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  • Mice  (847)
  • Population Dynamics  (252)
  • 2005-2009  (1,099)
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  • 1
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    p53 controls radiation-induced gastrointestinal syndrome in mice independent of apoptosis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-19
    Description: Acute exposure to ionizing radiation can cause lethal damage to the gastrointestinal (GI) tract, a condition called the GI syndrome. Whether the target cells affected by radiation to cause the GI syndrome are derived from the epithelium or endothelium and whether the target cells die by apoptosis or other mechanisms are controversial issues. Studying mouse models, we found that selective deletion of the proapoptotic genes Bak1 and Bax from the GI epithelium or from endothelial cells did not protect mice from developing the GI syndrome after sub-total-body gamma irradiation. In contrast, selective deletion of p53 from the GI epithelium, but not from endothelial cells, sensitized irradiated mice to the GI syndrome. Transgenic mice overexpressing p53 in all tissues were protected from the GI syndrome after irradiation. These results suggest that the GI syndrome is caused by the death of GI epithelial cells and that these epithelial cells die by a mechanism that is regulated by p53 but independent of apoptosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2897160/" 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/PMC2897160/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kirsch, David G -- Santiago, Philip M -- di Tomaso, Emmanuelle -- Sullivan, Julie M -- Hou, Wu-Shiun -- Dayton, Talya -- Jeffords, Laura B -- Sodha, Pooja -- Mercer, Kim L -- Cohen, Rhianna -- Takeuchi, Osamu -- Korsmeyer, Stanley J -- Bronson, Roderick T -- Kim, Carla F -- Haigis, Kevin M -- Jain, Rakesh K -- Jacks, Tyler -- K08 CA 114176/CA/NCI NIH HHS/ -- K08 CA114176/CA/NCI NIH HHS/ -- K08 CA114176-05/CA/NCI NIH HHS/ -- P01 CA080124/CA/NCI NIH HHS/ -- P01 CA080124-01A1/CA/NCI NIH HHS/ -- P01 CA80124/CA/NCI NIH HHS/ -- P30 CA014051/CA/NCI NIH HHS/ -- P30 CA014051-38/CA/NCI NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- RC1 AI078521/AI/NIAID NIH HHS/ -- RC1 AI078521-01/AI/NIAID NIH HHS/ -- RC1-AI078521/AI/NIAID NIH HHS/ -- U19-AI06775/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jan 29;327(5965):593-6. doi: 10.1126/science.1166202. Epub 2009 Dec 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉David H. Koch Institute for Integrative Cancer Research, 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/20019247" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cell Death ; Epithelial Cells/cytology/physiology/radiation effects ; Gamma Rays/*adverse effects ; Gene Deletion ; Genes, p53 ; Intestinal Diseases/etiology/pathology/*physiopathology ; Intestinal Mucosa/pathology/physiopathology/*radiation effects ; Intestine, Small/pathology/physiopathology/*radiation effects ; Mesoderm/cytology ; Mice ; Mice, Transgenic ; Models, Biological ; Radiation Dosage ; Radiation Injuries/etiology/pathology/*physiopathology ; Tumor Suppressor Protein p53/*physiology ; bcl-2 Homologous Antagonist-Killer Protein/genetics/metabolism ; bcl-2-Associated X Protein/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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  • 2
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    Medicine. A reinnervating microRNA (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Robert H -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1494-5. doi: 10.1126/science.1183842.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurology, Biochemistry and Molecular Pharmacology and Program in Neuroscience, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA. robert.brown@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007892" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/pathology/*physiopathology ; Animals ; Binding Sites ; Carrier Proteins/metabolism ; Disease Models, Animal ; Histone Deacetylases/metabolism ; Mice ; Mice, Transgenic ; MicroRNAs/genetics/*metabolism ; Muscle Cells/enzymology ; Muscle Denervation ; Muscle, Skeletal/innervation/metabolism ; Myostatin/genetics ; Neuromuscular Junction/*pathology/*physiology ; RNA Interference ; Sequence Analysis, RNA ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Norbin is an endogenous regulator of metabotropic glutamate receptor 5 signaling (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: Metabotropic glutamate receptor 5 (mGluR5) is highly expressed in the mammalian central nervous system (CNS). It is involved in multiple physiological