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  • 1
    Publication Date: 2016-06-19
    Description: The causes of Late Pleistocene megafaunal extinctions (60,000 to 11,650 years ago, hereafter 60 to 11.65 ka) remain contentious, with major phases coinciding with both human arrival and climate change around the world. The Americas provide a unique opportunity to disentangle these factors as human colonization took place over a narrow time frame (~15 to 14.6 ka) but during contrasting temperature trends across each continent. Unfortunately, limited data sets in South America have so far precluded detailed comparison. We analyze genetic and radiocarbon data from 89 and 71 Patagonian megafaunal bones, respectively, more than doubling the high-quality Pleistocene megafaunal radiocarbon data sets from the region. We identify a narrow megafaunal extinction phase 12,280 ± 110 years ago, some 1 to 3 thousand years after initial human presence in the area. Although humans arrived immediately prior to a cold phase, the Antarctic Cold Reversal stadial, megafaunal extinctions did not occur until the stadial finished and the subsequent warming phase commenced some 1 to 3 thousand years later. The increased resolution provided by the Patagonian material reveals that the sequence of climate and extinction events in North and South America were temporally inverted, but in both cases, megafaunal extinctions did not occur until human presence and climate warming coincided. Overall, metapopulation processes involving subpopulation connectivity on a continental scale appear to have been critical for megafaunal species survival of both climate change and human impacts.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-11-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bradshaw, R A -- Adler, A J -- Chytil, F -- Goldberg, N D -- Litman, B J -- New York, N.Y. -- Science. 1990 Nov 2;250(4981):611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173136" target="_blank"〉PubMed〈/a〉
    Keywords: History, 20th Century ; *Scientific Misconduct ; United States ; *United States Office of Research Integrity
    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: 2013-09-28
    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
    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: 2013-07-23
    Description: The melanocortin-4 receptor (MC4R) is essential for control of energy homeostasis in vertebrates. MC4R interacts with melanocortin receptor accessory protein 2 (MRAP2) in vitro, but its functions in vivo are unknown. We found that MRAP2a, a larval form, stimulates growth of zebrafish by specifically blocking the action of MC4R. In cell culture, this protein binds MC4R and reduces the ability of the receptor to bind its ligand, alpha-melanocyte-stimulating hormone (alpha-MSH). A paralog, MRAP2b, expressed later in development, also binds MC4R but increases ligand sensitivity. Thus, MRAP2 proteins allow for developmental control of MC4R activity, with MRAP2a blocking its function and stimulating growth during larval development, whereas MRAP2b enhances responsiveness to alpha-MSH once the zebrafish begins feeding, thus increasing the capacity for regulated feeding and growth.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4255277/" 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/PMC4255277/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sebag, Julien A -- Zhang, Chao -- Hinkle, Patricia M -- Bradshaw, Amanda M -- Cone, Roger D -- DK020593/DK/NIDDK NIH HHS/ -- DK070332/DK/NIDDK NIH HHS/ -- DK075721/DK/NIDDK NIH HHS/ -- DK19974/DK/NIDDK NIH HHS/ -- F23DK091055/DK/NIDDK NIH HHS/ -- R01 DK070332/DK/NIDDK NIH HHS/ -- R01 DK075721/DK/NIDDK NIH HHS/ -- T32 DK007563/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2013 Jul 19;341(6143):278-81. doi: 10.1126/science.1232995.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23869017" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Embryo, Nonmammalian/metabolism ; Energy Metabolism ; HEK293 Cells ; Humans ; Receptor Activity-Modifying Proteins/genetics/*metabolism ; Receptor, Melanocortin, Type 4/*metabolism ; Zebrafish/*embryology/metabolism ; Zebrafish Proteins/genetics/*metabolism ; alpha-MSH/metabolism/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2013-08-03
    Description: The rapid, reductive early divisions of many metazoan embryos are followed by the midblastula transition (MBT), during which the cell cycle elongates and zygotic transcription begins. It has been proposed that the increasing nuclear to cytoplasmic (N/C) ratio is critical for controlling the events of the MBT. We show that four DNA replication factors--Cut5, RecQ4, Treslin, and Drf1--are limiting for replication initiation at increasing N/C ratios in vitro and in vivo in Xenopus laevis. The levels of these factors regulate multiple events of the MBT, including the slowing of the cell cycle, the onset of zygotic transcription, and the developmental activation of the kinase Chk1. This work provides a mechanism for how the N/C ratio controls the MBT and shows that the regulation of replication initiation is fundamental for normal embryogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898016/" 