds its phenotype's age patterns of mortality and fertility in an environment; these two patterns in turn determine the genotype's fitness in that environment. Hence, to understand the evolution of ageing, age patterns of mortality and reproduction need to be compared for species across the tree of life. However, few studies have done so and only for a limited range of taxa. Here we contrast standardized patterns over age for 11 mammals, 12 other vertebrates, 10 invertebrates, 12 vascular plants and a green alga. Although it has been predicted that evolution should inevitably lead to increasing mortality and declining fertility with age after maturity, there is great variation among these species, including increasing, constant, decreasing, humped and bowed trajectories for both long- and short-lived species. This diversity challenges theoreticians to develop broader perspectives on the evolution of ageing and empiricists to study the demography of more species.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157354/" 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/PMC4157354/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, Owen R -- Scheuerlein, Alexander -- Salguero-Gomez, Roberto -- Camarda, Carlo Giovanni -- Schaible, Ralf -- Casper, Brenda B -- Dahlgren, Johan P -- Ehrlen, Johan -- Garcia, Maria B -- Menges, Eric S -- Quintana-Ascencio, Pedro F -- Caswell, Hal -- Baudisch, Annette -- Vaupel, James W -- P01 AG-031719/AG/NIA NIH HHS/ -- P01 AG031719/AG/NIA NIH HHS/ -- England -- Nature. 2014 Jan 9;505(7482):169-73. doi: 10.1038/nature12789. Epub 2013 Dec 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Max-Planck Odense Center on the Biodemography of Aging, Campusvej 55, 5230 Odense M, Denmark [2] Department of Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark [3]. ; 1] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [2]. ; 1] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [2] School of Biological Sciences, Centre for Biodiversity and Conservation Science, University of Queensland, Brisbane QLD 4072, Australia. ; Institut National d'Etudes Demographiques, 133 Boulevard Davout, 75980 Paris Cedex 20, France. ; Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany. ; Department of Biology, University of Pennsylvania, 433 South University Avenue, Philadelphia, Pennsylvania 19104-6018, USA. ; 1] Max-Planck Odense Center on the Biodemography of Aging, Campusvej 55, 5230 Odense M, Denmark [2] Department of Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark. ; Department of Ecology, Environment and Plant Sciences, Stockholm University, Lilla Frescativagen 5, 10691 Stockholm, Sweden. ; Pyrenean Institute of Ecology (CSIC), Avenida Montanana 1005, 50059 Zaragoza, Spain. ; Archbold Biological Station, 123 Main Drive, Venus, Florida 33960, USA. ; Department of Biology, University of Central Florida, 4110 Libra Drive, Orlando, Florida 32816-2368, USA. ; 1] Department of Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark [2] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [3] Woods Hole Oceanographic Institution, Biology Department MS-34, Woods Hole, Massachusetts 02543 USA [4] Institute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, PO Box 94248, 1090GE Amsterdam, The Netherlands. ; 1] Max-Planck Odense Center on the Biodemography of Aging, Campusvej 55, 5230 Odense M, Denmark [2] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [3] Duke Population Research Institute, Duke University, Durham, North Carolina 27705, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24317695" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Biological Evolution ; Chlorophyta ; Fertility/*physiology ; Longevity/*physiology ; *Phylogeny ; Plants ; Reproduction/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2013-11-23
    Description: Oxamniquine resistance evolved in the human blood fluke (Schistosoma mansoni) in Brazil in the 1970s. We crossed parental parasites differing ~500-fold in drug response, determined drug sensitivity and marker segregation in clonally derived second-generation progeny, and identified a single quantitative trait locus (logarithm of odds = 31) on chromosome 6. A sulfotransferase was identified as the causative gene by using RNA interference knockdown and biochemical complementation assays, and we subsequently demonstrated independent origins of loss-of-function mutations in field-derived and laboratory-selected resistant parasites. These results demonstrate the utility of linkage mapping in a human helminth parasite, while crystallographic analyses of protein-drug interactions illuminate the mode of drug action and provide a framework for rational design of oxamniquine derivatives that kill both S. mansoni and S. haematobium, the two species responsible for 〉99% of schistosomiasis cases worldwide.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4136436/" 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/PMC4136436/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Valentim, Claudia L L -- Cioli, Donato -- Chevalier, Frederic D -- Cao, Xiaohang -- Taylor, Alexander B -- Holloway, Stephen P -- Pica-Mattoccia, Livia -- Guidi, Alessandra -- Basso, Annalisa -- Tsai, Isheng J -- Berriman, Matthew -- Carvalho-Queiroz, Claudia -- Almeida, Marcio -- Aguilar, Hector -- Frantz, Doug E -- Hart, P John -- LoVerde, Philip T -- Anderson, Timothy J C -- 098051/Wellcome Trust/United Kingdom -- 5R21-AI072704/AI/NIAID NIH HHS/ -- 5R21-AI096277/AI/NIAID NIH HHS/ -- C06 RR013556/RR/NCRR NIH HHS/ -- HHSN272201000005I/PHS HHS/ -- R01 AI097576/AI/NIAID NIH HHS/ -- R01-AI097576/AI/NIAID NIH HHS/ -- R21 AI072704/AI/NIAID NIH HHS/ -- R21 AI096277/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Dec 13;342(6164):1385-9. doi: 10.1126/science.1243106. Epub 2013 Nov 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Biochemistry and Pathology, University of Texas Health Science Center, San Antonio, TX 78229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24263136" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Drug Resistance/*genetics ; Gene Knockdown Techniques ; Genetic Linkage ; Helminth Proteins/*genetics ; Humans ; Molecular Sequence Data ; Mutation ; Oxamniquine/*pharmacology ; Phylogeny ; Protein Conformation ; Quantitative Trait Loci ; RNA Interference ; Schistosoma mansoni/*drug effects/*genetics ; Schistosomicides/*pharmacology ; Sulfotransferases/chemistry/classification/*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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  • 3
    Publication Date: 2013-06-08
    Description: Evolutionarily young genes that serve essential functions represent a paradox; they must perform a function that either was not required until after their birth or was redundant with another gene. How young genes rapidly acquire essential function is largely unknown. We traced the evolutionary steps by which the Drosophila gene Umbrea acquired an essential role in chromosome segregation in D. melanogaster since the gene's origin less than 15 million years ago. Umbrea neofunctionalization occurred via loss of an ancestral heterochromatin-localizing domain, followed by alterations that rewired its protein interaction network and led to species-specific centromere localization. Our evolutionary cell biology approach provides temporal and mechanistic detail about how young genes gain essential function. Such innovations may constantly alter the repertoire of centromeric proteins in eukaryotes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4119826/" 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/PMC4119826/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ross, Benjamin D -- Rosin, Leah -- Thomae, Andreas W -- Hiatt, Mary Alice -- Vermaak, Danielle -- de la Cruz, Aida Flor A -- Imhof, Axel -- Mellone, Barbara G -- Malik, Harmit S -- R01 GM074108/GM/NIGMS NIH HHS/ -- R01GM074108/GM/NIGMS NIH HHS/ -- T32HG000035/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Jun 7;340(6137):1211-4. doi: 10.1126/science.1234393.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cellular Biology Program, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23744945" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Centromere/genetics/*physiology ; Chromosomal Proteins, Non-Histone/*genetics ; Drosophila/*genetics ; Drosophila Proteins/*genetics ; *Evolution, Molecular ; Gene Duplication ; Genes, Insect/*physiology ; Molecular Sequence Data
    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: 2013-08-31
    Description: Invasion of microbial DNA into the cytoplasm of animal cells triggers a cascade of host immune reactions that help clear the infection; however, self DNA in the cytoplasm can cause autoimmune diseases. Biochemical approaches led to the identification of cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) synthase (cGAS) as a cytosolic DNA sensor that triggers innate immune responses. Here, we show that cells from cGAS-deficient (cGas(-/-)) mice, including fibroblasts, macrophages, and dendritic cells, failed to produce type I interferons and other cytokines in response to DNA transfection or DNA virus infection. cGas(-/-) mice were more susceptible to lethal infection with herpes simplex virus 1 (HSV1) than wild-type mice. We also show that cGAMP is an adjuvant that boosts antigen-specific T cell activation and antibody production in mice.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3863637/" 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/PMC3863637/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Xiao-Dong -- Wu, Jiaxi -- Gao, Daxing -- Wang, Hua -- Sun, Lijun -- Chen, Zhijian J -- 5T32AI070116/AI/NIAID NIH HHS/ -- AI-093967/AI/NIAID NIH HHS/ -- R01 AI093967/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Sep 20;341(6152):1390-4. doi: 10.1126/science.1244040. Epub 2013 Aug 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23989956" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/biosynthesis ; DNA, Viral/genetics/immunology ; Dendritic Cells/immunology ; Fibroblasts/immunology ; Herpes Simplex/*immunology ; *Herpesvirus 1, Human ; Interferon Regulatory Factor-3/genetics ; Interferon-beta/*biosynthesis/genetics ; Lymphocyte Activation ; Macrophages/immunology ; Mice ; Mice, Knockout ; Nucleotidyltransferases/genetics/*immunology ; Signal Transduction ; T-Lymphocytes/immunology ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2013-08-10
    Description: Chromosome translocations are a hallmark of cancer cells. We have developed an experimental system to visualize the formation of translocations in living cells and apply it to characterize the spatial and dynamic properties of translocation formation. We demonstrate that translocations form within hours of the occurrence of double-strand breaks (DSBs) and that their formation is cell cycle-independent. Translocations form preferentially between prepositioned genome elements, and perturbation of key factors of the DNA repair machinery uncouples DSB pairing from translocation formation. These observations generate a spatiotemporal framework for the formation of translocations in living cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roukos, Vassilis -- Voss, Ty C -- Schmidt, Christine K -- Lee, Seungtaek -- Wangsa, Darawalee -- Misteli, Tom -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2013 Aug 9;341(6146):660-4. doi: 10.1126/science.1237150.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23929981" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/genetics ; Carrier Proteins/genetics ; Cell Cycle ; *DNA Breaks, Double-Stranded ; DNA Repair ; DNA-Activated Protein Kinase/antagonists & inhibitors ; DNA-Binding Proteins/antagonists & inhibitors ; Green Fluorescent Proteins/genetics ; High-Throughput Screening Assays ; Lac Operon ; Lac Repressors/genetics ; Mice ; Microscopy/methods ; NIH 3T3 Cells ; Neoplasms/genetics ; Nuclear Proteins/antagonists & inhibitors ; *Time-Lapse Imaging ; *Translocation, 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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  • 6
    Publication Date: 2013-10-26
    Description: Painful venoms are used to deter predators. Pain itself, however, can signal damage and thus serves an important adaptive function. Evolution to reduce general pain responses, although valuable for preying on venomous species, is rare, likely because it comes with the risk of reduced response to tissue damage. Bark scorpions capitalize on the protective pain pathway of predators by inflicting intensely painful stings. However, grasshopper mice regularly attack and consume bark scorpions, grooming only briefly when stung. Bark scorpion venom induces pain in many mammals (house mice, rats, humans) by activating the voltage-gated Na(+) channel Nav1.7, but has no effect on Nav1.8. Grasshopper mice Nav1.8 has amino acid variants that bind bark scorpion toxins and inhibit Na(+) currents, blocking action potential propagation and inducing analgesia. Thus, grasshopper mice have solved the predator-pain problem by using a toxin bound to a nontarget channel to block transmission of the pain signals the venom itself is initiating.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4172297/" 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/PMC4172297/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rowe, Ashlee H -- Xiao, Yucheng -- Rowe, Matthew P -- Cummins, Theodore R -- Zakon, Harold H -- NS 053422/NS/NINDS NIH HHS/ -- R01 NS053422/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2013 Oct 25;342(6157):441-6. doi: 10.1126/science.1236451.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neurobiology, The University of Texas at Austin, Austin, TX 78712, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24159039" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects/physiology ; Amino Acid Sequence ; Animals ; Arvicolinae/*metabolism ; *Food Chain ; Formaldehyde/pharmacology ; Mice ; Molecular Sequence Data ; NAV1.7 Voltage-Gated Sodium Channel/chemistry/genetics/*metabolism ; NAV1.8 Voltage-Gated Sodium Channel/chemistry/genetics/*metabolism ; Pain/chemically induced/*metabolism ; *Predatory Behavior ; Protein Structure, Tertiary ; Scorpion Venoms
    Print ISSN: 0036-8075
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  • 7
    Publication Date: 2013-10-12
    Description: Diverse eukaryotic hosts produce virus-derived small interfering RNAs (siRNAs) to direct antiviral immunity by RNA interference (RNAi). However, it remains unknown whether the mammalian RNAi pathway has a natural antiviral function. Here, we show that infection of hamster cells and suckling mice by Nodamura virus (NoV), a mosquito-transmissible RNA virus, requires RNAi suppression by its B2 protein. Loss of B2 expression or its suppressor activity leads to abundant production of viral siRNAs and rapid clearance of the mutant viruses in mice. However, viral small RNAs detected during virulent infection by NoV do not have the properties of canonical siRNAs. These findings have parallels with the induction and suppression of antiviral RNAi by the related Flock house virus in fruit flies and nematodes and reveal a mammalian antiviral immunity mechanism mediated by RNAi.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3875315/" 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/PMC3875315/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Yang -- Lu, Jinfeng -- Han, Yanhong -- Fan, Xiaoxu -- Ding, Shou-Wei -- AI52447/AI/NIAID NIH HHS/ -- GM94396/GM/NIGMS NIH HHS/ -- R01 AI052447/AI/NIAID NIH HHS/ -- R01 GM094396/GM/NIGMS NIH HHS/ -- RC1 GM091896/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Oct 11;342(6155):231-4. doi: 10.1126/science.1241911.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Pathology and Microbiology, University of California, Riverside, CA 92521, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24115437" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cricetinae ; Mice ; Nodaviridae/genetics/*pathogenicity ; RNA Interference/*immunology ; RNA Virus Infections/*immunology ; RNA, Small Interfering/*immunology ; RNA, Viral/genetics/*immunology ; Viral Nonstructural Proteins/genetics/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-02-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van der Oost, John -- New York, N.Y. -- Science. 2013 Feb 15;339(6121):768-70. doi: 10.1126/science.1234726.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Microbiology, Wageningen University, Wageningen, Netherlands. john.vanderoost@wur.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23413345" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caspase 9/*chemistry ; *DNA Cleavage ; Gene Targeting/*methods ; Genetic Engineering/*methods ; Genome/*genetics ; Genome, Human/*genetics ; Humans ; Inverted Repeat Sequences/*genetics ; Microarray Analysis/*methods ; RNA/*chemistry
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  • 9
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-11-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carboneras, C -- Walton, P -- Vila, M -- New York, N.Y. -- Science. 2013 Nov 22;342(6161):930-1. doi: 10.1126/science.342.6161.930-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Royal Society for the Protection of Birds, The Lodge, Sandy, Bedfordshire, SG19 2DL, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24264976" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Europe ; European Union ; Introduced Species/economics/*legislation & jurisprudence/statistics & numerical ; data ; Social Control, Formal
