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  • 11
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    Seventy-five genetic loci influencing the human red blood cell (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-12-12
    Description: Anaemia is a chief determinant of global ill health, contributing to cognitive impairment, growth retardation and impaired physical capacity. To understand further the genetic factors influencing red blood cells, we carried out a genome-wide association study of haemoglobin concentration and related parameters in up to 135,367 individuals. Here we identify 75 independent genetic loci associated with one or more red blood cell phenotypes at P 〈 10(-8), which together explain 4-9% of the phenotypic variance per trait. Using expression quantitative trait loci and bioinformatic strategies, we identify 121 candidate genes enriched in functions relevant to red blood cell biology. The candidate genes are expressed preferentially in red blood cell precursors, and 43 have haematopoietic phenotypes in Mus musculus or Drosophila melanogaster. Through open-chromatin and coding-variant analyses we identify potential causal genetic variants at 41 loci. Our findings provide extensive new insights into genetic mechanisms and biological pathways controlling red blood cell formation and function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3623669/" 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/PMC3623669/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van der Harst, Pim -- Zhang, Weihua -- Mateo Leach, Irene -- Rendon, Augusto -- Verweij, Niek -- Sehmi, Joban -- Paul, Dirk S -- Elling, Ulrich -- Allayee, Hooman -- Li, Xinzhong -- Radhakrishnan, Aparna -- Tan, Sian-Tsung -- Voss, Katrin -- Weichenberger, Christian X -- Albers, Cornelis A -- Al-Hussani, Abtehale -- Asselbergs, Folkert W -- Ciullo, Marina -- Danjou, Fabrice -- Dina, Christian -- Esko, Tonu -- Evans, David M -- Franke, Lude -- Gogele, Martin -- Hartiala, Jaana -- Hersch, Micha -- Holm, Hilma -- Hottenga, Jouke-Jan -- Kanoni, Stavroula -- Kleber, Marcus E -- Lagou, Vasiliki -- Langenberg, Claudia -- Lopez, Lorna M -- Lyytikainen, Leo-Pekka -- Melander, Olle -- Murgia, Federico -- Nolte, Ilja M -- O'Reilly, Paul F -- Padmanabhan, Sandosh -- Parsa, Afshin -- Pirastu, Nicola -- Porcu, Eleonora -- Portas, Laura -- Prokopenko, Inga -- Ried, Janina S -- Shin, So-Youn -- Tang, Clara S -- Teumer, Alexander -- Traglia, Michela -- Ulivi, Sheila -- Westra, Harm-Jan -- Yang, Jian -- Zhao, Jing Hua -- Anni, Franco -- Abdellaoui, Abdel -- Attwood, Antony -- Balkau, Beverley -- Bandinelli, Stefania -- Bastardot, Francois -- Benyamin, Beben -- Boehm, Bernhard O -- Cookson, William O -- Das, Debashish -- de Bakker, Paul I W -- de Boer, Rudolf A -- de Geus, Eco J C -- de Moor, Marleen H -- Dimitriou, Maria -- Domingues, Francisco S -- Doring, Angela -- Engstrom, Gunnar -- Eyjolfsson, Gudmundur Ingi -- Ferrucci, Luigi -- Fischer, Krista -- Galanello, Renzo -- Garner, Stephen F -- Genser, Bernd -- Gibson, Quince D -- Girotto, Giorgia -- Gudbjartsson, Daniel Fannar -- Harris, Sarah E -- Hartikainen, Anna-Liisa -- Hastie, Claire E -- Hedblad, Bo -- Illig, Thomas -- Jolley, Jennifer -- Kahonen, Mika -- Kema, Ido P -- Kemp, John P -- Liang, Liming -- Lloyd-Jones, Heather -- Loos, Ruth J F -- Meacham, Stuart -- Medland, Sarah E -- Meisinger, Christa -- Memari, Yasin -- Mihailov, Evelin -- Miller, Kathy -- Moffatt, Miriam F -- Nauck, Matthias -- Novatchkova, Maria -- Nutile, Teresa -- Olafsson, Isleifur -- Onundarson, Pall T -- Parracciani, Debora -- Penninx, Brenda W -- Perseu, Lucia -- Piga, Antonio -- Pistis, Giorgio -- Pouta, Anneli -- Puc, Ursula -- Raitakari, Olli -- Ring, Susan M -- Robino, Antonietta -- Ruggiero, Daniela -- Ruokonen, Aimo -- Saint-Pierre, Aude -- Sala, Cinzia -- Salumets, Andres -- Sambrook, Jennifer -- Schepers, Hein -- Schmidt, Carsten Oliver -- Sillje, Herman H W -- Sladek, Rob -- Smit, Johannes H -- Starr, John M -- Stephens, Jonathan -- Sulem, Patrick -- Tanaka, Toshiko -- Thorsteinsdottir, Unnur -- Tragante, Vinicius -- van Gilst, Wiek H -- van Pelt, L Joost -- van Veldhuisen, Dirk J -- Volker, Uwe -- Whitfield, John