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  • 1
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    Identification of small molecule activators of cryptochrome (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-17
    Description: Impairment of the circadian clock has been associated with numerous disorders, including metabolic disease. Although small molecules that modulate clock function might offer therapeutic approaches to such diseases, only a few compounds have been identified that selectively target core clock proteins. From an unbiased cell-based circadian phenotypic screen, we identified KL001, a small molecule that specifically interacts with cryptochrome (CRY). KL001 prevented ubiquitin-dependent degradation of CRY, resulting in lengthening of the circadian period. In combination with mathematical modeling, our studies using KL001 revealed that CRY1 and CRY2 share a similar functional role in the period regulation. Furthermore, KL001-mediated CRY stabilization inhibited glucagon-induced gluconeogenesis in primary hepatocytes. KL001 thus provides a tool to study the regulation of CRY-dependent physiology and aid development of clock-based therapeutics of diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3589997/" 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/PMC3589997/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hirota, Tsuyoshi -- Lee, Jae Wook -- St John, Peter C -- Sawa, Mariko -- Iwaisako, Keiko -- Noguchi, Takako -- Pongsawakul, Pagkapol Y -- Sonntag, Tim -- Welsh, David K -- Brenner, David A -- Doyle, Francis J 3rd -- Schultz, Peter G -- Kay, Steve A -- GM074868/GM/NIGMS NIH HHS/ -- GM085764/GM/NIGMS NIH HHS/ -- GM096873/GM/NIGMS NIH HHS/ -- MH051573/MH/NIMH NIH HHS/ -- MH082945/MH/NIMH NIH HHS/ -- P50 GM085764/GM/NIGMS NIH HHS/ -- R01 GM041804/GM/NIGMS NIH HHS/ -- R01 GM074868/GM/NIGMS NIH HHS/ -- R01 GM096873/GM/NIGMS NIH HHS/ -- R01 MH051573/MH/NIMH NIH HHS/ -- R01 MH082945/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 31;337(6098):1094-7. doi: 10.1126/science.1223710. Epub 2012 Jul 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22798407" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Carbazoles/chemistry/isolation & purification/*pharmacology ; Cell Line, Tumor ; Circadian Clocks/*drug effects ; Cryptochromes/*agonists/metabolism ; Gluconeogenesis/drug effects/genetics ; Glucose-6-Phosphatase/genetics ; HEK293 Cells ; Hepatocytes/drug effects/metabolism ; Humans ; Liver/cytology/drug effects/metabolism ; Mice ; Molecular Sequence Data ; Phosphoenolpyruvate Carboxykinase (GTP)/genetics ; Protein Stability/drug effects ; Proteolysis/drug effects ; *Small Molecule Libraries ; Sulfonamides/chemistry/isolation & purification/*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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  • 2
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    Vascular endothelial growth factor B controls endothelial fatty acid uptake (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-03-17
    Description: The vascular endothelial growth factors (VEGFs) are major angiogenic regulators and are involved in several aspects of endothelial cell physiology. However, the detailed role of VEGF-B in blood vessel function has remained unclear. Here we show that VEGF-B has an unexpected role in endothelial targeting of lipids to peripheral tissues. Dietary lipids present in circulation have to be transported through the vascular endothelium to be metabolized by tissue cells, a mechanism that is poorly understood. Bioinformatic analysis showed that Vegfb was tightly co-expressed with nuclear-encoded mitochondrial genes across a large variety of physiological conditions in mice, pointing to a role for VEGF-B in metabolism. VEGF-B specifically controlled endothelial uptake of fatty acids via transcriptional regulation of vascular fatty acid transport proteins. As a consequence, Vegfb(-/-) mice showed less uptake and accumulation of lipids in muscle, heart and brown adipose tissue, and instead shunted lipids to white adipose tissue. This regulation was mediated by VEGF receptor 1 and neuropilin 1 expressed by the endothelium. The co-expression of VEGF-B and mitochondrial proteins introduces a novel regulatory mechanism, whereby endothelial lipid uptake and mitochondrial lipid use are tightly coordinated. The involvement of VEGF-B in lipid uptake may open up the possibility for novel strategies to modulate pathological lipid accumulation in diabetes, obesity and cardiovascular diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagberg, Carolina E -- Falkevall, Annelie -- Wang, Xun -- Larsson, Erik -- Huusko, Jenni -- Nilsson, Ingrid -- van Meeteren, Laurens A -- Samen, Erik -- Lu, Li -- Vanwildemeersch, Maarten -- Klar, Joakim -- Genove, Guillem -- Pietras, Kristian -- Stone-Elander, Sharon -- Claesson-Welsh, Lena -- Yla-Herttuala, Seppo -- Lindahl, Per -- Eriksson, Ulf -- England -- Nature. 