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2013 Dec 20;342(6165):1435-41. doi: 10.1126/science.342.6165.1444.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357296" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Science Disciplines/history/*trends ; History, 21st Century ; Humans
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  • 11
    Publication Date: 2013-03-30
    Description: Based on nuclear and mitochondrial DNA, Hailer et al. (Reports, 20 April 2012, p. 344) suggested early divergence of polar bears from a common ancestor with brown bears and subsequent introgression. Our population genetic analysis that traces each of the genealogies in the independent nuclear loci does not support the evolutionary model proposed by the authors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakagome, Shigeki -- Mano, Shuhei -- Hasegawa, Masami -- New York, N.Y. -- Science. 2013 Mar 29;339(6127):1522. doi: 10.1126/science.1227339.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Statistical Mathematics, Tachikawa, Tokyo, Japan. nakagome@ism.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23539580" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Genome ; *Multilocus Sequence Typing ; Ursidae/*genetics
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  • 12
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2013 Dec 20;342(6165):1442. doi: 10.1126/science.342.6165.1442-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357294" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior ; Brain/physiology/*ultrastructure ; Electrical Synapses/physiology/ultrastructure ; Humans ; Immunotherapy/*methods ; Mice ; Neoplasms/*therapy ; Sequence Analysis, DNA/*trends ; Single-Cell Analysis/*trends
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  • 13
    Publication Date: 2013-06-15
    Description: The Root effect is a pH-dependent reduction in hemoglobin-O2 carrying capacity. Specific to ray-finned fishes, the Root effect has been ascribed specialized roles in retinal oxygenation and swimbladder inflation. We report that when rainbow trout are exposed to elevated water carbon dioxide (CO2), red muscle partial pressure of oxygen (PO2) increases by 65%--evidence that Root hemoglobins enhance general tissue O2 delivery during acidotic stress. Inhibiting carbonic anhydrase (CA) in the plasma abolished this effect. We argue that CA activity in muscle capillaries short-circuits red blood cell (RBC) pH regulation. This acidifies RBCs, unloads O2 from hemoglobin, and elevates tissue PO2, which could double O2 delivery with no change in perfusion. This previously undescribed mechanism to enhance O2 delivery during stress may represent the incipient function of Root hemoglobins in fishes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rummer, Jodie L -- McKenzie, David J -- Innocenti, Alessio -- Supuran, Claudiu T -- Brauner, Colin J -- New York, N.Y. -- Science. 2013 Jun 14;340(6138):1327-9. doi: 10.1126/science.1233692.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of British Columbia, 6270 University Boulevard, Vancouver, British Columbia V6T 1Z4, Canada. jodie.rummer@jcu.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23766325" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbon Dioxide/metabolism ; Erythrocytes/metabolism ; Hemoglobins/*metabolism ; Hydrogen-Ion Concentration ; Muscle, Skeletal/metabolism ; Oncorhynchus mykiss/*blood/*metabolism ; Oxygen/*blood/*metabolism ; Partial Pressure ; Stress, Physiological
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  • 14
    Publication Date: 2013-05-21
    Description: Evidence for transcriptional feedback in circadian timekeeping is abundant, yet little is known about the mechanisms underlying translational control. We found that ATAXIN-2 (ATX2), an RNA-associated protein involved in neurodegenerative disease, is a translational activator of the rate-limiting clock component PERIOD (PER) in Drosophila. ATX2 specifically interacted with TWENTY-FOUR (TYF), an activator of PER translation. RNA interference-mediated depletion of Atx2 or the expression of a mutant ATX2 protein that does not associate with polyadenylate-binding protein (PABP) suppressed behavioral rhythms and decreased abundance of PER. Although ATX2 can repress translation, depletion of Atx2 from Drosophila S2 cells inhibited translational activation by RNA-tethered TYF and disrupted the association between TYF and PABP. Thus, ATX2 coordinates an active translation complex important for PER expression and circadian rhythms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lim, Chunghun -- Allada, Ravi -- R01NS059042/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2013 May 17;340(6134):875-9. doi: 10.1126/science.1234785.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Northwestern University, Evanston, IL 60208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23687047" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxins ; Cell Line ; *Circadian Rhythm ; Drosophila Proteins/*biosynthesis/genetics/metabolism ; Drosophila melanogaster/metabolism/*physiology ; Mutation ; Nerve Tissue Proteins/genetics/*metabolism ; Period Circadian Proteins/*biosynthesis ; Poly(A)-Binding Proteins/metabolism ; Protein Biosynthesis ; RNA Interference
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-08-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaffe, Harold -- Patterson, Amy P -- Lurie, Nicole -- New York, N.Y. -- Science. 2013 Aug 16;341(6147):713-4. doi: 10.1126/science.1244158. Epub 2013 Aug 7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23926189" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biomedical Research ; Containment of Biohazards ; *Government Regulation ; *Influenza A virus/genetics/pathogenicity/physiology ; Mammals ; Orthomyxoviridae Infections/transmission/*virology ; Risk Assessment ; Safety Management ; United States ; *United States Dept. of Health and Human Services
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  • 16
    Publication Date: 2013-05-25
    Description: Cramer et al. (Reports, 23 March 2012, p. 1503; published online 9 February 2012) reported that bexarotene rapidly reduces beta-amyloid (Abeta) levels and plaque burden in two mouse models of Abeta deposition in Alzheimer's disease (AD). We now report that, although bexarotene reduces soluble Abeta40 levels in one of the mouse models, the drug has no impact on plaque burden in three strains that exhibit Abeta amyloidosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Veeraraghavalu, Karthikeyan -- Zhang, Can -- Miller, Sean -- Hefendehl, Jasmin K -- Rajapaksha, Tharinda W -- Ulrich, Jason -- Jucker, Mathias -- Holtzman, David M -- Tanzi, Rudolph E -- Vassar, Robert -- Sisodia, Sangram S -- New York, N.Y. -- Science. 2013 May 24;340(6135):924-f. doi: 10.1126/science.1235505.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23704555" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*drug therapy/*metabolism ; Amyloid beta-Peptides/*metabolism ; Animals ; Apolipoproteins E/*metabolism ; Brain/*metabolism ; Male ; Tetrahydronaphthalenes/*pharmacology/*therapeutic use
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  • 17
    Publication Date: 2013-12-07
    Description: The skin is a classical example of a tissue maintained by stem cells. However, the identity of the stem cells that maintain the interfollicular epidermis and the source of the signals that control their activity remain unclear. Using mouse lineage tracing and quantitative clonal analyses, we showed that the Wnt target gene Axin2 marks interfollicular epidermal stem cells. These Axin2-expressing cells constitute the majority of the basal epidermal layer, compete neutrally, and require Wnt/beta-catenin signaling to proliferate. The same cells contribute robustly to wound healing, with no requirement for a quiescent stem cell subpopulation. By means of double-labeling RNA in situ hybridization in mice, we showed that the Axin2-expressing cells themselves produce Wnt signals as well as long-range secreted Wnt inhibitors, suggesting an autocrine mechanism of stem cell self-renewal.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4081860/" 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/PMC4081860/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lim, Xinhong -- Tan, Si Hui -- Koh, Winston Lian Chye -- Chau, Rosanna Man Wah -- Yan, Kelley S -- Kuo, Calvin J -- van Amerongen, Renee -- Klein, Allon Moshe -- Nusse, Roel -- 1R01DK085720/DK/NIDDK NIH HHS/ -- 1U01DK085527/DK/NIDDK NIH HHS/ -- 5K08DK096048/DK/NIDDK NIH HHS/ -- K08 DK096048/DK/NIDDK NIH HHS/ -- P30 DK026743/DK/NIDDK NIH HHS/ -- R01 DK085720/DK/NIDDK NIH HHS/ -- U01 DK085527/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Dec 6;342(6163):1226-30. doi: 10.1126/science.1239730.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Howard Hughes Medical Institute (HHMI), Institute for Stem Cell Biology and Regenerative Medicine, School of Medicine, Stanford University, Stanford, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24311688" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autocrine Communication ; Axin Protein/genetics/metabolism ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Cells, Cultured ; Epidermis/*cytology/injuries/metabolism ; Epithelial Cells/cytology/metabolism ; Gene Expression ; Homeostasis ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Keratinocytes/cytology/metabolism ; Mice ; Regeneration ; Skin/injuries ; Stem Cell Niche ; Stem Cells/cytology/*physiology ; Wnt Proteins/metabolism ; *Wnt Signaling Pathway ; Wound Healing ; beta Catenin/genetics/metabolism
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  • 18
    Publication Date: 2013-03-16
    Description: Silicatein-alpha is responsible for the biomineralization of silicates in sponges. We used silicatein-alpha to guide the self-assembly of calcite "spicules" similar to the spicules of the calcareous sponge Sycon sp. The self-assembled spicules, 10 to 300 micrometers (mum) in length and 5 to 10 mum in diameter, are composed of aligned calcite nanocrystals. The spicules are initially amorphous but transform into calcite within months, exhibiting unusual growth along [100]. They scatter x-rays like twinned calcite crystals. Whereas natural spicules evidence brittle failure, the synthetic spicules show an elastic response, which greatly enhances bending strength. This remarkable feature is linked to a high protein content. With nano-thermogravimetric analysis, we measured the organic content of a single spicule to be 10 to 16%. In addition, the spicules exhibit waveguiding properties even when they are bent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Natalio, Filipe -- Corrales, Tomas P -- Panthofer, Martin -- Schollmeyer, Dieter -- Lieberwirth, Ingo -- Muller, Werner E G -- Kappl, Michael -- Butt, Hans-Jurgen -- Tremel, Wolfgang -- New York, N.Y. -- Science. 2013 Mar 15;339(6125):1298-302. doi: 10.1126/science.1216260.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Anorganische Chemie und Analytische Chemie, Johannes Gutenberg-Universitat, Mainz, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23493708" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium Carbonate/*chemistry ; Cathepsins/*chemistry ; Microscopy, Electron, Transmission ; Nanoparticles/chemistry ; Porifera ; Spectroscopy, Fourier Transform Infrared ; *Stress, Mechanical
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  • 19
    Publication Date: 2013-08-03
    Description: An inducible program of inflammatory gene expression is central to antimicrobial defenses. This response is controlled by a collaboration involving signal-dependent activation of transcription factors, transcriptional co-regulators, and chromatin-modifying factors. We have identified a long noncoding RNA (lncRNA) that acts as a key regulator of this inflammatory response. Pattern recognition receptors such as the Toll-like receptors induce the expression of numerous lncRNAs. One of these, lincRNA-Cox2, mediates both the activation and repression of distinct classes of immune genes. Transcriptional repression of target genes is dependent on interactions of lincRNA-Cox2 with heterogeneous nuclear ribonucleoprotein A/B and A2/B1. Collectively, these studies unveil a central role of lincRNA-Cox2 as a broad-acting regulatory component of the circuit that controls the inflammatory response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4376668/" 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/PMC4376668/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carpenter, Susan -- Aiello, Daniel -- Atianand, Maninjay K -- Ricci, Emiliano P -- Gandhi, Pallavi -- Hall, Lisa L -- Byron, Meg -- Monks, Brian -- Henry-Bezy, Meabh -- Lawrence, Jeanne B -- O'Neill, Luke A J -- Moore, Melissa J -- Caffrey, Daniel R -- Fitzgerald, Katherine A -- AI067497/AI/NIAID NIH HHS/ -- GM053234/GM/NIGMS NIH HHS/ -- R01 AI067497/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Aug 16;341(6147):789-92. doi: 10.1126/science.1240925. Epub 2013 Aug 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23907535" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Nucleus/metabolism ; Cyclooxygenase 2/genetics ; Cytokines/genetics/metabolism ; Cytosol/metabolism ; *Gene Expression Regulation ; Heterogeneous-Nuclear Ribonucleoproteins/metabolism ; Immunity, Innate/*genetics ; Inflammation/*genetics ; Macrophage Activation ; Macrophages/*immunology/*metabolism ; Mice ; Models, Immunological ; RNA Interference ; RNA, Long Noncoding/*genetics/metabolism ; Toll-Like Receptors/genetics/metabolism ; Transcription Factors/genetics/metabolism ; Transcription, Genetic ; Transcriptional Activation
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  • 20
    Publication Date: 2013-06-15
    Description: Epistatic interactions between mutant sites in the same protein can exert a strong influence on pathways of molecular evolution. We performed protein engineering experiments that revealed pervasive epistasis among segregating amino acid variants that contribute to adaptive functional variation in deer mouse hemoglobin (Hb). Amino acid mutations increased or decreased Hb-O2 affinity depending on the allelic state of other sites. Structural analysis revealed that epistasis for Hb-O2 affinity and allosteric regulatory control is attributable to indirect interactions between structurally remote sites. The prevalence of sign epistasis for fitness-related biochemical phenotypes has important implications for the evolutionary dynamics of protein polymorphism in natural populations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4409680/" 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/PMC4409680/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Natarajan, Chandrasekhar -- Inoguchi, Noriko -- Weber, Roy E -- Fago, Angela -- Moriyama, Hideaki -- Storz, Jay F -- HL087216-S1/HL/NHLBI NIH HHS/ -- R01 HL087216/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2013 Jun 14;340(6138):1324-7. doi: 10.1126/science.1236862.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biological Sciences, University of Nebraska, Lincoln, NE 68588, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23766324" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Biological/*genetics ; Alleles ; Animals ; *Epistasis, Genetic ; *Evolution, Molecular ; Exons ; Genetic Variation ; Hemoglobins/*chemistry/*genetics ; Hydrogen Bonding ; Mutation ; Oxygen/chemistry ; Peromyscus/genetics/*physiology ; Polymorphism, Genetic ; Protein Structure, Secondary ; alpha-Globins/chemistry/genetics ; beta-Globins/genetics
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  • 21
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2013 Dec 20;342(6165):1440-1. doi: 10.1126/science.342.6165.1440-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357292" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/administration & dosage ; Fusobacterium/physiology ; Gastrointestinal Tract/*microbiology ; *Health ; Humans ; Infant ; Infant Formula/chemistry ; Kidney/metabolism ; Kidney Calculi/chemically induced/etiology ; Klebsiella/drug effects/metabolism ; Malnutrition/microbiology ; Neoplasms/microbiology ; Rats ; Triazines/metabolism/toxicity
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  • 22
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2013 Dec 20;342(6165):1440. doi: 10.1126/science.342.6165.1440-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357291" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid beta-Peptides/metabolism ; Animals ; Biological Transport ; Brain/*metabolism ; Coloring Agents/analysis/pharmacokinetics ; Mice ; Sleep/*physiology
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  • 23
    Publication Date: 2013-08-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Verger, Philippe J P -- Boobis, Alan R -- New York, N.Y. -- Science. 2013 Aug 16;341(6147):717-8. doi: 10.1126/science.1241572.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉World Health Organization, Geneva, Switzerland. vergerp@who.int〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23950515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crops, Agricultural/*chemistry ; Developing Countries ; *Food Safety ; *Food Supply ; Humans ; International Cooperation ; *Pesticide Residues/analysis/toxicity ; *Pesticides/analysis/metabolism/toxicity ; Risk Assessment ; Toxicity Tests
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  • 24
    Publication Date: 2013-05-21