B -- Willemsen, Gonneke -- Winkelmann, Bernhard R -- Wirnsberger, Gerald -- Algra, Ale -- Cucca, Francesco -- d'Adamo, Adamo Pio -- Danesh, John -- Deary, Ian J -- Dominiczak, Anna F -- Elliott, Paul -- Fortina, Paolo -- Froguel, Philippe -- Gasparini, Paolo -- Greinacher, Andreas -- Hazen, Stanley L -- Jarvelin, Marjo-Riitta -- Khaw, Kay Tee -- Lehtimaki, Terho -- Maerz, Winfried -- Martin, Nicholas G -- Metspalu, Andres -- Mitchell, Braxton D -- Montgomery, Grant W -- Moore, Carmel -- Navis, Gerjan -- Pirastu, Mario -- Pramstaller, Peter P -- Ramirez-Solis, Ramiro -- Schadt, Eric -- Scott, James -- Shuldiner, Alan R -- Smith, George Davey -- Smith, J Gustav -- Snieder, Harold -- Sorice, Rossella -- Spector, Tim D -- Stefansson, Kari -- Stumvoll, Michael -- Tang, W H Wilson -- Toniolo, Daniela -- Tonjes, Anke -- Visscher, Peter M -- Vollenweider, Peter -- Wareham, Nicholas J -- Wolffenbuttel, Bruce H R -- Boomsma, Dorret I -- Beckmann, Jacques S -- Dedoussis, George V -- Deloukas, Panos -- Ferreira, Manuel A -- Sanna, Serena -- Uda, Manuela -- Hicks, Andrew A -- Penninger, Josef Martin -- Gieger, Christian -- Kooner, Jaspal S -- Ouwehand, Willem H -- Soranzo, Nicole -- Chambers, John C -- 092731/Wellcome Trust/United Kingdom -- 097117/Wellcome Trust/United Kingdom -- 14136/Cancer Research UK/United Kingdom -- CZB/4/505/Chief Scientist Office/United Kingdom -- ETM/55/Chief Scientist Office/United Kingdom -- G0600705/Medical Research Council/United Kingdom -- G0700704/Medical Research Council/United Kingdom -- G0801056/Medical Research Council/United Kingdom -- G1000143/Medical Research Council/United Kingdom -- G1002084/Medical Research Council/United Kingdom -- G9815508/Medical Research Council/United Kingdom -- HHSN268201100005C/HL/NHLBI NIH HHS/ -- HHSN268201100006C/HL/NHLBI NIH HHS/ -- HHSN268201100007C/HL/NHLBI NIH HHS/ -- HHSN268201100008C/HL/NHLBI NIH HHS/ -- HHSN268201100009C/HL/NHLBI NIH HHS/ -- HHSN268201100010C/HL/NHLBI NIH HHS/ -- HHSN268201100011C/HL/NHLBI NIH HHS/ -- HHSN268201100012C/HL/NHLBI NIH HHS/ -- HHSN271201100005C/DA/NIDA NIH HHS/ -- K12 RR023250/RR/NCRR NIH HHS/ -- MC_U106179471/Medical Research Council/United Kingdom -- MC_U106188470/Medical Research Council/United Kingdom -- N01AG12109/AG/NIA NIH HHS/ -- P01 HL076491/HL/NHLBI NIH HHS/ -- P01 HL098055/HL/NHLBI NIH HHS/ -- P20 HL113452/HL/NHLBI NIH HHS/ -- P30 DK072488/DK/NIDDK NIH HHS/ -- R01 AG018728/AG/NIA NIH HHS/ -- R01 CA165001/CA/NCI NIH HHS/ -- R01 GM053275/GM/NIGMS NIH HHS/ -- R01 HD042157/HD/NICHD NIH HHS/ -- R01 HL059367/HL/NHLBI NIH HHS/ -- R01 HL086694/HL/NHLBI NIH HHS/ -- R01 HL087641/HL/NHLBI NIH HHS/ -- R01 HL087679/HL/NHLBI NIH HHS/ -- R01 HL088119/HL/NHLBI NIH HHS/ -- R01 HL103866/HL/NHLBI NIH HHS/ -- R01 HL103931/HL/NHLBI NIH HHS/ -- R01 LM010098/LM/NLM NIH HHS/ -- R01 MH081802/MH/NIMH NIH HHS/ -- RG/09/012/28096/British Heart Foundation/United Kingdom -- RL1 MH083268/MH/NIMH NIH HHS/ -- U01 GM074518/GM/NIGMS NIH HHS/ -- U01 HG004402/HG/NHGRI NIH HHS/ -- U01 HL072515/HL/NHLBI NIH HHS/ -- U01 HL084756/HL/NHLBI NIH HHS/ -- U24 MH068457/MH/NIMH NIH HHS/ -- U54 RR020278/RR/NCRR NIH HHS/ -- UL1 RR025005/RR/NCRR NIH HHS/ -- UL1 TR000439/TR/NCATS NIH HHS/ -- England -- Nature. 2012 Dec 20;492(7429):369-75. doi: 10.1038/nature11677. Epub 2012 Dec 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, University of Groningen, University Medical Center Groningen, 9700 RB Groningen, The Netherlands. p.van.der.harst@umcg.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23222517" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/genetics ; Cytokines/metabolism ; Drosophila melanogaster/genetics ; Erythrocytes/cytology/*metabolism ; Female ; Gene Expression Regulation/genetics ; *Genetic Loci ; *Genome-Wide Association Study ; Hematopoiesis/genetics ; Hemoglobins/genetics ; Humans ; Male ; Mice ; Organ Specificity ; *Phenotype ; Polymorphism, Single Nucleotide/genetics ; RNA Interference ; Signal Transduction/genetics
    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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  • 12
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    Maternal retinoids control type 3 innate lymphoid cells and set the offspring immunity (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-03-29