2010 Apr 8;464(7290):917-21. doi: 10.1038/nature08945. Epub 2010 Mar 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tissue Biology Group, Division of Matrix Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, SE-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20228789" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue, Brown/metabolism ; Adipose Tissue, White/metabolism ; Animals ; Biological Transport ; Cell Line ; Cell Nucleus/genetics ; Cells, Cultured ; Endothelium/cytology/*metabolism ; Fatty Acid Transport Proteins/genetics ; Fatty Acids/*metabolism ; Gene Expression Regulation ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/genetics/metabolism ; Mitochondrial Proteins/genetics/metabolism ; Muscles/metabolism ; Myocardium/metabolism ; Neuropilin-1/genetics/metabolism ; Oligonucleotide Array Sequence Analysis ; Organ Specificity ; Signal Transduction ; Transcription, Genetic ; Vascular Endothelial Growth Factor B/deficiency/genetics/*metabolism ; Vascular Endothelial Growth Factor Receptor-1/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Natural killer cells act as rheostats modulating antiviral T cells (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-11-22
    Description: Antiviral T cells are thought to regulate whether hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections result in viral control, asymptomatic persistence or severe disease, although the reasons for these different outcomes remain unclear. Recent genetic evidence, however, has indicated a correlation between certain natural killer (NK)-cell receptors and progression of both HIV and HCV infection, implying that NK cells have a role in these T-cell-associated diseases. Although direct NK-cell-mediated lysis of virus-infected cells may contribute to antiviral defence during some virus infections--especially murine cytomegalovirus (MCMV) infections in mice and perhaps HIV in humans--NK cells have also been suspected of having immunoregulatory functions. For instance, NK cells may indirectly regulate T-cell responses by lysing MCMV-infected antigen-presenting cells. In contrast to MCMV, lymphocytic choriomeningitis virus (LCMV) infection in mice seems to be resistant to any direct antiviral effects of NK cells. Here we examine the roles of NK cells in regulating T-cell-dependent viral persistence and immunopathology in mice infected with LCMV, an established model for HIV and HCV infections in humans. We describe a three-way interaction, whereby activated NK cells cytolytically eliminate activated CD4 T cells that affect CD8 T-cell function and exhaustion. At high virus doses, NK cells prevented fatal pathology while enabling T-cell exhaustion and viral persistence, but at medium doses NK cells paradoxically facilitated lethal T-cell-mediated pathology. Thus, NK cells can act as rheostats, regulating CD4 T-cell-mediated support for the antiviral CD8 T cells that control viral pathogenesis and persistence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3539796/" 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/PMC3539796/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waggoner, Stephen N -- Cornberg, Markus -- Selin, Liisa K -- Welsh, Raymond M -- AI-081675/AI/NIAID NIH HHS/ -- AI-17672/AI/NIAID NIH HHS/ -- AI07349/AI/NIAID NIH HHS/ -- AI46578/AI/NIAID NIH HHS/ -- CA34461/CA/NCI NIH HHS/ -- DK52530/DK/NIDDK NIH HHS/ -- R01 AI017672/AI/NIAID NIH HHS/ -- R01 AI046578/AI/NIAID NIH HHS/ -- R01 AI046578-10/AI/NIAID NIH HHS/ -- R01 AR035506/AR/NIAMS NIH HHS/ -- R01 AR035506-22/AR/NIAMS NIH HHS/ -- R01 CA034461/CA/NCI NIH HHS/ -- R01 CA034461-22/CA/NCI NIH HHS/ -- R01 DK052530/DK/NIDDK NIH HHS/ -- R01 DK052530-05/DK/NIDDK NIH HHS/ -- R37 AI017672/AI/NIAID NIH HHS/ -- R37 AI017672-31/AI/NIAID NIH HHS/ -- T32 AI007349/AI/NIAID NIH HHS/ -- T32 AI007349-21/AI/NIAID NIH HHS/ -- England -- Nature. 2011 Nov 20;481(7381):394-8. doi: 10.1038/nature10624.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Program in Immunology and Virology, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22101430" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/cytology/immunology ; CD8-Positive T-Lymphocytes/cytology/immunology ; Disease Models, Animal ; HIV Infections/immunology ; Hepatitis C/immunology ; Humans ; Interferon-gamma/immunology ; Killer Cells, Natural/cytology/*immunology ; Lymphocyte Count ; Lymphocytic Choriomeningitis/immunology/pathology/virology ; Lymphocytic choriomeningitis virus/*immunology/pathogenicity ; Mice ; Mice, Inbred C57BL ; *Models, Immunological ; T-Lymphocytes/cytology/*immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Reduced airway surface pH impairs bacterial killing in the porcine cystic fibrosis lung (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-07-06
