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  • 1
    Publication Date: 2018-05-07
    Description: Niphargus is a speciose amphipod genus found in groundwater habitats across Europe. Three Niphargus species living in the sulphidic Frasassi caves in Italy harbour sulphur-oxidizing Thiothrix bacterial ectosymbionts. These three species are distantly related, implying that the ability to form ectosymbioses with Thiothrix may be common among Niphargus. Therefore, Niphargus-Thiothrix associations may also be found in sulphidic aquifers other than Frasassi. In this study, we examined this possibility by analysing niphargids of the genera Niphargus and Pontoniphargus collected from the partly sulphidic aquifers of the Southern Dobrogea region of Romania, which are accessible through springs, wells and Movile Cave. Molecular and morphological analyses revealed seven niphargid species in this region. Five of these species occurred occasionally or exclusively in sulphidic locations, whereas the remaining two were restricted to nonsulphidic areas. Thiothrix were detected by PCR on all seven Dobrogean niphargid species and observed using microscopy to be predominantly attached to their hosts' appendages. 16S rRNA gene sequences of the Thiothrix epibionts fell into two main clades, one of which (herein named T4) occurred solely on niphargids collected in sulphidic locations. The other Thiothrix clade was present on niphargids from both sulphidic and nonsulphidic areas and indistinguishable from the T3 ectosymbiont clade previously identified on Frasassi-dwelling Niphargus. Although niphargids from Frasassi and Southern Dobrogea are not closely related, the patterns of their association with Thiothrix are remarkably alike. The finding of similar Niphargus-Thiothrix associations in aquifers located 1200 km apart suggests that they may be widespread in European groundwater ecosystems.
    Keywords: amphipods; ecology; sulphide; symbiosis; systematics; taxonomy ; Amphipoda ; Animals ; DNA, Bacterial ; Ecosystem ; Groundwater ; Molecular Sequence Data ; Phylogeny ; RNA, Ribosomal, 16S ; Romania ; Sequence Analysis, DNA ; Sulfur ; Symbiosis ; Thiothrix
    Language: English , English
    Type: article , publishedVersion
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kupferschmidt, Kai -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1143. doi: 10.1126/science.351.6278.1143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965608" target="_blank"〉PubMed〈/a〉
    Keywords: Acinetobacter/*growth & development ; Animals ; *Death ; Humans ; Mice ; Moraxellaceae/*growth & development ; Rhizobiaceae/*growth & development ; 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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  • 3
    Publication Date: 2016-03-19
    Description: Maintaining energy homeostasis is crucial for the survival and health of organisms. The brain regulates feeding by responding to dietary factors and metabolic signals from peripheral organs. It is unclear how the brain interprets these signals. O-GlcNAc transferase (OGT) catalyzes the posttranslational modification of proteins by O-GlcNAc and is regulated by nutrient access. Here, we show that acute deletion of OGT from alphaCaMKII-positive neurons in adult mice caused obesity from overeating. The hyperphagia derived from the paraventricular nucleus (PVN) of the hypothalamus, where loss of OGT was associated with impaired satiety. These results identify O-GlcNAcylation in alphaCaMKII neurons of the PVN as an important molecular mechanism that regulates feeding behavior.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4817221/" 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/PMC4817221/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lagerlof, Olof -- Slocomb, Julia E -- Hong, Ingie -- Aponte, Yeka -- Blackshaw, Seth -- Hart, Gerald W -- Huganir, Richard L -- N01-HV-00240/HV/NHLBI NIH HHS/ -- P01 HL107153/HL/NHLBI NIH HHS/ -- P01HL107153/HL/NHLBI NIH HHS/ -- R01 DK061671/DK/NIDDK NIH HHS/ -- R01 NS036715/NS/NINDS NIH HHS/ -- R01DK6167/DK/NIDDK NIH HHS/ -- R01NS036715/NS/NINDS NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1293-6. doi: 10.1126/science.aad5494.