    Description: The impact of nutritional status during fetal life on the overall health of adults has been recognized; however, dietary effects on the developing immune system are largely unknown. Development of secondary lymphoid organs occurs during embryogenesis and is considered to be developmentally programmed. Secondary lymphoid organ formation depends on a subset of type 3 innate lymphoid cells (ILC3) named lymphoid tissue inducer (LTi) cells. Here we show that mouse fetal ILC3s are controlled by cell-autonomous retinoic acid (RA) signalling in utero, which pre-sets the immune fitness in adulthood. We found that embryonic lymphoid organs contain ILC progenitors that differentiate locally into mature LTi cells. Local LTi cell differentiation was controlled by maternal retinoid intake and fetal RA signalling acting in a haematopoietic cell-autonomous manner. RA controlled LTi cell maturation upstream of the transcription factor RORgammat. Accordingly, enforced expression of Rorgt restored maturation of LTi cells with impaired RA signalling, whereas RA receptors directly regulated the Rorgt locus. Finally, we established that maternal levels of dietary retinoids control the size of secondary lymphoid organs and the efficiency of immune responses in the adult offspring. Our results reveal a molecular link between maternal nutrients and the formation of immune structures required for resistance to infection in the offspring.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van de Pavert, Serge A -- Ferreira, Manuela -- Domingues, Rita G -- Ribeiro, Helder -- Molenaar, Rosalie -- Moreira-Santos, Lara -- Almeida, Francisca F -- Ibiza, Sales -- Barbosa, Ines -- Goverse, Gera -- Labao-Almeida, Carlos -- Godinho-Silva, Cristina -- Konijn, Tanja -- Schooneman, Dennis -- O'Toole, Tom -- Mizee, Mark R -- Habani, Yasmin -- Haak, Esther -- Santori, Fabio R -- Littman, Dan R -- Schulte-Merker, Stefan -- Dzierzak, Elaine -- Simas, J Pedro -- Mebius, Reina E -- Veiga-Fernandes, Henrique -- R01 AI080885/AI/NIAID NIH HHS/ -- R01AI080885/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Apr 3;508(7494):123-7. doi: 10.1038/nature13158. Epub 2014 Mar 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Molecular Cell Biology and Immunology, VU University Medical Center, van der Boechorststraat 7, 1081BT Amsterdam, The Netherlands [2] Hubrecht Institute-KNAW (Royal Netherlands Academy of Arts and Sciences) and University Medical Center Utrecht, 3584 CT Utrecht, Netherlands. [3]. ; 1] Instituto de Medicina Molecular, Faculdade de Medicina de Lisboa, Av. Prof. Egas Moniz, Edificio Egas Moniz, 1649-028 Lisboa, Portugal [2]. ; Instituto de Medicina Molecular, Faculdade de Medicina de Lisboa, Av. Prof. Egas Moniz, Edificio Egas Moniz, 1649-028 Lisboa, Portugal. ; Department of Molecular Cell Biology and Immunology, VU University Medical Center, van der Boechorststraat 7, 1081BT Amsterdam, The Netherlands. ; Erasmus Stem Cell Institute, Department of Cell Biology, Erasmus Medical Center, 3000 CA Rotterdam, The Netherlands. ; Howard Hughes Medical Institute, Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, New York 10016, USA. ; Hubrecht Institute-KNAW (Royal Netherlands Academy of Arts and Sciences) and University Medical Center Utrecht, 3584 CT Utrecht, Netherlands. ; 1] Department of Molecular Cell Biology and Immunology, VU University Medical Center, van der Boechorststraat 7, 1081BT Amsterdam, The Netherlands [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670648" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects/immunology ; Diet ; Female ; Fetus/drug effects/*immunology ; Immunity, Innate/drug effects/*immunology ; Lymphoid Tissue/cytology/drug effects/embryology/immunology ; Mice ; Mice, Inbred C57BL ; Pregnancy ; Prenatal Exposure Delayed Effects/*immunology ; Receptors, Retinoic Acid/metabolism ; Signal Transduction/drug effects ; Stem Cells/cytology/drug effects/immunology ; Tretinoin/administration & dosage/*immunology/metabolism/*pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 13