    Description: Cystic fibrosis (CF) is a life-shortening disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Although bacterial lung infection and the resulting inflammation cause most of the morbidity and mortality, how the loss of CFTR function first disrupts airway host defence has remained uncertain. To investigate the abnormalities that impair elimination when a bacterium lands on the pristine surface of a newborn CF airway, we interrogated the viability of individual bacteria immobilized on solid grids and placed onto the airway surface. As a model, we studied CF pigs, which spontaneously develop hallmark features of CF lung disease. At birth, their lungs lack infection and inflammation, but have a reduced ability to eradicate bacteria. Here we show that in newborn wild-type pigs, the thin layer of airway surface liquid (ASL) rapidly kills bacteria in vivo, when removed from the lung and in primary epithelial cultures. Lack of CFTR reduces bacterial killing. We found that the ASL pH was more acidic in CF pigs, and reducing pH inhibited the antimicrobial activity of ASL. Reducing ASL pH diminished bacterial killing in wild-type pigs, and, conversely, increasing ASL pH rescued killing in CF pigs. These results directly link the initial host defence defect to the loss of CFTR, an anion channel that facilitates HCO(3)(-) transport. Without CFTR, airway epithelial HCO(3)(-) secretion is defective, the ASL pH falls and inhibits antimicrobial function, and thereby impairs the killing of bacteria that enter the newborn lung. These findings suggest that increasing ASL pH might prevent the initial infection in patients with CF, and that assaying bacterial killing could report on the benefit of therapeutic interventions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390761/" 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/PMC3390761/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pezzulo, Alejandro A -- Tang, Xiao Xiao -- Hoegger, Mark J -- Alaiwa, Mahmoud H Abou -- Ramachandran, Shyam -- Moninger, Thomas O -- Karp, Phillip H -- Wohlford-Lenane, Christine L -- Haagsman, Henk P -- van Eijk, Martin -- Banfi, Botond -- Horswill, Alexander R -- Stoltz, David A -- McCray, Paul B Jr -- Welsh, Michael J -- Zabner, Joseph -- AI076671/AI/NIAID NIH HHS/ -- HL091842/HL/NHLBI NIH HHS/ -- HL102288/HL/NHLBI NIH HHS/ -- HL51670/HL/NHLBI NIH HHS/ -- P01 HL051670/HL/NHLBI NIH HHS/ -- P01 HL051670-15/HL/NHLBI NIH HHS/ -- P01 HL091842/HL/NHLBI NIH HHS/ -- P01 HL091842-05/HL/NHLBI NIH HHS/ -- R01 AI078921/AI/NIAID NIH HHS/ -- U01 HL102288/HL/NHLBI NIH HHS/ -- U01 HL102288-03/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jul 4;487(7405):109-13. doi: 10.1038/nature11130.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763554" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Anti-Infective Agents/pharmacology ; Bicarbonates/metabolism ; Body Fluids/drug effects/metabolism ; Cystic Fibrosis/*metabolism/*microbiology/pathology/therapy ; Cystic Fibrosis Transmembrane Conductance Regulator/genetics/metabolism ; Disease Models, Animal ; Female ; Hydrogen-Ion Concentration/drug effects ; Ion Transport ; Lung/*metabolism/*microbiology/pathology ; Male ; *Microbial Viability/drug effects ; Respiratory System/*metabolism/secretion ; Sus scrofa/microbiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Impaired mucus detachment disrupts mucociliary transport in a piglet model of cystic fibrosis (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-08-16
    Description: Lung disease in people with cystic fibrosis (CF) is initiated by defective host defense that predisposes airways to bacterial infection. Advanced CF is characterized by a deficit in mucociliary transport (MCT), a process that traps and propels bacteria out of the lungs, but whether this deficit occurs first or is secondary to airway remodeling has been unclear. To assess MCT, we tracked movement of radiodense microdisks in airways of newborn piglets with CF. Cholinergic stimulation, which elicits mucus secretion, substantially reduced microdisk movement. Impaired MCT was not due to periciliary liquid depletion; rather, CF submucosal glands secreted mucus strands that remained tethered to gland ducts. Inhibiting anion secretion in non-CF airways replicated CF abnormalities. Thus, impaired MCT is a primary defect in CF, suggesting that submucosal glands and tethered mucus may be targets for early CF treatment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4346163/" 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/PMC4346163/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoegger, Mark J -- Fischer, Anthony J -- McMenimen, James D -- Ostedgaard, Lynda S -- Tucker, Alex J -- Awadalla, Maged A -- Moninger, Thomas O -- Michalski, Andrew S -- Hoffman, Eric A -- Zabner, Joseph -- Stoltz, David A -- Welsh, Michael J -- DK054759/DK/NIDDK NIH HHS/ -- DP2 HL117744/DP/NCCDPHP CDC HHS/ -- DP2 HL117744/HL/NHLBI NIH HHS/ -- HL051670/HL/NHLBI NIH HHS/ -- HL091842/HL/NHLBI NIH HHS/ -- P01 HL051670/HL/NHLBI NIH HHS/ -- P01 HL091842/HL/NHLBI NIH HHS/ -- P30 DK054759/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):818-22. doi: 10.1126/science.1255825.