    Description: The generation of high-affinity antibodies depends on the ability of B cells to extract antigens from the surfaces of antigen-presenting cells. B cells that express high-affinity B cell receptors (BCRs) acquire more antigen and obtain better T cell help. However, the mechanisms by which B cells extract antigen remain unclear. Using fluid and flexible membrane substrates to mimic antigen-presenting cells, we showed that B cells acquire antigen by dynamic myosin IIa-mediated contractions that pull out and invaginate the presenting membranes. The forces generated by myosin IIa contractions ruptured most individual BCR-antigen bonds and promoted internalization of only high-affinity, multivalent BCR microclusters. Thus, B cell contractility contributes to affinity discrimination by mechanically testing the strength of antigen binding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3713314/" 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/PMC3713314/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Natkanski, Elizabeth -- Lee, Wing-Yiu -- Mistry, Bhakti -- Casal, Antonio -- Molloy, Justin E -- Tolar, Pavel -- MC_U117570592/Medical Research Council/United Kingdom -- MC_U117597138/Medical Research Council/United Kingdom -- U117570592/Medical Research Council/United Kingdom -- U117597138/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2013 Jun 28;340(6140):1587-90. doi: 10.1126/science.1237572. Epub 2013 May 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immune Cell Biology, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23686338" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody Affinity ; *Antigen Presentation ; Antigens/*immunology ; B-Lymphocytes/*immunology ; Cells, Cultured ; Mechanical Processes ; Mice ; Mice, Inbred C57BL ; Microscopy, Atomic Force ; Nonmuscle Myosin Type IIA/*physiology ; Receptors, Antigen, B-Cell/immunology
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  • 25
    Publication Date: 2013-06-15
    Description: Different stimulus intensities elicit distinct perceptions, implying that input signals are either conveyed through an overlapping but distinct subpopulation of sensory neurons or channeled into divergent brain circuits according to intensity. In Drosophila, carbon dioxide (CO2) is detected by a single type of olfactory sensory neuron, but information is conveyed to higher brain centers through second-order projection neurons (PNs). Two distinct pathways, PN(v)-1 and PN(v)-2, are necessary and sufficient for avoidance responses to low and high CO2 concentrations, respectively. Whereas low concentrations activate PN(v)-1, high concentrations activate both PN(v)s and GABAergic PN(v)-3, which may inhibit PN(v)-1 pathway-mediated avoidance behavior. Channeling a sensory input into distinct neural pathways allows the perception of an odor to be further modulated by both stimulus intensity and context.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Hui-Hao -- Chu, Li-An -- Fu, Tsai-Feng -- Dickson, Barry J -- Chiang, Ann-Shyn -- New York, N.Y. -- Science. 2013 Jun 14;340(6138):1338-41. doi: 10.1126/science.1236693.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Biotechnology, National Tsing Hua University, Hsinchu 30013, Taiwan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23766327" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carbon Dioxide ; Drosophila melanogaster/*physiology ; Escape Reaction/*physiology ; Olfactory Pathways/*physiology ; Olfactory Receptor Neurons/cytology/*physiology
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  • 26
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-02-23
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4240228/" 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/PMC4240228/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ryan, Karen K -- Seeley, Randy J -- DK093848/DK/NIDDK NIH HHS/ -- HL111319/HL/NHLBI NIH HHS/ -- K99 HL111319/HL/NHLBI NIH HHS/ -- R01 DK093848/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 22;339(6122):918-9. doi: 10.1126/science.1234062.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Metabolic Diseases Institute, University of Cincinnati, Cincinnati, OH 45237, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23430646" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids, Branched-Chain/metabolism ; Animals ; Bacteria/metabolism ; Diet ; Dietary Carbohydrates/*metabolism ; Dietary Fats/*metabolism ; Digestive System/microbiology ; Fatty Acids/metabolism ; *Food ; *Hormones ; Humans ; Nutritional Physiological Phenomena ; *Signal Transduction
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  • 27
    Publication Date: 2013-04-27
    Description: Secondary bacterial pneumonia leads to increased morbidity and mortality from influenza virus infections. What causes this increased susceptibility, however, is not well defined. Host defense from infection relies not only on immune resistance mechanisms but also on the ability to tolerate a given level of pathogen burden. Failure of either resistance or tolerance can contribute to disease severity, making it hard to distinguish their relative contribution. We employ a coinfection mouse model of influenza virus and Legionella pneumophila in which we can separate resistance and tolerance. We demonstrate that influenza virus can promote susceptibility to lethal bacterial coinfection, even when bacterial infection is controlled by the immune system. We propose that this failure of host defense is due to impaired ability to tolerate tissue damage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3933032/" 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/PMC3933032/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jamieson, Amanda M -- Pasman, Lesley -- Yu, Shuang -- Gamradt, Pia -- Homer, Robert J -- Decker, Thomas -- Medzhitov, Ruslan -- AI R01 055502/AI/NIAID NIH HHS/ -- R01 046688/PHS HHS/ -- R01 AI046688/AI/NIAID NIH HHS/ -- R01 AI055502/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Jun 7;340(6137):1230-4. doi: 10.1126/science.1233632. Epub 2013 Apr 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA. amanda_jamieson@brown.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23618765" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caspase 1 ; Coinfection/*immunology/pathology ; Disease Models, Animal ; Host-Pathogen Interactions/immunology ; Interleukin-1beta/metabolism ; *Legionella pneumophila ; Legionnaires' Disease/*immunology/pathology ; Lung/microbiology/pathology/virology ; Mice ; Mice, Inbred C57BL ; *Orthomyxoviridae ; Orthomyxoviridae Infections/*immunology/pathology ; Pneumonia, Bacterial/*immunology/pathology ; Toll-Like Receptor 2/metabolism ; Toll-Like Receptor 3/metabolism ; Toll-Like Receptor 4/metabolism ; Tumor Necrosis Factor-alpha/metabolism
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  • 28
    Publication Date: 2013-12-18
    Description: An understanding of ctenophore biology is critical for reconstructing events that occurred early in animal evolution. Toward this goal, we have sequenced, assembled, and annotated the genome of the ctenophore Mnemiopsis leidyi. Our phylogenomic analyses of both amino acid positions and gene content suggest that ctenophores rather than sponges are the sister lineage to all other animals. Mnemiopsis lacks many of the genes found in bilaterian mesodermal cell types, suggesting that these cell types evolved independently. The set of neural genes in Mnemiopsis is similar to that of sponges, indicating that sponges may have lost a nervous system. These results present a newly supported view of early animal evolution that accounts for major losses and/or gains of sophisticated cell types, including nerve and muscle cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3920664/" 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/PMC3920664/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ryan, Joseph F -- Pang, Kevin -- Schnitzler, Christine E -- Nguyen, Anh-Dao -- Moreland, R Travis -- Simmons, David K -- Koch, Bernard J -- Francis, Warren R -- Havlak, Paul -- NISC Comparative Sequencing Program -- Smith, Stephen A -- Putnam, Nicholas H -- Haddock, Steven H D -- Dunn, Casey W -- Wolfsberg, Tyra G -- Mullikin, James C -- Martindale, Mark Q -- Baxevanis, Andreas D -- ZIA HG000140-13/Intramural NIH HHS/ -- ZIA HG000140-14/Intramural NIH HHS/ -- ZIA HG000140-15/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2013 Dec 13;342(6164):1242592. doi: 10.1126/science.1242592.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genome Technology Branch, Division of Intramural Research, National Human Genome Research Institute, 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/24337300" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Biological Evolution ; Cell Lineage/*genetics ; Ctenophora/classification/*cytology/*genetics ; *Genome ; Mesoderm/cytology ; Molecular Sequence Data ; Muscle Development/genetics ; Neurogenesis/genetics ; Phylogeny
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  • 29
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-11-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Verissimo, Diogo -- New York, N.Y. -- Science. 2013 Nov 15;342(6160):798-9. doi: 10.1126/science.342.6160.798-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Durrell Institute of Conservation and Ecology, University of Kent, Canterbury, CT2 7NZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24233705" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Crops, Agricultural ; Insect Control/*methods ; *Insecticides ; *Oryza
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  • 30
    Publication Date: 2013-11-23
    Description: Cancer is a disease in which cells accumulate genetic aberrations that are believed to confer a clonal advantage over cells in the surrounding tissue. However, the quantitative benefit of frequently occurring mutations during tumor development remains unknown. We quantified the competitive advantage of Apc loss, Kras activation, and P53 mutations in the mouse intestine. Our findings indicate that the fate conferred by these mutations is not deterministic, and many mutated stem cells are replaced by wild-type stem cells after biased, but still stochastic events. Furthermore, P53 mutations display a condition-dependent advantage, and especially in colitis-affected intestines, clones harboring mutations in this gene are favored. Our work confirms the previously theoretical notion that the tissue architecture of the intestine suppresses the accumulation of mutated lineages.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vermeulen, Louis -- Morrissey, Edward -- van der Heijden, Maartje -- Nicholson, Anna M -- Sottoriva, Andrea -- Buczacki, Simon -- Kemp, Richard -- Tavare, Simon -- Winton, Douglas J -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2013 Nov 22;342(6161):995-8. doi: 10.1126/science.1243148.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK, Cambridge Institute, University of Cambridge, Robinson Way, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24264992" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein/genetics ; Animals ; Cell Transformation, Neoplastic/*genetics/*pathology ; *Gene Expression Regulation, Neoplastic ; Intestinal Neoplasms/*genetics/*pathology ; Mice ; Mice, Mutant Strains ; Models, Biological ; Mutation ; Neoplastic Stem Cells/metabolism/*pathology ; Proto-Oncogene Proteins p21(ras)/genetics ; Transcriptional Activation ; Tumor Suppressor Protein p53/genetics
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  • 31
    Publication Date: 2013-09-28
    Description: The growing prevalence of overeating disorders is a key contributor to the worldwide obesity epidemic. Dysfunction of particular neural circuits may trigger deviations from adaptive feeding behaviors. The lateral hypothalamus (LH) is a crucial neural substrate for motivated behavior, including feeding, but the precise functional neurocircuitry that controls LH neuronal activity to engage feeding has not been defined. We observed that inhibitory synaptic inputs from the extended amygdala preferentially innervate and suppress the activity of LH glutamatergic neurons to control food intake. These findings help explain how dysregulated activity at a number of unique nodes can result in a cascading failure within a defined brain network to produce maladaptive feeding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4131546/" 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/PMC4131546/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jennings, Joshua H -- Rizzi, Giorgio -- Stamatakis, Alice M -- Ung, Randall L -- Stuber, Garret D -- AA011605/AA/NIAAA NIH HHS/ -- AA022234/AA/NIAAA NIH HHS/ -- DA032750/DA/NIDA NIH HHS/ -- DA034472/DA/NIDA NIH HHS/ -- F31 DA034472/DA/NIDA NIH HHS/ -- NS007431/NS/NINDS NIH HHS/ -- P30 NS045892/NS/NINDS NIH HHS/ -- P50 AA011605/AA/NIAAA NIH HHS/ -- R01 DA032750/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2013 Sep 27;341(6153):1517-21. doi: 10.1126/science.1241812.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24072922" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Amygdala/physiology ; Animals ; Bacterial Proteins/genetics/metabolism ; Eating/*physiology ; Feeding Behavior/*physiology ; GABAergic Neurons/*physiology ; Hypothalamus/*physiology ; Luminescent Proteins/genetics/metabolism ; Male ; Mice ; Mice, Mutant Strains ; Obesity/physiopathology ; Rhodopsin/genetics/metabolism ; Septal Nuclei/physiology ; Synapses/physiology ; gamma-Aminobutyric Acid/metabolism/physiology
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  • 32
    Publication Date: 2013-04-27
    Description: Color patterns of bird plumage affect animal behavior and speciation. Diverse patterns are present in different species and within the individual. Here, we study the cellular and molecular basis of feather pigment pattern formation. Melanocyte progenitors are distributed as a horizontal ring in the proximal follicle, sending melanocytes vertically up into the epithelial cylinder, which gradually emerges as feathers grow. Different pigment patterns form by modulating the presence, arrangement, or differentiation of melanocytes. A layer of peripheral pulp further regulates pigmentation via patterned agouti expression. Lifetime feather cyclic regeneration resets pigment patterns for physiological needs. Thus, the evolution of stem cell niche topology allows complex pigment patterning through combinatorial co-option of simple regulatory mechanisms.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4144997/" 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/PMC4144997/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, S J -- Foley, J -- Jiang, T X -- Yeh, C Y -- Wu, P -- Foley, A -- Yen, C M -- Huang, Y C -- Cheng, H C -- Chen, C F -- Reeder, B -- Jee, S H -- Widelitz, R B -- Chuong, C M -- AR060306/AR/NIAMS NIH HHS/ -- AR42177/AR/NIAMS NIH HHS/ -- AR47364/AR/NIAMS NIH HHS/ -- R01 AR042177/AR/NIAMS NIH HHS/ -- R01 AR047364/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Jun 21;340(6139):1442-5. doi: 10.1126/science.1230374. Epub 2013 Apr 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23618762" target="_blank"〉PubMed〈/a〉
    Keywords: Agouti Signaling Protein/metabolism ; Animals ; Birds/*anatomy & histology/physiology ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Chickens/anatomy & histology/physiology ; Columbidae/anatomy & histology/physiology ; Feathers/*cytology/growth & development ; Female ; Galliformes/anatomy & histology/physiology ; Male ; Melanocytes/*cytology/physiology ; Models, Biological ; *Pigmentation ; Regeneration ; *Stem Cell Niche ; Stem Cells/*cytology/physiology
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  • 33
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2013 Dec 20;342(6165):1436-7. doi: 10.1126/science.342.6165.1436-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357288" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/anatomy & histology/blood supply/*growth & development ; Humans ; Induced Pluripotent Stem Cells/*cytology ; Neural Stem Cells/*cytology ; *Neurogenesis ; *Organ Culture Techniques
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  • 34
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2013 Dec 20;342(6165):1436. doi: 10.1126/science.342.6165.1436-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357287" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Separation ; Cloning, Organism/*methods ; Female ; Humans ; *Induced Pluripotent Stem Cells ; Nuclear Transfer Techniques ; Pregnancy ; *Research Embryo Creation ; Surrogate Mothers
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  • 35
    Publication Date: 2013-11-02
    Description: Central nervous system injuries are accompanied by scar formation. It has been difficult to delineate the precise role of the scar, as it is made by several different cell types, which may limit the damage but also inhibit axonal regrowth. We show that scarring by neural stem cell-derived astrocytes is required to restrict secondary enlargement of the lesion and further axonal loss after spinal cord injury. Moreover, neural stem cell progeny exerts a neurotrophic effect required for survival of neurons adjacent to the lesion. One distinct component of the glial scar, deriving from resident neural stem cells, is required for maintaining the integrity of the injured spinal cord.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sabelstrom, Hanna -- Stenudd, Moa -- Reu, Pedro -- Dias, David O -- Elfineh, Marta -- Zdunek, Sofia -- Damberg, Peter -- Goritz, Christian -- Frisen, Jonas -- New York, N.Y. -- Science. 2013 Nov 1;342(6158):637-40. doi: 10.1126/science.1242576.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Molecular Biology, Karolinska Institute, SE-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24179227" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Astrocytes/physiology ; Axons/*physiology ; Cell Survival ; Cicatrix/*pathology ; Forkhead Transcription Factors/genetics ; Genes, ras ; Mice ; Mice, Mutant Strains ; Neural Stem Cells/*physiology ; Spinal Cord Injuries/*pathology