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/PMC3898016/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Collart, Clara -- Allen, George E -- Bradshaw, Charles R -- Smith, James C -- Zegerman, Philip -- 092096/Wellcome Trust/United Kingdom -- 10-0908/Worldwide Cancer Research/United Kingdom -- C6946/A14492/Cancer Research UK/United Kingdom -- U117597140/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2013 Aug 23;341(6148):893-6. doi: 10.1126/science.1241530. Epub 2013 Aug 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust/Cancer Research UK Gurdon Institute, The Henry Wellcome Building of Cancer and Developmental Biology, University of Cambridge, Cambridge CB2 1QN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23907533" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastula/*embryology/metabolism ; Carrier Proteins/*metabolism ; Cell Cycle Proteins/*metabolism ; Chromosomal Proteins, Non-Histone/*metabolism ; *DNA Replication ; RecQ Helicases/*metabolism ; Xenopus Proteins/*metabolism ; Xenopus laevis/*embryology/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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  • 6
    Publication Date: 2004-10-16
    Description: Adsorption and desorption of hydrogen from nanoporous materials, such as activated carbon, is usually fully reversible. We have prepared nanoporous metal-organic framework materials with flexible linkers in which the pore openings, as characterized in the static structures, appear to be too small to allow H2 to pass. We observe hysteresis in their adsorption and desorption kinetics above the supercritical temperature of H2 that reflects the dynamical opening of the "windows" between pores. This behavior would allow H2 to be adsorbed at high pressures but stored at lower pressures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Xuebo -- Xiao, Bo -- Fletcher, Ashleigh J -- Thomas, K Mark -- Bradshaw, Darren -- Rosseinsky, Matthew J -- New York, N.Y. -- Science. 2004 Nov 5;306(5698):1012-5. Epub 2004 Oct 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Northern Carbon Research Laboratories, School of Natural Sciences, Bedson Building, University of Newcastle upon Tyne, Newcastle upon Tyne, NE1 7RU, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15486255" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1996-06-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bradshaw, R A -- New York, N.Y. -- Science. 1996 Jun 21;272(5269):1723.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650556" target="_blank"〉PubMed〈/a〉
    Keywords: Commerce/*economics ; Financing, Government ; National Institutes of Health (U.S.)/*economics ; *Research Support as Topic ; Societies, Scientific ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-09-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bradshaw, J L -- New York, N.Y. -- Science. 1993 Sep 24;261(5129):1755-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17794882" target="_blank"〉PubMed〈/a〉
    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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  • 9
    Publication Date: 1993-11-05
    Description: Stimulation of T cell proliferation generally requires two signals: The first signal is provided by the T cell receptor binding to antigen, and the second signal or costimulus is provided by a different receptor-ligand interaction. In mouse and human, the CD28-B7 interaction has been identified as a source of costimulatory signals. We have identified a cell surface molecule (GL1) that is distinct from B7 and abundantly expressed on activated B cells. On activated B cells GL1, rather than B7, is the predominant ligand for the T cell-activation molecule CTLA-4. GL1 provides a critical signal for T cell-dependent responses in vitro and in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hathcock, K S -- Laszlo, G -- Dickler, H B -- Bradshaw, J -- Linsley, P -- Hodes, R J -- New York, N.Y. -- Science. 1993 Nov 5;262(5135):905-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7694361" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antibodies, Monoclonal ; Antigens, CD/metabolism ; Antigens, CD18 ; Antigens, CD80/immunology/*metabolism ; Antigens, Differentiation/*metabolism ; Antigens, Surface/immunology/*metabolism ; B-Lymphocytes/*immunology ; CHO Cells ; CTLA-4 Antigen ; Cricetinae ; *Immunoconjugates ; Interleukin-2/biosynthesis ; *Lymphocyte Activation ; Mice ; T-Lymphocytes/*immunology
    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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  • 10
    Publication Date: 2006-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bradshaw, William E -- Holzapfel, Christina M -- New York, N.Y. -- Science. 2006 Jun 9;312(5779):1477-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Ecology and Evolutionary Biology, University of Oregon, Eugene, OR 97403, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16763134" target="_blank"〉PubMed〈/a〉
    Keywords: *Acclimatization/genetics ; Animals ; *Biological Evolution ; Climate
    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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