functions and is a target for treatment of various CNS disorders, including schizophrenia. We report that Norbin, a neuron-specific protein, physically interacts with mGluR5 in vivo, increases the cell surface localization of the receptor, and positively regulates mGluR5 signaling. Genetic deletion of Norbin attenuates mGluR5-dependent stable changes in synaptic function measured as long-term depression or long-term potentiation of synaptic transmission in the hippocampus. As with mGluR5 knockout mice or mice treated with mGluR5-selective antagonists, Norbin knockout mice showed a behavioral phenotype associated with a rodent model of schizophrenia, as indexed by alterations both in sensorimotor gating and psychotomimetic-induced locomotor activity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796550/" 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/PMC2796550/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Hong -- Westin, Linda -- Nong, Yi -- Birnbaum, Shari -- Bendor, Jacob -- Brismar, Hjalmar -- Nestler, Eric -- Aperia, Anita -- Flajolet, Marc -- Greengard, Paul -- DA 10044/DA/NIDA NIH HHS/ -- MH074866/MH/NIMH NIH HHS/ -- MH66172/MH/NIMH NIH HHS/ -- P01 DA010044/DA/NIDA NIH HHS/ -- P01 DA010044-020002/DA/NIDA NIH HHS/ -- P01 DA010044-030002/DA/NIDA NIH HHS/ -- P01 DA010044-04/DA/NIDA NIH HHS/ -- P01 DA010044-040002/DA/NIDA NIH HHS/ -- P01 DA010044-05/DA/NIDA NIH HHS/ -- P01 DA010044-050002/DA/NIDA NIH HHS/ -- P01 DA010044-06/DA/NIDA NIH HHS/ -- P01 DA010044-060002/DA/NIDA NIH HHS/ -- P01 DA010044-07/DA/NIDA NIH HHS/ -- P01 DA010044-070002/DA/NIDA NIH HHS/ -- P01 DA010044-08/DA/NIDA NIH HHS/ -- P01 DA010044-080002/DA/NIDA NIH HHS/ -- P01 DA010044-09/DA/NIDA NIH HHS/ -- P01 DA010044-090002/DA/NIDA NIH HHS/ -- P01 DA010044-10/DA/NIDA NIH HHS/ -- P01 DA010044-100002/DA/NIDA NIH HHS/ -- P01 DA010044-11/DA/NIDA NIH HHS/ -- P01 DA010044-110005/DA/NIDA NIH HHS/ -- P01 DA010044-12/DA/NIDA NIH HHS/ -- P01 DA010044-120005/DA/NIDA NIH HHS/ -- P01 DA010044-129002/DA/NIDA NIH HHS/ -- P01 DA010044-13/DA/NIDA NIH HHS/ -- P01 DA010044-130005/DA/NIDA NIH HHS/ -- P01 DA010044-139002/DA/NIDA NIH HHS/ -- P01 DA010044-14/DA/NIDA NIH HHS/ -- P01 DA010044-140005/DA/NIDA NIH HHS/ -- P01 DA010044-149002/DA/NIDA NIH HHS/ -- P01 DA010044-14S1/DA/NIDA NIH HHS/ -- P01 DA010044-14S10005/DA/NIDA NIH HHS/ -- P01 DA010044-14S19002/DA/NIDA NIH HHS/ -- P50 MH074866/MH/NIMH NIH HHS/ -- P50 MH074866-010001/MH/NIMH NIH HHS/ -- P50 MH074866-020001/MH/NIMH NIH HHS/ -- P50 MH074866-030001/MH/NIMH NIH HHS/ -- P50 MH074866-039001/MH/NIMH NIH HHS/ -- P50 MH074866-040001/MH/NIMH NIH HHS/ -- P50 MH074866-050001/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1554-7. doi: 10.1126/science.1178496.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007903" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Calcium/metabolism ; Calcium Signaling ; Cell Line ; Cell Membrane/metabolism ; Humans ; Mice ; Mice, Knockout ; Motor Activity ; Nerve Tissue Proteins/genetics/*metabolism ; Neuronal Plasticity ; Protein Binding ; Rats ; Receptor, Metabotropic Glutamate 5 ; Receptors, Metabotropic Glutamate/genetics/*metabolism ; Reflex, Startle ; Schizophrenia/physiopathology ; *Signal Transduction ; Synaptic Transmission ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    MicroRNA-206 delays ALS progression and promotes regeneration of neuromuscular synapses in mice (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by loss of motor neurons, denervation of target muscles, muscle atrophy, and paralysis. Understanding ALS pathogenesis may require a fuller understanding of the bidirectional signaling between motor neurons and skeletal muscle fibers at neuromuscular synapses. Here, we show that a key regulator of this signaling is miR-206, a skeletal muscle-specific microRNA that is dramatically induced in a mouse model of ALS. Mice that are genetically deficient in miR-206 form normal neuromuscular synapses during development, but deficiency of miR-206 in the ALS mouse model accelerates disease progression. miR-206 is required for efficient regeneration of neuromuscular synapses after acute nerve injury, which probably accounts for its salutary effects in ALS. miR-206 mediates these effects at least in part through histone deacetylase 4 and fibroblast growth factor signaling pathways. Thus, miR-206 slows ALS progression by sensing motor neuron injury and promoting the compensatory regeneration of neuromuscular synapses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796560/" 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/PMC2796560/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, Andrew H -- Valdez, Gregorio -- Moresi, Viviana -- Qi, Xiaoxia -- McAnally, John -- Elliott, Jeffrey L -- Bassel-Duby, Rhonda -- Sanes, Joshua R -- Olson, Eric N -- 1F32NS061464-01A1/NS/NINDS NIH HHS/ -- R01 HL093039/HL/NHLBI NIH HHS/ -- R01 HL093039-01A1/HL/NHLBI NIH HHS/ -- T32HL007360/HL/NHLBI NIH HHS/ -- U24 CA126608/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1549-54. doi: 10.1126/science.1181046.