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  • 36
    Publication Date: 2013-11-30
    Description: Hypercholesterolemia is a risk factor for estrogen receptor (ER)-positive breast cancers and is associated with a decreased response of tumors to endocrine therapies. Here, we show that 27-hydroxycholesterol (27HC), a primary metabolite of cholesterol and an ER and liver X receptor (LXR) ligand, increases ER-dependent growth and LXR-dependent metastasis in mouse models of breast cancer. The effects of cholesterol on tumor pathology required its conversion to 27HC by the cytochrome P450 oxidase CYP27A1 and were attenuated by treatment with CYP27A1 inhibitors. In human breast cancer specimens, CYP27A1 expression levels correlated with tumor grade. In high-grade tumors, both tumor cells and tumor-associated macrophages exhibited high expression levels of the enzyme. Thus, lowering circulating cholesterol levels or interfering with its conversion to 27HC may be a useful strategy to prevent and/or treat breast cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3899689/" 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/PMC3899689/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, Erik R -- Wardell, Suzanne E -- Jasper, Jeff S -- Park, Sunghee -- Suchindran, Sunil -- Howe, Matthew K -- Carver, Nicole J -- Pillai, Ruchita V -- Sullivan, Patrick M -- Sondhi, Varun -- Umetani, Michihisa -- Geradts, Joseph -- McDonnell, Donald P -- K99CA172357/CA/NCI NIH HHS/ -- R37 DK048807/DK/NIDDK NIH HHS/ -- R37DK048807/DK/NIDDK NIH HHS/ -- T32 CA059365/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2013 Nov 29;342(6162):1094-8. doi: 10.1126/science.1241908.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24288332" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/blood/*metabolism/*pathology ; Cell Line, Tumor ; Cholestanetriol 26-Monooxygenase/antagonists & inhibitors/metabolism ; Disease Models, Animal ; Female ; Humans ; Hydroxycholesterols/antagonists & inhibitors/blood/*metabolism ; Hypercholesterolemia/blood/*metabolism ; Lung Neoplasms/secondary ; Mice ; Tumor Cells, Cultured
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  • 37
    Publication Date: 2013-08-03
    Description: Insects often undergo regular outbreaks in population density but identifying the causal mechanism for such outbreaks in any particular species has proven difficult. Here, we show that outbreak cycles in the tea tortrix Adoxophyes honmai can be explained by temperature-driven changes in system stability. Wavelet analysis of a 51-year time series spanning more than 200 outbreaks reveals a threshold in outbreak amplitude each spring when temperature exceeds 15 degrees C and a secession of outbreaks each fall as temperature decreases. This is in close agreement with our independently parameterized mathematical model that predicts the system crosses a Hopf bifurcation from stability to sustained cycles as temperature increases. These results suggest that temperature can alter system stability and provide an explanation for generation cycles in multivoltine insects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, William A -- Bjornstad, Ottar N -- Yamanaka, Takehiko -- New York, N.Y. -- Science. 2013 Aug 16;341(6147):796-9. doi: 10.1126/science.1238477. Epub 2013 Aug 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Queen's University, Kingston, Ontario, Canada. nelsonw@queensu.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23907532" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Life Cycle Stages ; Models, Biological ; Moths/growth & development/*physiology ; Population Density ; Population Dynamics ; *Seasons ; *Temperature ; Wavelet Analysis
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  • 38
    Publication Date: 2013-08-03
    Description: Whereas reward (appetitiveness) and aversiveness (punishment) have been distinguished as two discrete dimensions within psychology and behavior, physiological and computational models of their neural representation have treated them as opposite sides of a single continuous dimension of "value." Here, I show that although dopamine neurons of the primate ventral midbrain are activated by evidence for reward and suppressed by evidence against reward, they are insensitive to aversiveness. This indicates that reward and aversiveness are represented independently as two dimensions, even by neurons that are closely related to motor function. Because theory and experiment support the existence of opponent neural representations for value, the present results imply four types of value-sensitive neurons corresponding to reward-ON (dopamine), reward-OFF, aversive-ON, and aversive-OFF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fiorillo, Christopher D -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Aug 2;341(6145):546-9. doi: 10.1126/science.1238699.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bio and Brain Engineering, KAIST (Korea Advanced Institute of Science and Technology), Yuseong-gu, Daejeon, Republic of Korea. fiorillo@kaist.ac.kr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23908236" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Appetitive Behavior/*physiology ; Conditioning, Classical/physiology ; Dopaminergic Neurons/*physiology ; Female ; Macaca mulatta ; Male ; Mesencephalon/cytology/*physiology ; Punishment/*psychology ; *Reward
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  • 39
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2013 Dec 20;342(6165):1434-5. doi: 10.1126/science.342.6165.1434-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357286" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*ultrastructure ; Cell Count/methods ; Cell Membrane/chemistry ; Humans ; Imaging, Three-Dimensional/*methods ; Membrane Lipids/*chemistry ; Mice ; Neurons/chemistry/*ultrastructure ; Staining and Labeling/*methods
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  • 40
    Publication Date: 2013-04-20
    Description: Recovery of overexploited marine populations has been slow, and most remain below target biomass levels. A key question is whether this is due to insufficient reductions in harvest rates or the erosion of population resilience. Using a global meta-analysis of overfished stocks, we find that resilience of those stocks subjected to moderate levels of overfishing is enhanced, not compromised, offering the possibility of swift recovery. However, prolonged intense overexploitation, especially for collapsed stocks, not only delays rebuilding but also substantially increases the uncertainty in recovery times, despite predictable influences of fishing and life history. Timely and decisive reductions in harvest rates could mitigate this uncertainty. Instead, current harvest and low biomass levels render recovery improbable for the majority of the world's depleted stocks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neubauer, Philipp -- Jensen, Olaf P -- Hutchings, Jeffrey A -- Baum, Julia K -- New York, N.Y. -- Science. 2013 Apr 19;340(6130):347-9. doi: 10.1126/science.1230441.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Marine and Coastal Sciences, Rutgers University, New Brunswick, NJ 08901, USA. neubauer.phil@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23599493" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomass ; *Conservation of Natural Resources ; *Fisheries ; Fishes/*growth & development/physiology ; Population Density
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  • 41
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Victora, Gabriel D -- New York, N.Y. -- Science. 2013 Dec 6;342(6163):1186. doi: 10.1126/science.1247567.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24311676" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/genetics/*immunology ; Antibody Affinity ; Antibody Formation ; Awards and Prizes ; B-Lymphocytes/*immunology ; Cell Movement ; Cell Proliferation ; *Evolution, Molecular ; Germinal Center/cytology/*immunology ; History, 21st Century ; Mice ; Mice, Transgenic ; Somatic Hypermutation, Immunoglobulin ; T-Lymphocytes, Helper-Inducer/immunology ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 42
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2013 Dec 20;342(6165):1434-5. doi: 10.1126/science.342.6165.1434-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357285" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/genetics/metabolism ; Clustered Regularly Interspaced Short Palindromic Repeats/*genetics ; DNA/genetics ; Genetic Diseases, Inborn/*surgery ; Genetic Therapy/*methods ; Humans ; Mice ; Microsurgery/*methods ; *RNA Editing ; RNA, Guide/genetics/metabolism ; Rats
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  • 43
    Publication Date: 2013-11-23
    Description: Cyclophosphamide is one of several clinically important cancer drugs whose therapeutic efficacy is due in part to their ability to stimulate antitumor immune responses. Studying mouse models, we demonstrate that cyclophosphamide alters the composition of microbiota in the small intestine and induces the translocation of selected species of Gram-positive bacteria into secondary lymphoid organs. There, these bacteria stimulate the generation of a specific subset of "pathogenic" T helper 17 (pT(H)17) cells and memory T(H)1 immune responses. Tumor-bearing mice that were germ-free or that had been treated with antibiotics to kill Gram-positive bacteria showed a reduction in pT(H)17 responses, and their tumors were resistant to cyclophosphamide. Adoptive transfer of pT(H)17 cells partially restored the antitumor efficacy of cyclophosphamide. These results suggest that the gut microbiota help shape the anticancer immune response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4048947/" 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/PMC4048947/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Viaud, Sophie -- Saccheri, Fabiana -- Mignot, Gregoire -- Yamazaki, Takahiro -- Daillere, Romain -- Hannani, Dalil -- Enot, David P -- Pfirschke, Christina -- Engblom, Camilla -- Pittet, Mikael J -- Schlitzer, Andreas -- Ginhoux, Florent -- Apetoh, Lionel -- Chachaty, Elisabeth -- Woerther, Paul-Louis -- Eberl, Gerard -- Berard, Marion -- Ecobichon, Chantal -- Clermont, Dominique -- Bizet, Chantal -- Gaboriau-Routhiau, Valerie -- Cerf-Bensussan, Nadine -- Opolon, Paule -- Yessaad, Nadia -- Vivier, Eric -- Ryffel, Bernhard -- Elson, Charles O -- Dore, Joel -- Kroemer, Guido -- Lepage, Patricia -- Boneca, Ivo Gomperts -- Ghiringhelli, Francois -- Zitvogel, Laurence -- P01 DK071176/DK/NIDDK NIH HHS/ -- P01DK071176/DK/NIDDK NIH HHS/ -- P50 CA086355/CA/NCI NIH HHS/ -- R01 AI084880/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Nov 22;342(6161):971-6. doi: 10.1126/science.1240537.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut National de la Sante et de la Recherche Medicale, U1015, Equipe labellisee Ligue Nationale Contre le Cancer, Institut Gustave Roussy, Villejuif, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24264990" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Anti-Bacterial Agents/administration & dosage ; Antineoplastic Agents/*therapeutic use ; Bacterial Translocation/*drug effects ; Cyclophosphamide/*therapeutic use ; Germ-Free Life ; Gram-Positive Bacteria/drug effects/physiology ; Immunologic Memory ; Immunosuppressive Agents/*therapeutic use ; Intestine, Small/*microbiology ; Lymphoid Tissue/immunology/microbiology ; Mice ; Microbiota/drug effects/*physiology ; Neoplasms/*drug therapy/*immunology ; Th17 Cells/immunology/transplantation
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  • 44
    Publication Date: 2013-10-19
    Description: The chytrid fungus, Batrachochytrium dendrobatidis, causes chytridiomycosis and is a major contributor to global amphibian declines. Although amphibians have robust immune defenses, clearance of this pathogen is impaired. Because inhibition of host immunity is a common survival strategy of pathogenic fungi, we hypothesized that B. dendrobatidis evades clearance by inhibiting immune functions. We found that B. dendrobatidis cells and supernatants impaired lymphocyte proliferation and induced apoptosis; however, fungal recognition and phagocytosis by macrophages and neutrophils was not impaired. Fungal inhibitory factors were resistant to heat, acid, and protease. Their production was absent in zoospores and reduced by nikkomycin Z, suggesting that they may be components of the cell wall. Evasion of host immunity may explain why this pathogen has devastated amphibian populations worldwide.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3956111/" 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/PMC3956111/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fites, J Scott -- Ramsey, Jeremy P -- Holden, Whitney M -- Collier, Sarah P -- Sutherland, Danica M -- Reinert, Laura K -- Gayek, A Sophia -- Dermody, Terence S -- Aune, Thomas M -- Oswald-Richter, Kyra -- Rollins-Smith, Louise A -- 1K01HL103179-01/HL/NHLBI NIH HHS/ -- AI007281/AI/NIAID NIH HHS/ -- AI038296/AI/NIAID NIH HHS/ -- AI044924/AI/NIAID NIH HHS/ -- K01 HL103179/HL/NHLBI NIH HHS/ -- R01 AI038296/AI/NIAID NIH HHS/ -- R37 AI038296/AI/NIAID NIH HHS/ -- R56 AI044924/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Oct 18;342(6156):366-9. doi: 10.1126/science.1243316.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Vanderbilt University, Nashville, TN 37235, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24136969" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoglycosides/pharmacology ; Amphibians/*immunology/*microbiology ; Animals ; Apoptosis/immunology ; Cell Proliferation ; Chytridiomycota/*pathogenicity ; Host-Pathogen Interactions/*immunology ; Lymphocytes/drug effects/*immunology/*microbiology ; Mycoses/immunology/*veterinary ; Spores, Fungal/pathogenicity ; Xenopus laevis
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 45
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vafai, Scott B -- Mootha, Vamsi K -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Dec 20;342(6165):1453-4. doi: 10.1126/science.1248449.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Departments of Molecular Biology and Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357304" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Leigh Disease/*drug therapy ; Mitochondrial Diseases/*drug therapy ; *Molecular Targeted Therapy ; Multiprotein Complexes/*antagonists & inhibitors ; Neuroprotective Agents/*therapeutic use ; Sirolimus/*therapeutic use ; TOR Serine-Threonine Kinases/*antagonists & inhibitors
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  • 46
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-05-11
    Description: The possibility that market interaction may erode moral values is a long-standing, but controversial, hypothesis in the social sciences, ethics, and philosophy. To date, empirical evidence on decay of moral values through market interaction has been scarce. We present controlled experimental evidence on how market interaction changes how human subjects value harm and damage done to third parties. In the experiment, subjects decide between either saving the life of a mouse or receiving money. We compare individual decisions to those made in a bilateral and a multilateral market. In both markets, the willingness to kill the mouse is substantially higher than in individual decisions. Furthermore, in the multilateral market, prices for life deteriorate tremendously. In contrast, for morally neutral consumption choices, differences between institutions are small.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Falk, Armin -- Szech, Nora -- New York, N.Y. -- Science. 2013 May 10;340(6133):707-11. doi: 10.1126/science.1231566.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Economics and Neuroscience, University of Bonn, Bonn, Germany. armin.falk@uni-bonn.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23661753" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Commerce/*ethics ; Decision Making ; Humans ; Mice ; *Morals
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  • 47
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-03-23
    Description: The theories of aero- and hydrodynamics predict animal movement and device design in air and water through the computation of lift, drag, and thrust forces. Although models of terrestrial legged locomotion have focused on interactions with solid ground, many animals move on substrates that flow in response to intrusion. However, locomotor-ground interaction models on such flowable ground are often unavailable. We developed a force model for arbitrarily-shaped legs and bodies moving freely in granular media, and used this "terradynamics" to predict a small legged robot's locomotion on granular media using various leg shapes and stride frequencies. Our study reveals a complex but generic dependence of stresses in granular media on intruder depth, orientation, and movement direction and gives insight into the effects of leg morphology and kinematics on movement.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Chen -- Zhang, Tingnan -- Goldman, Daniel I -- New York, N.Y. -- Science. 2013 Mar 22;339(6126):1408-12. doi: 10.1126/science.1229163.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Physics, Georgia Institute of Technology, Atlanta, GA 30332, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23520106" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomechanical Phenomena ; Extremities/*physiology ; *Locomotion ; *Models, Biological ; Robotics ; Stress, Mechanical