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology and Biophysics, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, USA. ; Department of Pediatrics, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, USA. ; Department of Internal Medicine, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, USA. ; Central Microscopy Research Facility, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, USA. ; Department of Internal Medicine, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, USA. Department of Radiology, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, USA. Department of Biomedical Engineering, University of Iowa, Iowa City, IA 52242, USA. ; Department of Molecular Physiology and Biophysics, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, USA. Department of Internal Medicine, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, USA. Department of Biomedical Engineering, University of Iowa, Iowa City, IA 52242, USA. david-stoltz@uiowa.edu michael-welsh@uiowa.edu. ; Department of Molecular Physiology and Biophysics, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, USA. Department of Internal Medicine, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, USA. Howard Hughes Medical Institute (HHMI), University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, USA. david-stoltz@uiowa.edu michael-welsh@uiowa.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25124441" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Anions/metabolism ; Cilia/physiology ; Cystic Fibrosis/*physiopathology ; Cystic Fibrosis Transmembrane Conductance Regulator/physiology ; Disease Models, Animal ; Exocrine Glands/*secretion ; Lung/physiopathology ; Methacholine Chloride/pharmacology ; *Mucociliary Clearance ; Mucus/*secretion ; Respiratory Mucosa/*physiopathology ; Respiratory System/*physiopathology ; Swine ; Trachea/physiopathology
    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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    Reorganization of Southern Ocean plankton ecosystem at the onset of Antarctic glaciation (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-04-20
    Description: The circum-Antarctic Southern Ocean is an important region for global marine food webs and carbon cycling because of sea-ice formation and its unique plankton ecosystem. However, the mechanisms underlying the installation of this distinct ecosystem and the geological timing of its development remain unknown. Here, we show, on the basis of fossil marine dinoflagellate cyst records, that a major restructuring of the Southern Ocean plankton ecosystem occurred abruptly and concomitant with the first major Antarctic glaciation in the earliest Oligocene (~33.6 million years ago). This turnover marks a regime shift in zooplankton-phytoplankton interactions and community structure, which indicates the appearance of eutrophic and seasonally productive environments on the Antarctic margin. We conclude that earliest Oligocene cooling, ice-sheet expansion, and subsequent sea-ice formation were important drivers of biotic evolution in the Southern Ocean.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Houben, Alexander J P -- Bijl, Peter K -- Pross, Jorg -- Bohaty, Steven M -- Passchier, Sandra -- Stickley, Catherine E -- Rohl, Ursula -- Sugisaki, Saiko -- Tauxe, Lisa -- van de Flierdt, Tina -- Olney, Matthew -- Sangiorgi, Francesca -- Sluijs, Appy -- Escutia, Carlota -- Brinkhuis, Henk -- Expedition 318 Scientists -- Dotti, Carlota Escutia -- Klaus, Adam -- Fehr, Annick -- Williams, Trevor -- Bendle, James A P -- Carr, Stephanie A -- Dunbar, Robert B -- Flores, Jose-Abel -- Gonzalez, Jhon J -- Hayden, Travis G -- Iwai, Masao -- Jimenez-Espejo, Francisco J -- Katsuki, Kota -- Kong, Gee Soo -- McKay, Robert M -- Nakai, Mutsumi -- Pekar, Stephen F -- Riesselman, Christina -- Sakai, Toyosaburo -- Salzmann, Ulrich -- Shrivastava, Prakash K -- Tuo, Shouting -- Welsh, Kevin -- Yamane, Masako -- New York, N.Y. -- Science. 2013 Apr 19;340(6130):341-4. doi: 10.1126/science.1223646.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Earth Sciences, Laboratory of Palaeobotany and Palynology, Faculty of Geosciences, Utrecht University, Budapestlaan 4, 3584 CD Utrecht, Netherlands. Alexander.Houben@TNO.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23599491" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; Antarctic Regions ; Cold Temperature ; Dinoflagellida/*physiology ; *Ecosystem ; Fossils ; *Ice Cover ; *Oceans and Seas ; Phytoplankton/*physiology ; Zooplankton/*physiology
    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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