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon H. Snyder Department of Neuroscience, Kavli Neuroscience Discovery Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. ; National Institute on Drug Abuse + National Institutes of Health/Johns Hopkins University Graduate Partnership Program, Baltimore, MD 21224, USA. ; Solomon H. Snyder Department of Neuroscience, Kavli Neuroscience Discovery Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. ; Solomon H. Snyder Department of Neuroscience, Kavli Neuroscience Discovery Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Intramural Research Program, Neuronal Circuits and Behavior Unit, National Institute on Drug Abuse, Baltimore, MD 21224, USA. ; Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. ; Solomon H. Snyder Department of Neuroscience, Kavli Neuroscience Discovery Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. rhuganir@jhmi.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989246" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylglucosamine/metabolism ; Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Energy Metabolism/genetics/*physiology ; Feeding Behavior/*physiology ; Gene Deletion ; Homeostasis/genetics ; Hyperphagia/*genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; N-Acetylglucosaminyltransferases/genetics/*physiology ; Neurons/enzymology ; Obesity/genetics ; Paraventricular Hypothalamic Nucleus/cytology/enzymology/*physiology ; Protein Processing, Post-Translational ; Satiety Response/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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  • 4
    Publication Date: 2016-01-30
    Description: Cystic fibrosis (CF) is caused by mutations in the gene that encodes the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel. In humans and pigs, the loss of CFTR impairs respiratory host defenses, causing airway infection. But CF mice are spared. We found that in all three species, CFTR secreted bicarbonate into airway surface liquid. In humans and pigs lacking CFTR, unchecked H(+) secretion by the nongastric H(+)/K(+) adenosine triphosphatase (ATP12A) acidified airway surface liquid, which impaired airway host defenses. In contrast, mouse airways expressed little ATP12A and secreted minimal H(+); consequently, airway surface liquid in CF and non-CF mice had similar pH. Inhibiting ATP12A reversed host defense abnormalities in human and pig airways. Conversely, expressing ATP12A in CF mouse airways acidified airway surface liquid, impaired defenses, and increased airway bacteria. These findings help explain why CF mice are protected from infection and nominate ATP12A as a potential therapeutic target for CF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shah, Viral S -- Meyerholz, David K -- Tang, Xiao Xiao -- Reznikov, Leah -- Abou Alaiwa, Mahmoud -- Ernst, Sarah E -- Karp, Philip H -- Wohlford-Lenane, Christine L -- Heilmann, Kristopher P -- Leidinger, Mariah R -- Allen, Patrick D -- Zabner, Joseph -- McCray, Paul B Jr -- Ostedgaard, Lynda S -- Stoltz, David A -- Randak, Christoph O -- Welsh, Michael J -- 5T32GM007337/GM/NIGMS NIH HHS/ -- DK054759/DK/NIDDK NIH HHS/ -- F30 HL123239/HL/NHLBI NIH HHS/ -- F30HL123239/HL/NHLBI NIH HHS/ -- HL091842/HL/NHLBI NIH HHS/ -- HL117744/HL/NHLBI NIH HHS/ -- HL51670/HL/NHLBI NIH HHS/ -- K08HL097071/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):503-7. doi: 10.1126/science.aad5589.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Iowa, Iowa City, IA 52242, USA. Department of Molecular Physiology and Biophysics, Pappajohn Biomedical Institute, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA. ; Department of Pathology, University of Iowa, Iowa City, IA 52242, USA. ; Department of Medicine, University of Iowa, Iowa City, IA 52242, USA. Howard Hughes Medical Institute, University of Iowa, Iowa City, IA 52242, USA. ; Department of Medicine, University of Iowa, Iowa City, IA 52242, USA. ; Department of Pediatrics University of Iowa, Iowa City, IA 52242, USA. ; Department of Microbiology, University of Iowa, Iowa City, IA 52242, USA. ; Department of Pediatrics University of Iowa, Iowa City, IA 52242, USA. Department of Microbiology, University of Iowa, Iowa City, IA 52242, USA. ; Department of Medicine, University of Iowa, Iowa City, IA 52242, USA. Department of Molecular Physiology and Biophysics, Pappajohn Biomedical Institute, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA. Department of Biomedical Engineering, College of Engineering, University of Iowa, Iowa City, IA 52242, USA. ; Department of Medicine, University of Iowa, Iowa City, IA 52242, USA. Department of Molecular Physiology and Biophysics, Pappajohn Biomedical Institute, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA. Howard Hughes Medical Institute, University of Iowa, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823428" target="_blank"〉PubMed〈/a〉