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  • 48
    Publication Date: 2013-05-25
    Description: Cramer et al. (Reports, 23 March 2012, p. 1503; published online 9 February 2012) demonstrated in a mouse model for Alzheimer's disease (AD) that treatment of APP/PS1DeltaE9 mice with bexarotene decreased Abeta pathology and ameliorated memory deficits. We confirm the reversal of memory deficits in APP/PS1DeltaE9 mice expressing human APOE3 or APOE4 to the levels of their nontransgenic controls and the significant decrease of interstitial fluid Abeta, but not the effects on amyloid deposition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4086452/" 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/PMC4086452/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fitz, Nicholas F -- Cronican, Andrea A -- Lefterov, Iliya -- Koldamova, Radosveta -- F32AG034031/AG/NIA NIH HHS/ -- R01 AG037481/AG/NIA NIH HHS/ -- R01 AG037919/AG/NIA NIH HHS/ -- R01AG037481/AG/NIA NIH HHS/ -- R01AG037919/AG/NIA NIH HHS/ -- R21 ES021243/ES/NIEHS NIH HHS/ -- R21ES021243/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2013 May 24;340(6135):924-c. doi: 10.1126/science.1235809.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Environmental and Occupational Health, University of Pittsburgh, 100 Technology Drive, Pittsburgh, PA 15219, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23704552" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*drug therapy/*metabolism ; Amyloid beta-Peptides/*metabolism ; Animals ; Apolipoproteins E/*metabolism ; Brain/*metabolism ; Male ; Tetrahydronaphthalenes/*pharmacology/*therapeutic use
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  • 49
    Publication Date: 2013-10-05
    Description: Dominant mutations in sarcomere proteins such as the myosin heavy chains (MHC) are the leading genetic causes of human hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy. We found that expression of the HCM-causing cardiac MHC gene (Myh6) R403Q mutation in mice can be selectively silenced by an RNA interference (RNAi) cassette delivered by an adeno-associated virus vector. RNAi-transduced MHC(403/+) mice developed neither hypertrophy nor myocardial fibrosis, the pathologic manifestations of HCM, for at least 6 months. Because inhibition of HCM was achieved by only a 25% reduction in the levels of the mutant transcripts, we suggest that the variable clinical phenotype in HCM patients reflects allele-specific expression and that partial silencing of mutant transcripts may have therapeutic benefit.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4100553/" 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/PMC4100553/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, Jianming -- Wakimoto, Hiroko -- Seidman, J G -- Seidman, Christine E -- R01 HL084553/HL/NHLBI NIH HHS/ -- R01HL084553/HL/NHLBI NIH HHS/ -- U01 HL066582/HL/NHLBI NIH HHS/ -- U01 HL098166/HL/NHLBI NIH HHS/ -- U01HL098166/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Oct 4;342(6154):111-4. doi: 10.1126/science.1236921.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24092743" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cardiomyopathy, Hypertrophic/*diagnosis/genetics/pathology ; Dependovirus ; Fibrosis ; Gene Silencing ; *Genetic Therapy ; HEK293 Cells ; Humans ; Mice ; Mutation ; Myosin Heavy Chains/*genetics ; *RNA Interference
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  • 50
    Publication Date: 2013-04-27
    Description: Leathers and Olson (Reports, 5 October 2012, p. 132) draw the strong conclusion that neurons in the monkey lateral intraparietal (LIP) cortical area encode only cue salience, and not action value, during value-based decision-making. Although their findings regarding cue salience are interesting, their broader conclusions are problematic because (i) their primary conclusion is based on responses observed during a brief interval at the beginning of behavioral trials but is extended to all subsequent temporal epochs and (ii) the authors failed to replicate basic hallmarks of LIP physiology observed in those subsequent temporal epochs by many laboratories.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4045496/" 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/PMC4045496/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Newsome, William T -- Glimcher, Paul W -- Gottlieb, Jacqueline -- Lee, Daeyeol -- Platt, Michael L -- R01 MH096875/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2013 Apr 26;340(6131):430. doi: 10.1126/science.1233214.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23620037" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cues ; Decision Making/*physiology ; Male ; Motivation/*physiology ; Neurons/*physiology ; Saccades/*physiology ; *Social Values
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  • 51
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-02-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cemma, Marija -- Brumell, John H -- New York, N.Y. -- Science. 2013 Feb 22;339(6122):912-3. doi: 10.1126/science.1235639.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology Program, Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23430642" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caspases/*metabolism ; *Cell Death ; Cytosol/*microbiology ; Gram-Negative Bacterial Infections/*immunology ; Macrophages/*microbiology ; Vacuoles/*microbiology
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  • 52
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-08-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2013 Aug 16;341(6147):730-1. doi: 10.1126/science.341.6147.730.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23950524" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crops, Agricultural ; Developing Countries ; Humans ; Malaria/prevention & control ; *Pest Control/methods/statistics & numerical data ; *Pesticides/poisoning/toxicity ; Plant Weeds
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  • 53
    Publication Date: 2013-05-21
    Description: Invasive species that proliferate after colonizing new habitats have a negative environmental and economic impact. The reason why some species become successful invaders, whereas others, even closely related species, remain noninvasive is often unclear. The harlequin ladybird Harmonia axyridis, introduced for biological pest control, has become an invader that is outcompeting indigenous ladybird species in many countries. Here, we show that Harmonia carries abundant spores of obligate parasitic microsporidia closely related to Nosema thompsoni. These microsporidia, while not harming the carrier Harmonia, are lethal pathogens for the native ladybird Coccinella septempunctata. We propose that intraguild predation, representing a major selective force among competing ladybird species, causes the infection and ultimate death of native ladybirds when they feed on microsporidia-contaminated Harmonia eggs or larvae.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vilcinskas, Andreas -- Stoecker, Kilian -- Schmidtberg, Henrike -- Rohrich, Christian R -- Vogel, Heiko -- New York, N.Y. -- Science. 2013 May 17;340(6134):862-3. doi: 10.1126/science.1234032.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Phytopathology and Applied Zoology, Heinrich-Buff-Ring 26-32, Justus-Liebig-University of Giessen, D-35392 Giessen, Germany. andreas.vilcinskas@agrar.uni-giessen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23687046" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Beetles/*parasitology/*physiology ; *Food Chain ; Hemocytes/parasitology ; Hemolymph/parasitology ; *Introduced Species ; Nosema/*physiology/ultrastructure
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  • 54
    Publication Date: 2013-03-16
    Description: The identification of precise mutations is required for a complete understanding of the underlying molecular and evolutionary mechanisms driving adaptive phenotypic change. Using plasticine models in the field, we show that the light coat color of deer mice that recently colonized the light-colored soil of the Nebraska Sand Hills provides a strong selective advantage against visually hunting predators. Color variation in an admixed population suggests that this light Sand Hills phenotype is composed of multiple traits. We identified distinct regions within the Agouti locus associated with each color trait and found that only haplotypes associated with light trait values have evidence of selection. Thus, local adaptation is the result of independent selection on many mutations within a single locus, each with a specific effect on an adaptive phenotype, thereby minimizing pleiotropic consequences.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3836219/" 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/PMC3836219/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Linnen, Catherine R -- Poh, Yu-Ping -- Peterson, Brant K -- Barrett, Rowan D H -- Larson, Joanna G -- Jensen, Jeffrey D -- Hoekstra, Hopi E -- 308796/European Research Council/International -- New York, N.Y. -- Science. 2013 Mar 15;339(6125):1312-6. doi: 10.1126/science.1233213.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Kentucky, Lexington, KY 40506, USA. catherine.linnen@uky.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23493712" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/*genetics ; Agouti Signaling Protein/genetics ; Animals ; *Biological Evolution ; Color ; Food Chain ; *Multifactorial Inheritance ; Mutation ; Organic Chemicals ; Peromyscus/genetics/*physiology ; Pigmentation/*genetics ; Selection, Genetic
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  • 55
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-03-02
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4005781/" 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/PMC4005781/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flak, Magdalena B -- Neves, Joana F -- Blumberg, Richard S -- DK0034854/DK/NIDDK NIH HHS/ -- DK044319/DK/NIDDK NIH HHS/ -- DK051362/DK/NIDDK NIH HHS/ -- DK053056/DK/NIDDK NIH HHS/ -- DK088199/DK/NIDDK NIH HHS/ -- R01 DK088199/DK/NIDDK NIH HHS/ -- R37 DK044319/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2013 Mar 1;339(6123):1044-5. doi: 10.1126/science.1236226.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Gastroenterology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School and Harvard Digestive Diseases Center, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23449586" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autoimmunity ; Diabetes Mellitus, Type 1/*microbiology ; Female ; Gonadal Steroid Hormones/*immunology ; Intestines/*microbiology ; Male ; *Metagenome ; *Sex Characteristics
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  • 56
    Publication Date: 2013-07-06
    Description: DNA methylation is implicated in mammalian brain development and plasticity underlying learning and memory. We report the genome-wide composition, patterning, cell specificity, and dynamics of DNA methylation at single-base resolution in human and mouse frontal cortex throughout their lifespan. Widespread methylome reconfiguration occurs during fetal to young adult development, coincident with synaptogenesis. During this period, highly conserved non-CG methylation (mCH) accumulates in neurons, but not glia, to become the dominant form of methylation in the human neuronal genome. Moreover, we found an mCH signature that identifies genes escaping X-chromosome inactivation. Last, whole-genome single-base resolution 5-hydroxymethylcytosine (hmC) maps revealed that hmC marks fetal brain cell genomes at putative regulatory regions that are CG-demethylated and activated in the adult brain and that CG demethylation at these hmC-poised loci depends on Tet2 activity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3785061/" 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/PMC3785061/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lister, Ryan -- Mukamel, Eran A -- Nery, Joseph R -- Urich, Mark -- Puddifoot, Clare A -- Johnson, Nicholas D -- Lucero, Jacinta -- Huang, Yun -- Dwork, Andrew J -- Schultz, Matthew D -- Yu, Miao -- Tonti-Filippini, Julian -- Heyn, Holger -- Hu, Shijun -- Wu, Joseph C -- Rao, Anjana -- Esteller, Manel -- He, Chuan -- Haghighi, Fatemeh G -- Sejnowski, Terrence J -- Behrens, M Margarita -- Ecker, Joseph R -- AI44432/AI/NIAID NIH HHS/ -- CA151535/CA/NCI NIH HHS/ -- HD065812/HD/NICHD NIH HHS/ -- HG006827/HG/NHGRI NIH HHS/ -- K99NS080911/NS/NINDS NIH HHS/ -- MH094670/MH/NIMH NIH HHS/ -- R01 AI044432/AI/NIAID NIH HHS/ -- R01 CA151535/CA/NCI NIH HHS/ -- R01 HD065812/HD/NICHD NIH HHS/ -- R01 HG006827/HG/NHGRI NIH HHS/ -- R01 MH094670/MH/NIMH NIH HHS/ -- R01 MH094774/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Aug 9;341(6146):1237905. doi: 10.1126/science.1237905. Epub 2013 Jul 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genomic Analysis Laboratory, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA. ryan.lister@uwa.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23828890" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/metabolism ; Adult ; Animals ; Base Sequence ; Conserved Sequence ; Cytosine/*analogs & derivatives/metabolism ; *DNA Methylation ; *Epigenesis, Genetic ; Epigenomics ; Frontal Lobe/*growth & development ; *Gene Expression Regulation, Developmental ; Genome-Wide Association Study ; Humans ; Longevity ; Mice ; Mice, Inbred C57BL ; X Chromosome Inactivation/genetics
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  • 57
    Publication Date: 2013-08-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malakoff, David -- New York, N.Y. -- Science. 2013 Aug 9;341(6146):601.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23926188" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drug Resistance, Multiple, Viral/*genetics ; Humans ; Influenza A virus/*genetics/*pathogenicity ; Influenza in Birds/*transmission/*virology ; Influenza, Human/*prevention & control ; Pandemics/*prevention & control
    Print ISSN: 0036-8075
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  • 58
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2013 Dec 6;342(6163):1156. doi: 10.1126/science.342.6163.1156.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24311652" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Bone and Bones ; *DNA, Mitochondrial ; *Fossils ; *Hominidae ; Humans ; Neanderthals ; Spain
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 59
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-07-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Argus, Joseph P -- Bensinger, Steven J -- New York, N.Y. -- Science. 2013 Jul 5;341(6141):37-8. doi: 10.1126/science.1242100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23828930" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Glycolysis ; *Lymphocyte Activation ; *Oxidative Phosphorylation ; T-Lymphocytes/*cytology/*metabolism
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  • 60
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-06-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, Thomas E -- New York, N.Y. -- Science. 2013 Jun 14;340(6138):1299-300. doi: 10.1126/science.1240843.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Behavioral Genetics and Department of Integrative Physiology, Box 447, University of Colorado, Boulder 80309, USA. johnsont@colorado.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23766322" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Gene Knockout Techniques ; Humans ; Membrane Proteins/*metabolism ; Metalloendopeptidases/*metabolism ; Progeria/*therapy ; Protein Methyltransferases/*genetics/*metabolism
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  • 61
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-11-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nijman, Sebastian M B -- Friend, Stephen H -- New York, N.Y. -- Science. 2013 Nov 15;342(6160):809-11. doi: 10.1126/science.1244669.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24233712" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila melanogaster/genetics ; Gene Targeting ; *Genes, Lethal ; *Genes, Modifier ; Genetic Therapy/*methods ; Humans ; Immunotherapy ; Molecular Targeted Therapy ; Mutation ; Neoplasms/*genetics/*therapy ; Saccharomyces cerevisiae/genetics ; Tumor Suppressor Proteins/genetics
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  • 62
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Christine -- New York, N.Y. -- Science. 2013 Nov 29;342(6162):1052-3. doi: 10.1126/science.1247833.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉New York University, Center for Genomics and Systems Biology, New York, NY 10003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24288321" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Evolution, Molecular ; *Gene Expression Regulation ; Humans ; Macaca mulatta/*genetics ; Pan troglodytes/*genetics ; Protein Biosynthesis/*genetics ; RNA, Messenger/*biosynthesis ; *Selection, Genetic ; *Transcription, Genetic
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  • 63