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    Aberrant neurites and synaptic vesicle protein deficiency in synapsin II-depleted neurons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-13
    Description: Synapsin I and synapsin II are neuron-specific phosphoproteins that have a role in the regulation of neurotransmitter release and in the formation of nerve terminals. After depletion of synapsin II by antisense oligonucleotides, rat hippocampal neurons in culture were unable to consolidate their minor processes and did not elongate axons. These aberrant morphological changes were accompanied by an abnormal distribution of intracellular filamentous actin (F-actin). In addition, synapsin II suppression resulted in a selective decrease in the amounts of several synaptic vesicle-associated proteins. These data suggest that synapsin II participates in cytoskeletal organization during the early stages of nerve cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferreira, A -- Kosik, K S -- Greengard, P -- Han, H Q -- New York, N.Y. -- Science. 1994 May 13;264(5161):977-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurological Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178158" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Base Sequence ; *Calcium-Binding Proteins ; Cells, Cultured ; Hippocampus/cytology ; Membrane Glycoproteins/*metabolism ; Microtubule-Associated Proteins/metabolism ; Molecular Sequence Data ; Nerve Tissue Proteins/*metabolism ; Neurites/*physiology ; Neurons/*cytology/metabolism/ultrastructure ; Oligonucleotides, Antisense/pharmacology ; Rats ; Synapsins/genetics/*metabolism ; Synaptophysin/*metabolism ; Synaptotagmins ; Tubulin/metabolism ; tau Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 14
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    Synaptic pruning by microglia is necessary for normal brain development (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-23
    Description: Microglia are highly motile phagocytic cells that infiltrate and take up residence in the developing brain, where they are thought to provide a surveillance and scavenging function. However, although microglia have been shown to engulf and clear damaged cellular debris after brain insult, it remains less clear what role microglia play in the uninjured brain. Here, we show that microglia actively engulf synaptic material and play a major role in synaptic pruning during postnatal development in mice. These findings link microglia surveillance to synaptic maturation and suggest that deficits in microglia function may contribute to synaptic abnormalities seen in some neurodevelopmental disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paolicelli, Rosa C -- Bolasco, Giulia -- Pagani, Francesca -- Maggi, Laura -- Scianni, Maria -- Panzanelli, Patrizia -- Giustetto, Maurizio -- Ferreira, Tiago Alves -- Guiducci, Eva -- Dumas, Laura -- Ragozzino, Davide -- Gross, Cornelius T -- New York, N.Y. -- Science. 2011 Sep 9;333(6048):1456-8. doi: 10.1126/science.1202529. Epub 2011 Jul 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mouse Biology Unit, European Molecular Biology Laboratory (EMBL), Via Ramarini 32, 00015 Monterotondo, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21778362" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*growth & development/physiology ; Chemokine CX3CL1/metabolism ; Dendritic Spines/physiology/ultrastructure ; Excitatory Postsynaptic Potentials ; Guanylate Kinase/analysis ; Hippocampus/*growth & development/*physiology ; Long-Term Synaptic Depression ; Membrane Proteins/analysis ; Mice ; Mice, Knockout ; Microglia/*physiology ; Miniature Postsynaptic Potentials ; Neuronal Plasticity ; Patch-Clamp Techniques ; Pyramidal Cells/physiology ; Receptors, Chemokine/genetics/metabolism ; Receptors, Cytokine/genetics/metabolism ; Receptors, HIV/genetics/metabolism ; Signal Transduction ; Synapses/*physiology ; Synaptosomal-Associated Protein 25/analysis
    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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  • 15
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    Continental-scale effects of nutrient pollution on stream ecosystem functioning (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-16