    Keywords: Acids/metabolism ; Animals ; Bicarbonates/metabolism ; Cystic Fibrosis/*metabolism/*microbiology ; H(+)-K(+)-Exchanging ATPase/genetics/*metabolism ; Humans ; Hydrogen-Ion Concentration ; Lung/*metabolism/*microbiology ; Mice ; Mice, Inbred CFTR/genetics/metabolism ; Mice, Transgenic ; Swine
    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: 2016-01-02
    Description: Several recent studies link parental environments to phenotypes in subsequent generations. In this work, we investigate the mechanism by which paternal diet affects offspring metabolism. Protein restriction in mice affects small RNA (sRNA) levels in mature sperm, with decreased let-7 levels and increased amounts of 5' fragments of glycine transfer RNAs (tRNAs). In testicular sperm, tRNA fragments are scarce but increase in abundance as sperm mature in the epididymis. Epididymosomes (vesicles that fuse with sperm during epididymal transit) carry RNA payloads matching those of mature sperm and can deliver RNAs to immature sperm in vitro. Functionally, tRNA-glycine-GCC fragments repress genes associated with the endogenous retroelement MERVL, in both embryonic stem cells and embryos. Our results shed light on sRNA biogenesis and its dietary regulation during posttesticular sperm maturation, and they also link tRNA fragments to regulation of endogenous retroelements active in the preimplantation embryo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharma, Upasna -- Conine, Colin C -- Shea, Jeremy M -- Boskovic, Ana -- Derr, Alan G -- Bing, Xin Y -- Belleannee, Clemence -- Kucukural, Alper -- Serra, Ryan W -- Sun, Fengyun -- Song, Lina -- Carone, Benjamin R -- Ricci, Emiliano P -- Li, Xin Z -- Fauquier, Lucas -- Moore, Melissa J -- Sullivan, Robert -- Mello, Craig C -- Garber, Manuel -- Rando, Oliver J -- DP1ES025458/DP/NCCDPHP CDC HHS/ -- R01HD080224/HD/NICHD NIH HHS/ -- UL1 TR000161/TR/NCATS NIH HHS/ -- UL1 TR001453/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):391-6. doi: 10.1126/science.aad6780. Epub 2015 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA. Program in Bioinformatics and Integrative Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Department of Obstetrics, Gynecology and Reproduction, Universite Laval, Centre Hospitalier Universitaire de Quebec Research Center, Quebec City, Quebec G1V 4G2, Canada. ; RNAi Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA. RNAi Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA. RNAi Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA. RNAi Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA. oliver.rando@umassmed.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/metabolism ; Diet, Protein-Restricted ; Epididymis/metabolism ; *Fertilization ; *Gene Expression Regulation ; Male ; Mice ; MicroRNAs/metabolism ; RNA, Transfer, Gly/*metabolism/*physiology ; Retroelements/genetics ; *Sperm Maturation ; Spermatozoa/*metabolism ; Testis/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 6
    Publication Date: 2016-02-26
    Description: Mota and Herculano-Houzel (Reports, 3 July 2015, p. 74) assign power functions to neuroanatomical data and present a model to account for evolutionary patterns of cortical folding in the mammalian brain. We detail how the model assumptions are in conflict with experimental and observational work and show that the model itself does not accurately fit the data.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewitus, Eric -- Kelava, Iva -- Kalinka, Alex T -- Tomancak, Pavel -- Huttner, Wieland B -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):825. doi: 10.1126/science.aad2029.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Biologie, Ecole Normale Superieure, Paris, France. lewitus@biologie.ens.fr huttner@mpi-cbg.de. ; MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge Biomedical Campus, Cambridge CB2 0QH, UK. ; Institute of Population Genetics, Vetmeduni, Vienna, Austria. ; Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany. ; Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany. lewitus@biologie.ens.fr huttner@mpi-cbg.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cerebral Cortex ; Humans ; Lissencephaly/*pathology ; Neurons/*cytology
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  • 7
    Publication Date: 2016-02-26