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007902" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/pathology/*physiopathology ; Animals ; Axons/physiology ; Carrier Proteins/genetics/metabolism ; Disease Models, Animal ; Disease Progression ; Fibroblast Growth Factors/metabolism ; Histone Deacetylases/genetics/metabolism ; Mice ; Mice, Transgenic ; MicroRNAs/genetics/*metabolism ; Motor Neurons/pathology/*physiology ; Muscle Denervation ; Muscle, Skeletal/innervation/*metabolism/pathology ; MyoD Protein/genetics/metabolism ; Myogenin/genetics/metabolism ; Nerve Regeneration ; Neuromuscular Junction/growth & development/*pathology/*physiology ; RNA Interference ; Signal Transduction ; Transcriptional Activation ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Genetics. SNP study supports southern migration route to Asia (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Normile, Dennis -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1470. doi: 10.1126/science.326.5959.1470.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007876" target="_blank"〉PubMed〈/a〉
    Keywords: Asia ; Asian Continental Ancestry Group/*genetics/history ; *Emigration and Immigration/history ; Ethnic Groups/*genetics/history ; Haplotypes ; History, Ancient ; Humans ; *Polymorphism, Single Nucleotide ; Population Dynamics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Where are the parasites? (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kutz, Susan J -- Dobson, Andy P -- Hoberg, Eric P -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1187-8. doi: 10.1126/science.326.5957.1187-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965449" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arctic Regions/epidemiology ; *Climate Change ; *Ecosystem ; Host-Parasite Interactions ; Parasites/growth & development/*physiology ; Parasitic Diseases, Animal/epidemiology/parasitology/transmission ; Population Dynamics
    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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    A spindle assembly checkpoint protein functions in prophase I arrest and prometaphase progression (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: Two critical stages of mammalian oocyte regulation are prophase I arrest, which is important for sustaining the oocyte pool, and the progression through meiosis I (MI) to produce fertilizable eggs. We have found that the spindle assembly checkpoint protein BubR1 regulates both stages in mouse oocytes. We show that oocytes depleted of BubR1 cannot sustain prophase I arrest and readily undergo germinal vesicle breakdown, a marker for reentry into MI. BubR1-depleted oocytes then arrest before completing MI, marked by failure of polar body extrusion. Both meiotic defects in BubR1-depleted oocytes are due to reduced activity of the master regulator known as the anaphase-promoting complex (APC), brought about through diminished levels of the APC coactivator Cdh1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3428834/" 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/PMC3428834/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Homer, Hayden -- Gui, Liming -- Carroll, John -- 082587/Wellcome Trust/United Kingdom -- 082587/Z/07/Z/Wellcome Trust/United Kingdom -- G0400530/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):991-4. doi: 10.1126/science.1175326.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Oocyte and Embryo Research Laboratory, Department of Cell and Developmental Biology, Division of Biosciences and Institute for Women's Health, University College London, London, UK. h.homer@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965510" target="_blank"〉PubMed〈/a〉
    Keywords: Anaphase-Promoting Complex-Cyclosome ; Animals ; Carrier Proteins/metabolism ; Cdc20 Proteins ; Cdh1 Proteins ; Cell Cycle Proteins/metabolism ; Cyclin B1/metabolism ; Female ; Gene Silencing ; Meiosis/*physiology ; Meiotic Prophase I/*physiology ; Mice ; Oocytes/*physiology ; Prometaphase/*physiology/*radiation effects ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Securin ; Ubiquitin-Protein Ligase Complexes/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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  • 8