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sale, Julian E -- Patel, Ketan J -- Batista, Facundo D -- MC_U105178808/Medical Research Council/United Kingdom -- MC_U105178811/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2013 Dec 13;342(6164):1335. doi: 10.1126/science.1248808.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Laboratory of Molecular Biology, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24337288" target="_blank"〉PubMed〈/a〉
    Keywords: Allergy and Immunology/*history ; Animals ; Antibodies, Monoclonal, Humanized/*history ; *Antibody Diversity ; Biomedical Engineering/*history ; Great Britain ; History, 20th Century ; History, 21st Century ; Humans ; Mice ; Molecular Biology/*history
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  • 64
    Publication Date: 2013-02-23
    Description: Insects use several senses to forage, detecting floral cues such as color, shape, pattern, and volatiles. We report a formerly unappreciated sensory modality in bumblebees (Bombus terrestris), detection of floral electric fields. These fields act as floral cues, which are affected by the visit of naturally charged bees. Like visual cues, floral electric fields exhibit variations in pattern and structure, which can be discriminated by bumblebees. We also show that such electric field information contributes to the complex array of floral cues that together improve a pollinator's memory of floral rewards. Because floral electric fields can change within seconds, this sensory modality may facilitate rapid and dynamic communication between flowers and their pollinators.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clarke, Dominic -- Whitney, Heather -- Sutton, Gregory -- Robert, Daniel -- New York, N.Y. -- Science. 2013 Apr 5;340(6128):66-9. doi: 10.1126/science.1230883. Epub 2013 Feb 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biological Sciences, University of Bristol, Woodland Road, Bristol BS8 1UG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23429701" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bees/*physiology ; *Cues ; *Electromagnetic Fields ; Flowers/anatomy & histology/*physiology ; *Pollination
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 65
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-04-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2013 Apr 26;340(6131):427. doi: 10.1126/science.340.6131.427.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23620032" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthropology, Physical/*history ; *Biological Evolution ; Female ; Foot/*anatomy & histology/*physiology ; History, Ancient ; Hominidae/*anatomy & histology/*physiology ; Walking/*history
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  • 66
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-04-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2013 Apr 26;340(6131):426-7. doi: 10.1126/science.340.6131.426-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23620030" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthropology, Physical/*history ; Hand/*anatomy & histology/*physiology ; Hand Bones/*anatomy & histology ; *Hand Strength ; History, Ancient ; Hominidae/*physiology ; Humans
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  • 67
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-05-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clarke, Julia -- New York, N.Y. -- Science. 2013 May 10;340(6133):690-2. doi: 10.1126/science.1235463.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Geological Sciences, The University of Texas at Austin, Austin, TX 78712, USA. julia_clarke@jsg.utexas.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23661746" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Birds/anatomy & histology/growth & development ; Dinosaurs/anatomy & histology/growth & development ; Feathers/anatomy & histology/*growth & development/ultrastructure ; *Flight, Animal ; *Fossils ; Protein Structure, Secondary ; beta-Keratins/chemistry
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  • 68
    Publication Date: 2013-03-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malakoff, David -- Enserink, Martin -- New York, N.Y. -- Science. 2013 Mar 1;339(6123):1025. doi: 10.1126/science.339.6123.1025.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23449570" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomedical Research/*standards ; *Guidelines as Topic ; Humans ; Influenza A Virus, H5N1 Subtype/*genetics/*pathogenicity ; Influenza, Human/*prevention & control/*transmission ; Laboratories/standards ; United States
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  • 69
    Publication Date: 2013-12-07
    Description: In individual cells, transcription is a random process obeying single-molecule kinetics. Often, it occurs in a bursty, intermittent manner. The frequency and size of these bursts affect the magnitude of temporal fluctuations in messenger RNA and protein content within a cell, creating variation or "noise" in gene expression. It is still unclear to what degree transcriptional kinetics are specific to each gene and determined by its promoter sequence. Alternative scenarios have been proposed, in which the kinetics of transcription are governed by cellular constraints and follow universal rules across the genome. Evidence from genome-wide noise studies and from systematic perturbations of promoter sequences suggest that both scenarios-namely gene-specific versus genome-wide regulation of transcription kinetics-may be present to different degrees in bacteria, yeast, and animal cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4045091/" 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/PMC4045091/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez, Alvaro -- Golding, Ido -- R01 GM082837/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Dec 6;342(6163):1188-93. doi: 10.1126/science.1242975.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Rowland Institute at Harvard, Harvard University, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24311680" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Escherichia coli/genetics/metabolism ; Eukaryota/genetics/metabolism ; *Gene Expression Regulation ; Genome ; Kinetics ; Models, Genetic ; Promoter Regions, Genetic ; RNA, Messenger/genetics/metabolism ; Single-Cell Analysis ; Stochastic Processes ; *Transcription, Genetic ; Yeasts/genetics/metabolism
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  • 70
    Publication Date: 2013-01-26
    Description: Caspases are either apoptotic or inflammatory. Among inflammatory caspases, caspase-1 and -11 trigger pyroptosis, a form of programmed cell death. Whereas both can be detrimental in inflammatory disease, only caspase-1 has an established protective role during infection. Here, we report that caspase-11 is required for innate immunity to cytosolic, but not vacuolar, bacteria. Although Salmonella typhimurium and Legionella pneumophila normally reside in the vacuole, specific mutants (sifA and sdhA, respectively) aberrantly enter the cytosol. These mutants triggered caspase-11, which enhanced clearance of S. typhimurium sifA in vivo. This response did not require NLRP3, NLRC4, or ASC inflammasome pathways. Burkholderia species that naturally invade the cytosol also triggered caspase-11, which protected mice from lethal challenge with B. thailandensis and B. pseudomallei. Thus, caspase-11 is critical for surviving exposure to ubiquitous environmental pathogens.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3697099/" 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/PMC3697099/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aachoui, Youssef -- Leaf, Irina A -- Hagar, Jon A -- Fontana, Mary F -- Campos, Cristine G -- Zak, Daniel E -- Tan, Michael H -- Cotter, Peggy A -- Vance, Russell E -- Aderem, Alan -- Miao, Edward A -- AI057141/AI/NIAID NIH HHS/ -- AI063302/AI/NIAID NIH HHS/ -- AI065359/AI/NIAID NIH HHS/ -- AI075039/AI/NIAID NIH HHS/ -- AI080749/AI/NIAID NIH HHS/ -- AI097518/AI/NIAID NIH HHS/ -- P01 AI063302/AI/NIAID NIH HHS/ -- P30 CA016086/CA/NCI NIH HHS/ -- R01 AI075039/AI/NIAID NIH HHS/ -- R01 AI080749/AI/NIAID NIH HHS/ -- R01 AI097518/AI/NIAID NIH HHS/ -- U19 AI100627/AI/NIAID NIH HHS/ -- U54 AI057141/AI/NIAID NIH HHS/ -- U54 AI065359/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 22;339(6122):975-8. doi: 10.1126/science.1230751. Epub 2013 Jan 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23348507" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Burkholderia/pathogenicity/physiology ; Burkholderia Infections/enzymology/immunology/metabolism ; Burkholderia pseudomallei/pathogenicity/physiology ; Caspases/*metabolism ; *Cell Death ; Cytosol/*microbiology ; Gram-Negative Bacterial Infections/enzymology/*immunology/microbiology ; Immunity, Innate ; Inflammasomes/metabolism ; Macrophages/immunology/*microbiology ; Mice ; Mice, Inbred C57BL ; Phagosomes/microbiology ; Salmonella Infections, Animal/enzymology/immunology/microbiology ; Salmonella typhimurium/pathogenicity/physiology ; Vacuoles/*microbiology
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  • 71
    Publication Date: 2013-01-25
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3838856/" 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/PMC3838856/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fouchier, Ron A M -- Garcia-Sastre, Adolfo -- Kawaoka, Yoshihiro -- Barclay, Wendy S -- Bouvier, Nicole M -- Brown, Ian H -- Capua, Ilaria -- Chen, Hualan -- Compans, Richard W -- Couch, Robert B -- Cox, Nancy J -- Doherty, Peter C -- Donis, Ruben O -- Feldmann, Heinz -- Guan, Yi -- Katz, Jacqueline M -- Kiselev, Oleg I -- Klenk, H D -- Kobinger, Gary -- Liu, Jinhua -- Liu, Xiufan -- Lowen, Anice -- Mettenleiter, Thomas C -- Osterhaus, Albert D M E -- Palese, Peter -- Peiris, J S Malik -- Perez, Daniel R -- Richt, Jurgen A -- Schultz-Cherry, Stacey -- Steel, John -- Subbarao, Kanta -- Swayne, David E -- Takimoto, Toru -- Tashiro, Masato -- Taubenberger, Jeffery K -- Thomas, Paul G -- Tripp, Ralph A -- Tumpey, Terrence M -- Webby, Richard J -- Webster, Robert G -- ZIA AI001088-01/Intramural NIH HHS/ -- ZIA AI001088-02/Intramural NIH HHS/ -- ZIA AI001088-03/Intramural NIH HHS/ -- ZIA AI001088-04/Intramural NIH HHS/ -- ZIA AI001088-05/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 1;339(6119):520-1. doi: 10.1126/science.1235140. Epub 2013 Jan 23.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23345603" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomedical Research/*trends ; Birds ; Humans ; *Influenza A Virus, H5N1 Subtype ; Influenza in Birds/*transmission/*virology ; Influenza, Human/*transmission/*virology
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  • 72
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-03-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joshi, Nikhil S -- Jacks, Tyler -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Mar 8;339(6124):1160-1. doi: 10.1126/science.1235528.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Koch Institute for Integrative Cancer Research, Department of Biology, and Howard Hughes Medical Institute, 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/23471395" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; *Immune Tolerance ; Male ; Prostate/*immunology ; Prostatic Neoplasms/*immunology ; T-Lymphocytes, Regulatory/*immunology ; Thymus Gland/*growth & development/*immunology ; Transcription Factors/*immunology
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  • 73
    Publication Date: 2013-09-28
    Description: Tropical forests continue to be felled and fragmented around the world. A key question is how rapidly species disappear from forest fragments and how quickly humans must restore forest connectivity to minimize extinctions. We surveyed small mammals on forest islands in Chiew Larn Reservoir in Thailand 5 to 7 and 25 to 26 years after isolation and observed the near-total loss of native small mammals within 5 years from 〈10-hectare (ha) fragments and within 25 years from 10- to 56-ha fragments. Based on our results, we developed an island biogeographic model and estimated mean extinction half-life (50% of resident species disappearing) to be 13.9 years. These catastrophic extinctions were probably partly driven by an invasive rat species; such biotic invasions are becoming increasingly common in human-modified landscapes. Our results are thus particularly relevant to other fragmented forest landscapes and suggest that small fragments are potentially even more vulnerable to biodiversity loss than previously thought.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibson, Luke -- Lynam, Antony J -- Bradshaw, Corey J A -- He, Fangliang -- Bickford, David P -- Woodruff, David S -- Bumrungsri, Sara -- Laurance, William F -- New York, N.Y. -- Science. 2013 Sep 27;341(6153):1508-10. doi: 10.1126/science.1240495.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, National University of Singapore, 14 Science Drive 4, Singapore 117543, Singapore. lggibson@nus.edu.sg〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24072921" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodiversity ; *Conservation of Natural Resources ; *Extinction, Biological ; Humans ; Islands ; Mammals/*classification ; Thailand ; *Trees
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  • 74
    Publication Date: 2013-05-04
    Description: Byers and Dunn (Reports, 9 November 2012, p. 802) reported that sexual selection and natural selection are closely related in a wild population of pronghorns. Here, I argue that this conclusion is incorrect. Their main finding is due to the fact that, unsurprisingly, juvenile mortality and juvenile survival are negatively related across years.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arnqvist, Goran -- 294333/European Research Council/International -- New York, N.Y. -- Science. 2013 May 3;340(6132):549. doi: 10.1126/science.1233413.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Animal Ecology, Department of Ecology and Genetics, Uppsala University, Norbyvagen 18D, SE75236 Uppsala, Sweden. goran.arnqvist@ebc.uu.se〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23641095" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antelopes/*physiology ; Female ; Male ; *Mating Preference, Animal ; *Predatory Behavior ; *Sexual Behavior, Animal
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  • 75
    Publication Date: 2013-02-02
    Description: The geographic origins of breeds and the genetic basis of variation within the widely distributed and phenotypically diverse domestic rock pigeon (Columba livia) remain largely unknown. We generated a rock pigeon reference genome and additional genome sequences representing domestic and feral populations. We found evidence for the origins of major breed groups in the Middle East and contributions from a racing breed to North American feral populations. We identified the gene EphB2 as a strong candidate for the derived head crest phenotype shared by numerous breeds, an important trait in mate selection in many avian species. We also found evidence that this trait evolved just once and spread throughout the species, and that the crest originates early in development by the localized molecular reversal of feather bud polarity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3778192/" 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/PMC3778192/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shapiro, Michael D -- Kronenberg, Zev -- Li, Cai -- Domyan, Eric T -- Pan, Hailin -- Campbell, Michael -- Tan, Hao -- Huff, Chad D -- Hu, Haofu -- Vickrey, Anna I -- Nielsen, Sandra C A -- Stringham, Sydney A -- Hu, Hao -- Willerslev, Eske -- Gilbert, M Thomas P -- Yandell, Mark -- Zhang, Guojie -- Wang, Jun -- GO RC2HG005619/HG/NHGRI NIH HHS/ -- R01 GM104390/GM/NIGMS NIH HHS/ -- R01 HG004694/HG/NHGRI NIH HHS/ -- R01HG004694/HG/NHGRI NIH HHS/ -- R44 HG006579/HG/NHGRI NIH HHS/ -- RC2 HG005619/HG/NHGRI NIH HHS/ -- T32 GM007464/GM/NIGMS NIH HHS/ -- T32 HD007491/HD/NICHD NIH HHS/ -- T32GM007464/GM/NIGMS NIH HHS/ -- T32HD07491/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2013 Mar 1;339(6123):1063-7. doi: 10.1126/science.1230422. Epub 2013 Jan 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Utah, Salt Lake City, UT 84112, USA. mike.shapiro@utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23371554" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Domestic/anatomy & histology/classification/genetics ; Animals, Wild/anatomy & histology/classification/genetics ; Breeding ; Columbidae/anatomy & histology/*classification/*genetics ; *Evolution, Molecular ; Feathers/anatomy & histology ; *Genetic Variation ; Genome ; Head/*anatomy & histology ; Models, Genetic ; Molecular Sequence Data ; Phylogeny ; Polymorphism, Single Nucleotide ; *Quantitative Trait, Heritable ; Receptor, EphB2/genetics ; Sequence Analysis, DNA
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  • 76
    Publication Date: 2013-03-23