    Description: Excessive nutrient loading is a major threat to aquatic ecosystems worldwide that leads to profound changes in aquatic biodiversity and biogeochemical processes. Systematic quantitative assessment of functional ecosystem measures for river networks is, however, lacking, especially at continental scales. Here, we narrow this gap by means of a pan-European field experiment on a fundamental ecosystem process--leaf-litter breakdown--in 100 streams across a greater than 1000-fold nutrient gradient. Dramatically slowed breakdown at both extremes of the gradient indicated strong nutrient limitation in unaffected systems, potential for strong stimulation in moderately altered systems, and inhibition in highly polluted streams. This large-scale response pattern emphasizes the need to complement established structural approaches (such as water chemistry, hydrogeomorphology, and biological diversity metrics) with functional measures (such as litter-breakdown rate, whole-system metabolism, and nutrient spiraling) for assessing ecosystem health.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woodward, Guy -- Gessner, Mark O -- Giller, Paul S -- Gulis, Vladislav -- Hladyz, Sally -- Lecerf, Antoine -- Malmqvist, Bjorn -- McKie, Brendan G -- Tiegs, Scott D -- Cariss, Helen -- Dobson, Mike -- Elosegi, Arturo -- Ferreira, Veronica -- Graca, Manuel A S -- Fleituch, Tadeusz -- Lacoursiere, Jean O -- Nistorescu, Marius -- Pozo, Jesus -- Risnoveanu, Geta -- Schindler, Markus -- Vadineanu, Angheluta -- Vought, Lena B-M -- Chauvet, Eric -- New York, N.Y. -- Science. 2012 Jun 15;336(6087):1438-40. doi: 10.1126/science.1219534.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, Ecology and Plant Science, University College Cork, National University of Ireland, Cork, Enterprise Centre, Distillery Fields, Cork, Ireland. g.woodward@qmul.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22700929" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodiversity ; Biomass ; *Ecosystem ; Europe ; Eutrophication ; Ilex ; Invertebrates/*metabolism ; *Plant Leaves ; Quercus ; *Rivers/microbiology ; *Water Pollution, Chemical
    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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  • 16
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    A gut lipid messenger links excess dietary fat to dopamine deficiency (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-08-21
    Description: Excessive intake of dietary fats leads to diminished brain dopaminergic function. It has been proposed that dopamine deficiency exacerbates obesity by provoking compensatory overfeeding as one way to restore reward sensitivity. However, the physiological mechanisms linking prolonged high-fat intake to dopamine deficiency remain elusive. We show that administering oleoylethanolamine, a gastrointestinal lipid messenger whose synthesis is suppressed after prolonged high-fat exposure, is sufficient to restore gut-stimulated dopamine release in high-fat-fed mice. Administering oleoylethanolamine to high-fat-fed mice also eliminated motivation deficits during flavorless intragastric feeding and increased oral intake of low-fat emulsions. Our findings suggest that high-fat-induced gastrointestinal dysfunctions play a key role in dopamine deficiency and that restoring gut-generated lipid signaling may increase the reward value of less palatable, yet healthier, foods.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tellez, Luis A -- Medina, Sara -- Han, Wenfei -- Ferreira, Jozelia G -- Licona-Limon, Paula -- Ren, Xueying -- Lam, Tukiet T -- Schwartz, Gary J -- de Araujo, Ivan E -- DC009997/DC/NIDCD NIH HHS/ -- DK020541/DK/NIDDK NIH HHS/ -- DK026687/DK/NIDDK NIH HHS/ -- DK085579/DK/NIDDK NIH HHS/ -- P30 DK026687/DK/NIDDK NIH HHS/ -- UL1RR024139/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2013 Aug 16;341(6147):800-2. doi: 10.1126/science.1239275.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The John B. Pierce Laboratory, New Haven, CT 06519, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23950538" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Appetite ; Corpus Striatum/*metabolism ; Dietary Fats/*administration & dosage ; Dopamine/deficiency/*metabolism ; Endocannabinoids/*administration & dosage/biosynthesis/*physiology ; Energy Intake ; Ethanolamines/*administration & dosage ; Feeding Behavior ; Gastrointestinal Tract/*metabolism ; Homeostasis ; Intestine, Small/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Oleic Acids/*administration & dosage/biosynthesis/*physiology ; PPAR alpha/genetics/metabolism ; Reward ; Signal Transduction ; Vagus Nerve/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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  • 17