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    Epidemic dynamics at the human-animal interface (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: Few infectious diseases are entirely human-specific: Most human pathogens also circulate in animals or else originated in nonhuman hosts. Influenza, plague, and trypanosomiasis are classic examples of zoonotic infections that transmit from animals to humans. The multihost ecology of zoonoses leads to complex dynamics, and analytical tools, such as mathematical modeling, are vital to the development of effective control policies and research agendas. Much attention has focused on modeling pathogens with simpler life cycles and immediate global urgency, such as influenza and severe acute respiratory syndrome. Meanwhile, vector-transmitted, chronic, and protozoan infections have been neglected, as have crucial processes such as cross-species transmission. Progress in understanding and combating zoonoses requires a new generation of models that addresses a broader set of pathogen life histories and integrates across host species and scientific disciplines.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3891603/" 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/PMC3891603/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lloyd-Smith, James O -- George, Dylan -- Pepin, Kim M -- Pitzer, Virginia E -- Pulliam, Juliet R C -- Dobson, Andrew P -- Hudson, Peter J -- Grenfell, Bryan T -- R24 HD047879/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1362-7. doi: 10.1126/science.1177345.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, University of California at Los Angeles, Los Angeles, CA 90095, USA. jlloydsmith@ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965751" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Infections/epidemiology/transmission/veterinary ; *Disease Outbreaks ; Host-Pathogen Interactions ; Humans ; *Models, Statistical ; Population Dynamics ; Protozoan Infections/epidemiology/transmission ; Protozoan Infections, Animal/epidemiology/transmission ; Virus Diseases/epidemiology/transmission/veterinary ; *Zoonoses/epidemiology/transmission
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Climate-driven basin-scale decadal oscillations of oceanic phytoplankton (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: Phytoplankton--the microalgae that populate the upper lit layers of the ocean--fuel the oceanic food web and affect oceanic and atmospheric carbon dioxide levels through photosynthetic carbon fixation. Here, we show that multidecadal changes in global phytoplankton abundances are related to basin-scale oscillations of the physical ocean, specifically the Pacific Decadal Oscillation and the Atlantic Multidecadal Oscillation. This relationship is revealed in approximately 20 years of satellite observations of chlorophyll and sea surface temperature. Interaction between the main pycnocline and the upper ocean seasonal mixed layer is one mechanism behind this correlation. Our findings provide a context for the interpretation of contemporary changes in global phytoplankton and should improve predictions of their future evolution with climate change.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martinez, Elodie -- Antoine, David -- D'Ortenzio, Fabrizio -- Gentili, Bernard -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1253-6. doi: 10.1126/science.1177012.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UPMC University of Paris 06, UMR 7093, Laboratoire d'Oceanographie de Villefranche (LOV), 06230 Villefranche-sur-Mer, France. martinez@obs-vlfr.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965473" target="_blank"〉PubMed〈/a〉
    Keywords: Atlantic Ocean ; Biomass ; Chlorophyll/*analysis ; *Climate ; *Ecosystem ; Global Warming ; Indian Ocean ; Oceans and Seas ; Pacific Ocean ; Phytoplankton/*physiology ; Population Dynamics ; Seasons ; *Seawater/chemistry ; Temperature ; Time Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Paleontology. Megafaunal decline and fall (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, Christopher -- New York, N.Y. -- Science. 2009 Nov 20;326(5956):1072-3. doi: 10.1126/science.1182770.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Marine and Tropical Biology, James Cook University, Townsville, Queensland 4811, Australia. christopher.johnson@jcu.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Archaeology ; Ascomycota ; Biomass ; *Ecosystem ; *Extinction, Biological ; Fires ; Fossils ; *Geologic Sediments ; Humans ; Indiana ; *Mammals ; North America ; Paleontology ; Population Dynamics ; Spores, Fungal ; Trees/growth & development
    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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