    Description: The typical pattern of morphological evolution associated with the radiation of a group of related species is the emergence of a novel trait and its subsequent diversification. Yet the genetic mechanisms associated with these two evolutionary steps are poorly characterized. Here, we show that a spot of dark pigment on fly wings emerged from the assembly of a novel gene regulatory module in which a set of pigmentation genes evolved to respond to a common transcriptional regulator determining their spatial distribution. The primitive wing spot pattern subsequently diversified through changes in the expression pattern of this regulator. These results suggest that the genetic changes underlying the emergence and diversification of wing pigmentation patterns are partitioned within genetic networks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arnoult, Laurent -- Su, Kathy F Y -- Manoel, Diogo -- Minervino, Caroline -- Magrina, Justine -- Gompel, Nicolas -- Prud'homme, Benjamin -- New York, N.Y. -- Science. 2013 Mar 22;339(6126):1423-6. doi: 10.1126/science.1233749.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Aix-Marseille Universite, CNRS, UMR 7288, Institut de Biologie du Developpement de Marseille-Luminy, 13288 Marseille cedex 9, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23520110" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Biological Evolution ; Drosophila/anatomy & histology/genetics/growth & development ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/anatomy & histology/*genetics/growth & ; development/metabolism ; *Evolution, Molecular ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; *Gene Regulatory Networks ; *Genes, Insect ; Homeodomain Proteins/genetics/*metabolism ; Phylogeny ; Pigmentation/*genetics ; Pigments, Biological/analysis/metabolism ; Pupa ; RNA Interference ; Transcription Factors/genetics/*metabolism ; Wings, Animal/*anatomy & histology/chemistry
    Print ISSN: 0036-8075
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  • 77
    Publication Date: 2013-04-06
    Description: Coral reef recovery from major disturbance is hypothesized to depend on the arrival of propagules from nearby undisturbed reefs. Therefore, reefs isolated by distance or current patterns are thought to be highly vulnerable to catastrophic disturbance. We found that on an isolated reef system in north Western Australia, coral cover increased from 9% to 44% within 12 years of a coral bleaching event, despite a 94% reduction in larval supply for 6 years after the bleaching. The initial increase in coral cover was the result of high rates of growth and survival of remnant colonies, followed by a rapid increase in juvenile recruitment as colonies matured. We show that isolated reefs can recover from major disturbance, and that the benefits of their isolation from chronic anthropogenic pressures can outweigh the costs of limited connectivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gilmour, James P -- Smith, Luke D -- Heyward, Andrew J -- Baird, Andrew H -- Pratchett, Morgan S -- New York, N.Y. -- Science. 2013 Apr 5;340(6128):69-71. doi: 10.1126/science.1232310.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Australian Institute of Marine Science, University of Western Australia Oceans Institute, Perth, WA 6009, Australia. j.gilmour@aims.gov.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23559247" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthozoa/*growth & development ; Conservation of Natural Resources ; *Coral Reefs ; Reproduction ; Temperature ; Western Australia
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 78
    Publication Date: 2013-07-23
    Description: Melanocortin receptor accessory proteins (MRAPs) modulate signaling of melanocortin receptors in vitro. To investigate the physiological role of brain-expressed melanocortin 2 receptor accessory protein 2 (MRAP2), we characterized mice with whole-body and brain-specific targeted deletion of Mrap2, both of which develop severe obesity at a young age. Mrap2 interacts directly with melanocortin 4 receptor (Mc4r), a protein previously implicated in mammalian obesity, and it enhances Mc4r-mediated generation of the second messenger cyclic adenosine monophosphate, suggesting that alterations in Mc4r signaling may be one mechanism underlying the association between Mrap2 disruption and obesity. In a study of humans with severe, early-onset obesity, we found four rare, potentially pathogenic genetic variants in MRAP2, suggesting that the gene may also contribute to body weight regulation in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3788688/" 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/PMC3788688/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Asai, Masato -- Ramachandrappa, Shwetha -- Joachim, Maria -- Shen, Yuan -- Zhang, Rong -- Nuthalapati, Nikhil -- Ramanathan, Visali -- Strochlic, David E -- Ferket, Peter -- Linhart, Kirsten -- Ho, Caroline -- Novoselova, Tatiana V -- Garg, Sumedha -- Ridderstrale, Martin -- Marcus, Claude -- Hirschhorn, Joel N -- Keogh, Julia M -- O'Rahilly, Stephen -- Chan, Li F -- Clark, Adrian J -- Farooqi, I Sadaf -- Majzoub, Joseph A -- 098497/Wellcome Trust/United Kingdom -- G0802796/Medical Research Council/United Kingdom -- G0900554/Medical Research Council/United Kingdom -- G9824984/Medical Research Council/United Kingdom -- P30-HD18655/HD/NICHD NIH HHS/ -- R01 DK075787/DK/NIDDK NIH HHS/ -- R01DK075787/DK/NIDDK NIH HHS/ -- T32 DK007699/DK/NIDDK NIH HHS/ -- T32 MH020017/MH/NIMH NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2013 Jul 19;341(6143):275-8. doi: 10.1126/science.1233000.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Department of Medicine, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23869016" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Animals ; Body Mass Index ; Body Weight/*genetics ; Carrier Proteins/*genetics ; Child ; Child, Preschool ; Energy Metabolism/genetics ; Female ; Gene Deletion ; Humans ; Male ; Mice ; Mice, Knockout ; Obesity/*genetics/metabolism ; Receptor Activity-Modifying Proteins/genetics/*metabolism ; Receptor, Melanocortin, Type 4/genetics/*metabolism ; Young Adult
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  • 79
    Publication Date: 2013-03-02
    Description: Prenatal infection and exposure to traumatizing experiences during peripuberty have each been associated with increased risk for neuropsychiatric disorders. Evidence is lacking for the cumulative impact of such prenatal and postnatal environmental challenges on brain functions and vulnerability to psychiatric disease. Here, we show in a translational mouse model that combined exposure to prenatal immune challenge and peripubertal stress induces synergistic pathological effects on adult behavioral functions and neurochemistry. We further demonstrate that the prenatal insult markedly increases the vulnerability of the pubescent offspring to brain immune changes in response to stress. Our findings reveal interactions between two adverse environmental factors that have individually been associated with neuropsychiatric disease and support theories that mental illnesses with delayed onsets involve multiple environmental hits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giovanoli, Sandra -- Engler, Harald -- Engler, Andrea -- Richetto, Juliet -- Voget, Mareike -- Willi, Roman -- Winter, Christine -- Riva, Marco A -- Mortensen, Preben B -- Feldon, Joram -- Schedlowski, Manfred -- Meyer, Urs -- New York, N.Y. -- Science. 2013 Mar 1;339(6123):1095-9. doi: 10.1126/science.1228261.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Physiology and Behavior Laboratory, Swiss Federal Institute of Technology (ETH) Zurich, 8603 Schwerzenbach, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23449593" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytokines/immunology ; Disease Models, Animal ; Female ; Humans ; Mental Disorders/*immunology ; Mice ; Mice, Inbred C57BL ; Poly I-C/immunology/pharmacology ; Pregnancy ; Prenatal Exposure Delayed Effects/*immunology/virology ; Puberty/*immunology ; Stress, Physiological/*immunology
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  • 80
    Publication Date: 2013-02-23
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4011183/" 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/PMC4011183/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patterson, Amy P -- Tabak, Lawrence A -- Fauci, Anthony S -- Collins, Francis S -- Howard, Sally -- Z99 AI999999/Intramural NIH HHS/ -- Z99 OD999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2013 Mar 1;339(6123):1036-7. doi: 10.1126/science.1236194. Epub 2013 Feb 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institutes of Health, Bethesda, MD 20892, USA. pattersa@od.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23429700" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomedical Research/*education ; Birds ; Guidelines as Topic ; Humans ; Influenza A Virus, H5N1 Subtype/genetics/*pathogenicity ; Influenza in Birds/*transmission ; Influenza, Human/*transmission ; Safety
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  • 81
    Publication Date: 2013-01-19
    Description: Directional guidance of cells via gradients of chemokines is considered crucial for embryonic development, cancer dissemination, and immune responses. Nevertheless, the concept still lacks direct experimental confirmation in vivo. Here, we identify endogenous gradients of the chemokine CCL21 within mouse skin and show that they guide dendritic cells toward lymphatic vessels. Quantitative imaging reveals depots of CCL21 within lymphatic endothelial cells and steeply decaying gradients within the perilymphatic interstitium. These gradients match the migratory patterns of the dendritic cells, which directionally approach vessels from a distance of up to 90-micrometers. Interstitial CCL21 is immobilized to heparan sulfates, and its experimental delocalization or swamping the endogenous gradients abolishes directed migration. These findings functionally establish the concept of haptotaxis, directed migration along immobilized gradients, in tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weber, Michele -- Hauschild, Robert -- Schwarz, Jan -- Moussion, Christine -- de Vries, Ingrid -- Legler, Daniel F -- Luther, Sanjiv A -- Bollenbach, Tobias -- Sixt, Michael -- New York, N.Y. -- Science. 2013 Jan 18;339(6117):328-32. doi: 10.1126/science.1228456.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IST Austria (Institute of Science and Technology Austria), Klosterneuburg, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23329049" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chemokine CCL19/metabolism ; Chemokine CCL21/chemistry/*immunology ; Chemotaxis/*immunology ; Dendritic Cells/*immunology ; Heparitin Sulfate/chemistry ; Immobilized Proteins/chemistry/immunology ; Lymphatic Vessels/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Receptors, CCR7/genetics ; Skin/*immunology
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  • 82
    Publication Date: 2013-10-12
    Description: Lymphocytes face major metabolic challenges upon activation. They must meet the bioenergetic and biosynthetic demands of increased cell proliferation and also adapt to changing environmental conditions, in which nutrients and oxygen may be limiting. An emerging theme in immunology is that metabolic reprogramming and lymphocyte activation are intricately linked. However, why T cells adopt specific metabolic programs and the impact that these programs have on T cell function and, ultimately, immunological outcome remain unclear. Research on tumor cell metabolism has provided valuable insight into metabolic pathways important for cell proliferation and the influence of metabolites themselves on signal transduction and epigenetic programming. In this Review, we highlight emerging concepts regarding metabolic reprogramming in proliferating cells and discuss their potential impact on T cell fate and function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4486656/" 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/PMC4486656/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pearce, Erika L -- Poffenberger, Maya C -- Chang, Chih-Hao -- Jones, Russell G -- AI091965/AI/NIAID NIH HHS/ -- CA158823/CA/NCI NIH HHS/ -- MOP-93799/Canadian Institutes of Health Research/Canada -- R01 AI091965/AI/NIAID NIH HHS/ -- R01 CA181125/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2013 Oct 11;342(6155):1242454. doi: 10.1126/science.1242454.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. erikapearce@path.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24115444" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/metabolism ; Cell Differentiation ; Cell Proliferation ; *Citric Acid Cycle ; Gene Expression Regulation ; *Glycolysis ; Humans ; Ketoglutaric Acids/metabolism ; *Lymphocyte Activation ; Membrane Proteins/metabolism ; Mitochondria/immunology/metabolism ; Neoplasms/immunology/metabolism ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; T-Lymphocytes/*immunology/*metabolism ; Thyroid Hormones/metabolism
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  • 83
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-10-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aspinall, Richard -- Gregory, Peter -- New York, N.Y. -- Science. 2013 Oct 25;342(6157):421. doi: 10.1126/science.342.6157.421-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉James Hutton Institute, Craigiebuckler, Aberdeen, AB15 8QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24159029" target="_blank"〉PubMed〈/a〉
    Keywords: *Agriculture ; Animals ; *Climate Change ; *Conservation of Natural Resources ; *Decision Support Techniques ; *Ecosystem ; *Models, Economic
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  • 84
    Publication Date: 2013-05-21
    Description: Lazic criticizes the statistical analyses used to support the conclusions in our mouse model. His theory-biased criticism is disproportionate in view of the robustness of our findings (even if different statistical methods are applied) and falls short in explaining the postpubertal onset of effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giovanoli, Sandra -- Meyer, Urs -- New York, N.Y. -- Science. 2013 May 17;340(6134):811. doi: 10.1126/science.1238060.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Physiology and Behavior Laboratory, Swiss Federal Institute of Technology (ETH) Zurich, Schwerzenbach, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23687030" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Humans ; Mental Disorders/*immunology ; Pregnancy ; Prenatal Exposure Delayed Effects/*immunology ; Puberty/*immunology ; Stress, Physiological/*immunology
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  • 85
    Publication Date: 2013-09-07
    Description: Gaucher et al. suggest that their field observations and petrographic analysis of one thin section do not support an Ediacaran age for the trace fossils-bearing strata of the Tacuari Formation. We have strengthened our conclusion of an Ediacaran age for the Tacuari Formation based on reassessment of new and previously presented field and petrographic evidence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pecoits, Ernesto -- Konhauser, Kurt O -- Aubet, Natalie R -- Heaman, Larry M -- Veroslavsky, Gerardo -- Stern, Richard -- Gingras, Murray K -- New York, N.Y. -- Science. 2013 Feb 22;339(6122):906. doi: 10.1126/science.1230677.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Earth and Atmospheric Sciences, University of Alberta, Edmonton, Alberta, T6G 2E3, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23430639" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Fossils
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  • 86
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-05-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheetham, Seth W -- Brand, Andrea H -- 092096/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2013 May 17;340(6134):817-8. doi: 10.1126/science.1238525.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Gurdon Institute and Department of Physiology, Development, and Neuroscience, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN,UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23687033" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila Proteins/metabolism ; Drosophila melanogaster/*metabolism ; Insulin/*metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; *Signal Transduction ; Somatomedins/metabolism ; Stem Cells/metabolism
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  • 87
    Publication Date: 2013-01-05
    Description: The El Nino-Southern Oscillation (ENSO) drives large changes in global climate patterns from year to year, yet its sensitivity to continued anthropogenic greenhouse forcing is uncertain. We analyzed fossil coral reconstructions of ENSO spanning the past 7000 years from the Northern Line Islands, located in the center of action for ENSO. The corals document highly variable ENSO activity, with no evidence for a systematic trend in ENSO variance, which is contrary to some models that exhibit a response to insolation forcing over this same period. Twentieth-century ENSO variance is significantly higher than average fossil coral ENSO variance but is not unprecedented. Our results suggest that forced changes in ENSO, whether natural or anthropogenic, may be difficult to detect against a background of large internal variability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cobb, Kim M -- Westphal, Niko -- Sayani, Hussein R -- Watson, Jordan T -- Di Lorenzo, Emanuele -- Cheng, H -- Edwards, R L -- Charles, Christopher D -- New York, N.Y. -- Science. 2013 Jan 4;339(6115):67-70. doi: 10.1126/science.1228246.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Earth and Atmospheric Sciences, Georgia Institute of Technology, Atlanta, GA 30332, USA. kcobb@eas.gatech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23288537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthozoa/*growth & development ; *Climate Change ; *Fossils ; Islands