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    Drug resistance. Population transcriptomics of human malaria parasites reveals the mechanism of artemisinin resistance (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-12-17
    Description: Artemisinin resistance in Plasmodium falciparum threatens global efforts to control and eliminate malaria. Polymorphisms in the kelch domain-carrying protein K13 are associated with artemisinin resistance, but the underlying molecular mechanisms are unknown. We analyzed the in vivo transcriptomes of 1043 P. falciparum isolates from patients with acute malaria and found that artemisinin resistance is associated with increased expression of unfolded protein response (UPR) pathways involving the major PROSC and TRiC chaperone complexes. Artemisinin-resistant parasites also exhibit decelerated progression through the first part of the asexual intraerythrocytic development cycle. These findings suggest that artemisinin-resistant parasites remain in a state of decelerated development at the young ring stage, whereas their up-regulated UPR pathways mitigate protein damage caused by artemisinin. The expression profiles of UPR-related genes also associate with the geographical origin of parasite isolates, further suggesting their role in emerging artemisinin resistance in the Greater Mekong Subregion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mok, Sachel -- Ashley, Elizabeth A -- Ferreira, Pedro E -- Zhu, Lei -- Lin, Zhaoting -- Yeo, Tomas -- Chotivanich, Kesinee -- Imwong, Mallika -- Pukrittayakamee, Sasithon -- Dhorda, Mehul -- Nguon, Chea -- Lim, Pharath -- Amaratunga, Chanaki -- Suon, Seila -- Hien, Tran Tinh -- Htut, Ye -- Faiz, M Abul -- Onyamboko, Marie A -- Mayxay, Mayfong -- Newton, Paul N -- Tripura, Rupam -- Woodrow, Charles J -- Miotto, Olivo -- Kwiatkowski, Dominic P -- Nosten, Francois -- Day, Nicholas P J -- Preiser, Peter R -- White, Nicholas J -- Dondorp, Arjen M -- Fairhurst, Rick M -- Bozdech, Zbynek -- 089276/Wellcome Trust/United Kingdom -- 090770/Wellcome Trust/United Kingdom -- 093956/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2015 Jan 23;347(6220):431-5. doi: 10.1126/science.1260403. Epub 2014 Dec 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biological Sciences, Nanyang Technological University, Singapore. ; Mahidol-Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand. Centre for Tropical Medicine and Global Health, Nuffield Department of Medicine, University of Oxford, Oxford, UK. ; Department of Clinical Tropical Medicine, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand. ; Department of Molecular Tropical Medicine and Genetics, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand. ; Centre for Tropical Medicine and Global Health, Nuffield Department of Medicine, University of Oxford, Oxford, UK. WorldWide Antimalarial Resistance Network (WWARN), Asia Regional Centre, Mahidol University, Bangkok, Thailand. WorldWide Antimalarial Resistance Network, University of Maryland School of Medicine, Baltimore, MD, USA. ; National Center for Parasitology, Entomology and Malaria Control, Phnom Penh, Cambodia. ; National Center for Parasitology, Entomology and Malaria Control, Phnom Penh, Cambodia. Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. ; Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. ; Oxford University Clinical Research Unit (OUCRU), Hospital for Tropical Diseases, Ho Chi Minh City, Vietnam. ; Department of Medical Research, Lower Myanmar, Yangon, Myanmar. ; Malaria Research Group & Dev Care Foundation, Dhaka, Bangladesh. ; Kinshasa School of Public Health, Kinshasa, Democratic Republic of the Congo. ; Lao-Oxford-Mahosot Hospital-Wellcome Trust Research Unit, Mahosot Hospital, Vientiane, Lao PDR. Faculty of Postgraduate Studies, University of Health Sciences, Vientiane, Lao PDR. ; Mahidol-Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand. Centre for Tropical Medicine and Global Health, Nuffield Department of Medicine, University of Oxford, Oxford, UK. Lao-Oxford-Mahosot Hospital-Wellcome Trust Research Unit, Mahosot Hospital, Vientiane, Lao PDR. ; Mahidol-Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand. ; Mahidol-Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand. Medical Research Council (MRC) Centre for Genomics and Global Health, University of Oxford, Oxford, UK. Wellcome Trust Sanger Institute, Hinxton, Cambridge, UK. ; Medical Research Council (MRC) Centre for Genomics and Global Health, University of Oxford, Oxford, UK. Wellcome Trust Sanger Institute, Hinxton, Cambridge, UK. ; Centre for Tropical Medicine and Global Health, Nuffield Department of Medicine, University of Oxford, Oxford, UK. Shoklo Malaria Research Unit, Mahidol-Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, Mae Sot, Thailand. ; School of Biological Sciences, Nanyang Technological University, Singapore. zbozdech@ntu.edu.sg.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25502316" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimalarials/*pharmacology ; Artemisinins/*pharmacology ; Chaperonin Containing TCP-1/genetics/metabolism ; Drug Resistance/*genetics ; Humans ; Malaria/*drug therapy/parasitology ; Malaria, Falciparum/*drug therapy/parasitology ; Plasmodium falciparum/*drug effects/*genetics ; Transcriptome ; Unfolded Protein Response/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 18
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    Inhibition of development of exoerythrocytic forms of malaria parasites by gamma-interferon (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-16
    Description: A specific DNA probe was used to study the effect of recombinant rat, mouse, and human gamma-interferon (gamma-IFN) on the course of sporozoite-induced malaria infections. In mice and rats infected with sporozoites of Plasmodium berghei, mouse and rat gamma-IFN's strongly inhibited the development of the exoerythrocytic forms in the liver liver cells of the hosts, but not the development of the erythrocytic stages. The degree of inhibition of the exoerythrocytic forms was proportional to the dose of gamma-IFN administered, but was independent of the number of sporozoites used for challenge. A 30 percent reduction in the development of exoerythrocytic forms in rat liver was achieved when 150 units (about 15 nanograms of protein) of rat gamma-IFN were injected a few hours before sporozoite challenge; the reduction was 90 percent or more with higher doses of gamma-IFN. The effect was less pronounced if the gamma-IFN was administered 18 hours before or a few hours after challenge. Human gamma-IFN also diminished the parasitemia in chimpanzees infected with sporozoites of the human malaria parasite Plasmodium vivax. The target of gamma-IFN activity may be the infected hepatocytes themselves, as shown by in vitro experiments in which small doses of the human lymphokine inhibited the development of exoerythrocytic forms of Plasmodium berghei in a human hepatoma cell line. These results suggest that immunologically induced interferon may be involved in controlling malaria infection under natural conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferreira, A -- Schofield, L -- Enea, V -- Schellekens, H -- van der Meide, P -- Collins, W E -- Nussenzweig, R S -- Nussenzweig, V -- New York, N.Y. -- Science. 1986 May 16;232(4752):881-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3085218" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Humans ; Interferon-gamma/pharmacology/*therapeutic use ; Liver/cytology ; Malaria/*drug therapy ; Mice ; Pan troglodytes ; Plasmodium berghei/drug effects ; Plasmodium vivax/drug effects ; Toxoplasma/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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