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  • 88
    Publication Date: 2013-10-26
    Description: The shape of the human face and skull is largely genetically determined. However, the genomic basis of craniofacial morphology is incompletely understood and hypothesized to involve protein-coding genes, as well as gene regulatory sequences. We used a combination of epigenomic profiling, in vivo characterization of candidate enhancer sequences in transgenic mice, and targeted deletion experiments to examine the role of distant-acting enhancers in craniofacial development. We identified complex regulatory landscapes consisting of enhancers that drive spatially complex developmental expression patterns. Analysis of mouse lines in which individual craniofacial enhancers had been deleted revealed significant alterations of craniofacial shape, demonstrating the functional importance of enhancers in defining face and skull morphology. These results demonstrate that enhancers are involved in craniofacial development and suggest that enhancer sequence variation contributes to the diversity of human facial morphology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3991470/" 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/PMC3991470/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Attanasio, Catia -- Nord, Alex S -- Zhu, Yiwen -- Blow, Matthew J -- Li, Zirong -- Liberton, Denise K -- Morrison, Harris -- Plajzer-Frick, Ingrid -- Holt, Amy -- Hosseini, Roya -- Phouanenavong, Sengthavy -- Akiyama, Jennifer A -- Shoukry, Malak -- Afzal, Veena -- Rubin, Edward M -- FitzPatrick, David R -- Ren, Bing -- Hallgrimsson, Benedikt -- Pennacchio, Len A -- Visel, Axel -- 1R01DE01963/DE/NIDCR NIH HHS/ -- 1R01DE021708/DE/NIDCR NIH HHS/ -- 1U01DE020054/DE/NIDCR NIH HHS/ -- F32 GM105202/GM/NIGMS NIH HHS/ -- MC_PC_U127561093/Medical Research Council/United Kingdom -- MC_U127561093/Medical Research Council/United Kingdom -- R01 DE019638/DE/NIDCR NIH HHS/ -- R01 DE021708/DE/NIDCR NIH HHS/ -- R01 HG003988/HG/NHGRI NIH HHS/ -- R01 HG003991/HG/NHGRI NIH HHS/ -- R01HG003988/HG/NHGRI NIH HHS/ -- R01HG003991/HG/NHGRI NIH HHS/ -- U01 DE020054/DE/NIDCR NIH HHS/ -- U01 DE020060/DE/NIDCR NIH HHS/ -- U01DE020060/DE/NIDCR NIH HHS/ -- U54 HG006997/HG/NHGRI NIH HHS/ -- U54HG006997/HG/NHGRI NIH HHS/ -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2013 Oct 25;342(6157):1241006. doi: 10.1126/science.1241006.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24159046" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Craniofacial Abnormalities/genetics/pathology ; Enhancer Elements, Genetic/genetics/*physiology ; Epigenesis, Genetic ; Face/abnormalities/*anatomy & histology ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Gene Targeting ; Maxillofacial Development/*genetics ; Mice ; Mice, Transgenic ; Sequence Deletion ; Skull/abnormalities/anatomy & histology/*growth & development
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  • 89
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-07-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weimerskirch, Henri -- New York, N.Y. -- Science. 2013 Jul 5;341(6141):35-6. doi: 10.1126/science.1240316.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre d'Etudes Biologiques de Chize, CNRS, 79360 Villiers-en-Bois, France. henriw@cebc.cnrs.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23828928" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds/*physiology ; *Feeding Behavior ; *Homing Behavior ; *Territoriality
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  • 90
    Publication Date: 2013-11-16
    Description: Rapid and reductive cell divisions during embryogenesis require that intracellular structures adapt to a wide range of cell sizes. The mitotic spindle presents a central example of this flexibility, scaling with the dimensions of the cell to mediate accurate chromosome segregation. To determine whether spindle size regulation is achieved through a developmental program or is intrinsically specified by cell size or shape, we developed a system to encapsulate cytoplasm from Xenopus eggs and embryos inside cell-like compartments of defined sizes. Spindle size was observed to shrink with decreasing compartment size, similar to what occurs during early embryogenesis, and this scaling trend depended on compartment volume rather than shape. Thus, the amount of cytoplasmic material provides a mechanism for regulating the size of intracellular structures.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4094345/" 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/PMC4094345/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Good, Matthew C -- Vahey, Michael D -- Skandarajah, Arunan -- Fletcher, Daniel A -- Heald, Rebecca -- GM074751/GM/NIGMS NIH HHS/ -- GM098766/GM/NIGMS NIH HHS/ -- R01 GM074751/GM/NIGMS NIH HHS/ -- R01 GM098766/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Nov 15;342(6160):856-60. doi: 10.1126/science.1243147.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, University of California-Berkeley, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24233724" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Size ; Cytoplasm/chemistry/*physiology/ultrastructure ; *Embryonic Development ; Ovum ; Spindle Apparatus/chemistry/*physiology/ultrastructure ; Xenopus laevis
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  • 91
    Publication Date: 2013-04-06
    Description: Formins are potent activators of actin filament assembly in the cytoplasm. In turn, cytoplasmic actin polymerization can promote release of actin from megakaryocytic acute leukemia (MAL) protein for serum response factor (SRF) transcriptional activity. We found that formins polymerized actin inside the mammalian nucleus to drive serum-dependent MAL-SRF activity. Serum stimulated rapid assembly of actin filaments within the nucleus in a formin-dependent manner. The endogenous formin mDia was regulated with an optogenetic tool, which allowed for photoreactive release of nuclear formin autoinhibition. Activated mDia promoted rapid and reversible nuclear actin network assembly, subsequent MAL nuclear accumulation, and SRF activity. Thus, a dynamic polymeric actin structure within the nucleus is part of the serum response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baarlink, Christian -- Wang, Haicui -- Grosse, Robert -- New York, N.Y. -- Science. 2013 May 17;340(6134):864-7. doi: 10.1126/science.1235038. Epub 2013 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Pharmacology, Biochemical-Pharmacological Center, University of Marburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23558171" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*metabolism ; Animals ; Carrier Proteins/*metabolism ; Cell Nucleus/*metabolism ; HeLa Cells ; Humans ; Intracellular Signaling Peptides and Proteins/*metabolism ; *Metabolic Networks and Pathways ; Mice ; Microtubule-Associated Proteins/*metabolism ; NADPH Dehydrogenase/*metabolism ; NIH 3T3 Cells ; Nuclear Localization Signals/metabolism ; Polymerization ; Serum/metabolism ; Serum Response Factor/*agonists
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 92
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-09-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Good, Michael F -- New York, N.Y. -- Science. 2013 Sep 20;341(6152):1352-3. doi: 10.1126/science.1244157.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Glycomics, Griffith University, Gold Coast 4222, Australia. michael.good@griffith.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24052298" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Humans ; Malaria Vaccines/*administration & dosage/*immunology ; Malaria, Falciparum/*prevention & control ; Male ; Plasmodium falciparum/*immunology
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  • 93
    Publication Date: 2013-09-21
    Description: Circadian clocks are self-sustained cellular oscillators that synchronize oxidative and reductive cycles in anticipation of the solar cycle. We found that the clock transcription feedback loop produces cycles of nicotinamide adenine dinucleotide (NAD(+)) biosynthesis, adenosine triphosphate production, and mitochondrial respiration through modulation of mitochondrial protein acetylation to synchronize oxidative metabolic pathways with the 24-hour fasting and feeding cycle. Circadian control of the activity of the NAD(+)-dependent deacetylase sirtuin 3 (SIRT3) generated rhythms in the acetylation and activity of oxidative enzymes and respiration in isolated mitochondria, and NAD(+) supplementation restored protein deacetylation and enhanced oxygen consumption in circadian mutant mice. Thus, circadian control of NAD(+) bioavailability modulates mitochondrial oxidative function and organismal metabolism across the daily cycles of fasting and feeding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3963134/" 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/PMC3963134/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peek, Clara Bien -- Affinati, Alison H -- Ramsey, Kathryn Moynihan -- Kuo, Hsin-Yu -- Yu, Wei -- Sena, Laura A -- Ilkayeva, Olga -- Marcheva, Biliana -- Kobayashi, Yumiko -- Omura, Chiaki -- Levine, Daniel C -- Bacsik, David J -- Gius, David -- Newgard, Christopher B -- Goetzman, Eric -- Chandel, Navdeep S -- Denu, John M -- Mrksich, Milan -- Bass, Joseph -- 5P01HL071643-10/HL/NHLBI NIH HHS/ -- 5P30AR057216-05/AR/NIAMS NIH HHS/ -- F30 DK085936/DK/NIDDK NIH HHS/ -- F30 ES019815/ES/NIEHS NIH HHS/ -- F32 DK092034/DK/NIDDK NIH HHS/ -- P01 AG011412/AG/NIA NIH HHS/ -- P01AG011412-16/AG/NIA NIH HHS/ -- P01DK58398/DK/NIDDK NIH HHS/ -- P30 CA014520/CA/NCI NIH HHS/ -- R01 AG038679/AG/NIA NIH HHS/ -- R01 CA152601-01/CA/NCI NIH HHS/ -- R01 CA152799-01A1/CA/NCI NIH HHS/ -- R01 CA16383801A1/CA/NCI NIH HHS/ -- R01 CA168292/CA/NCI NIH HHS/ -- R01 CA168292-01A1/CA/NCI NIH HHS/ -- R01 DK090242/DK/NIDDK NIH HHS/ -- R01 DK090625/DK/NIDDK NIH HHS/ -- R01 GM065386/GM/NIGMS NIH HHS/ -- R01 HL097817/HL/NHLBI NIH HHS/ -- R01DK090242-03/DK/NIDDK NIH HHS/ -- R01DK090625-01A1/DK/NIDDK NIH HHS/ -- R01HL097817-01/HL/NHLBI NIH HHS/ -- R37 GM059785/GM/NIGMS NIH HHS/ -- T32 DK007169/DK/NIDDK NIH HHS/ -- T32 GM008152/GM/NIGMS NIH HHS/ -- T32 HL007909/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Nov 1;342(6158):1243417. doi: 10.1126/science.1243417. Epub 2013 Sep 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24051248" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/genetics/metabolism ; Acetylation ; Animals ; Circadian Clocks/genetics/*physiology ; *Energy Metabolism ; Fasting ; Lipid Metabolism ; Liver/metabolism ; Mice ; Mice, Knockout ; Mitochondria, Liver/*metabolism ; NAD/*metabolism ; Oxidation-Reduction ; Oxygen Consumption ; Sirtuin 3/genetics/metabolism
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  • 94
    Publication Date: 2013-02-09
    Description: Although many metazoan enzymes that add or remove specific modifications on histone proteins are essential transcriptional regulators, the functional significance of posttranslational modifications on histone proteins is not well understood. Here, we show in Drosophila that a point mutation in lysine 27 of histone H3 (H3-K27) fails to repress transcription of genes that are normally repressed by Polycomb repressive complex 2 (PRC2), the methyltransferase that modifies H3-K27. Moreover, differentiated H3-K27 mutant cells show homeotic transformations like those seen in PRC2 mutant cells. Taken together, these analyses demonstrate that H3-K27 is the crucial physiological substrate that PRC2 modifies for Polycomb repression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pengelly, Ana Raquel -- Copur, Omer -- Jackle, Herbert -- Herzig, Alf -- Muller, Jurg -- New York, N.Y. -- Science. 2013 Feb 8;339(6120):698-9. doi: 10.1126/science.1231382.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chromatin and Chromosome Biology Research Group, Max Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23393264" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Drosophila Proteins/chemistry/*genetics/*metabolism ; Drosophila melanogaster/*genetics/growth & development/metabolism ; *Gene Expression Regulation ; Genes, Homeobox ; Genes, Insect ; Histones/chemistry/*genetics/*metabolism ; Lysine ; Mutant Proteins/chemistry/metabolism ; Nucleosomes/metabolism ; Phenotype ; Point Mutation ; Polycomb Repressive Complex 2/*metabolism ; Protein Processing, Post-Translational ; Transcription, Genetic ; Transgenes
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  • 95
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-05-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiss, Robin A -- Stoye, Jonathan P -- MC_U117512710/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2013 May 17;340(6134):820-1. doi: 10.1126/science.1235148.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Infection and Immunity, University College London, Gower Street, London WC1E 6BT, UK. rweiss@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23687035" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Viral/genetics ; Endogenous Retroviruses/*genetics ; Female ; Genome, Human/*genetics ; Humans ; Placenta/virology ; Pregnancy ; Promoter Regions, Genetic ; Proviruses/*genetics ; Transcription, Genetic
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  • 96
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-04-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sherkow, Jacob S -- Greely, Henry T -- New York, N.Y. -- Science. 2013 Apr 5;340(6128):32-3. doi: 10.1126/science.1236965.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Law and the Biosciences, Stanford Law School, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23559235" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breeding/*methods ; Cloning, Organism/*methods ; *Endangered Species ; *Extinction, Biological ; Genetic Engineering ; Genomics ; Marsupialia/*genetics ; Selection, Genetic ; Tasmania
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  • 97
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2013 Dec 13;342(6164):1304. doi: 10.1126/science.342.6164.1304.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24337270" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Characidae/*growth & development ; *Evolution, Molecular ; Eye/*anatomy & histology ; HSP90 Heat-Shock Proteins/*genetics
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  • 98
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-10-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bae, Byoung-il -- Walsh, Christopher A -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Oct 11;342(6155):200-1. doi: 10.1126/science.1245812.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics and Genomics, Manton Center for Orphan Disease, and Howard Hughes Medical Institute, Children's Hospital Boston, Department of Neurology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24115427" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*growth & development/*pathology ; Humans ; Microcephaly/*pathology ; *Models, Biological ; Organoids/*cytology/*growth & development ; Tissue Culture Techniques/*methods
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  • 99
    Publication Date: 2013-09-07
    Description: An avian-origin human-infecting influenza (H7N9) virus was recently identified in China. We have evaluated the viral hemagglutinin (HA) receptor-binding properties of two human H7N9 isolates, A/Shanghai/1/2013 (SH-H7N9) (containing the avian-signature residue Gln(226)) and A/Anhui/1/2013 (AH-H7N9) (containing the mammalian-signature residue Leu(226)). We found that SH-H7N9 HA preferentially binds the avian receptor analog, whereas AH-H7N9 HA binds both avian and human receptor analogs. Furthermore, an AH-H7N9 mutant HA (Leu(226) --〉 Gln) was found to exhibit dual receptor-binding property, indicating that other amino acid substitutions contribute to the receptor-binding switch. The structures of SH-H7N9 HA, AH-H7N9 HA, and its mutant in complex with either avian or human receptor analogs show how AH-H7N9 can bind human receptors while still retaining the avian receptor-binding property.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shi, Yi -- Zhang, Wei -- Wang, Fei -- Qi, Jianxun -- Wu, Ying -- Song, Hao -- Gao, Feng -- Bi, Yuhai -- Zhang, Yanfang -- Fan, Zheng -- Qin, Chengfeng -- Sun, Honglei -- Liu, Jinhua -- Haywood, Joel -- Liu, Wenjun -- Gong, Weimin -- Wang, Dayan -- Shu, Yuelong -- Wang, Yu -- Yan, Jinghua -- Gao, George F -- New York, N.Y. -- Science. 2013 Oct 11;342(6155):243-7. doi: 10.1126/science.1242917. Epub 2013 Sep 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Network of Immunity and Health, Beijing Institutes of Life Science, Chinese Academy of Sciences, Beijing, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24009358" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds ; Crystallography, X-Ray ; Glycine/chemistry/genetics/metabolism ; Hemagglutinin Glycoproteins, Influenza Virus/*chemistry/metabolism ; Humans ; Influenza A virus/*metabolism ; Influenza in Birds/*virology ; Influenza, Human/*virology ; Protein Conformation ; Receptors, Cell Surface/*chemistry/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2013 Nov 29;342(6162):1028. doi: 10.1126/science.342.6162.1028.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24288308" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*metabolism/*pathology ; Female ; Humans ; Hydroxycholesterols/*metabolism ; Hypercholesterolemia/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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