    Description: Voltage-gated CaV1.2 channels (L-type calcium channel alpha1C subunits) are critical mediators of transcription-dependent neural plasticity. Whether these channels signal via the influx of calcium ion (Ca(2+)), voltage-dependent conformational change (VDeltaC), or a combination of the two has thus far been equivocal. We fused CaV1.2 to a ligand-gated Ca(2+)-permeable channel, enabling independent control of localized Ca(2+) and VDeltaC signals. This revealed an unexpected dual requirement: Ca(2+) must first mobilize actin-bound Ca(2+)/calmodulin-dependent protein kinase II, freeing it for subsequent VDeltaC-mediated accumulation. Neither signal alone sufficed to activate transcription. Signal order was crucial: Efficiency peaked when Ca(2+) preceded VDeltaC by 10 to 20 seconds. CaV1.2 VDeltaC synergistically augmented signaling by N-methyl-d-aspartate receptors. Furthermore, VDeltaC mistuning correlated with autistic symptoms in Timothy syndrome. Thus, nonionic VDeltaC signaling is vital to the function of CaV1.2 in synaptic and neuropsychiatric processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Boxing -- Tadross, Michael R -- Tsien, Richard W -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):863-7. doi: 10.1126/science.aad3647.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience and Physiology and New York University Neuroscience Institute, New York, NY 10016, USA. ; Department of Molecular and Cellular Physiology, Beckman Center, School of Medicine, Stanford University, Stanford, CA 94305, USA. Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147, USA. tadrossm@janelia.hhmi.org. ; Department of Neuroscience and Physiology and New York University Neuroscience Institute, New York, NY 10016, USA. Department of Molecular and Cellular Physiology, Beckman Center, School of Medicine, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912895" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/genetics/metabolism ; Calcium Channel Blockers/pharmacology ; Calcium Channels, L-Type/chemistry/*metabolism ; *Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; *Gene Expression Regulation ; HEK293 Cells ; Hippocampus/cytology ; Humans ; Long QT Syndrome/genetics/metabolism ; Neuronal Plasticity/*genetics ; Neurons/drug effects/*metabolism ; Nimodipine/pharmacology ; Protein Conformation/drug effects ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/metabolism ; Syndactyly/genetics/metabolism
    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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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheid, Johannes F -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1175. doi: 10.1126/science.aad7133.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital, Boston, MA 02114, USA. The Rockefeller University, New York, NY 10021, USA. fscheid@partners.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785466" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/genetics/immunology/isolation & purification ; Antibodies, Neutralizing/genetics/*immunology/isolation & purification ; B-Lymphocytes/*immunology ; Cell Separation/methods ; HIV Antibodies/genetics/*immunology/isolation & purification ; HIV Infections/*blood ; Humans ; Immunologic Memory ; Mice ; env Gene Products, Human Immunodeficiency Virus/*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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  • 9
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hurtley, Stella -- Roberts, Leslie -- Ray, L Bryan -- Purnell, Beverly A -- Ash, Caroline -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1180-1. doi: 10.1126/science.350.6265.1180.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785472" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics ; Animals ; Health ; Humans ; Mitochondria/metabolism ; Stem Cells/physiology ; Telomere/*genetics ; *Telomere Homeostasis
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    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: Mitochondria generate adenosine 5'-triphosphate (ATP) and are a source of potentially toxic reactive oxygen species (ROS). It has been suggested that the gradual mitochondrial dysfunction that is observed to accompany aging could in fact be causal to the aging process. Here we review findings that suggest that age-dependent mitochondrial dysfunction is not sufficient to limit life span. Furthermore, mitochondrial ROS are not always deleterious and can even stimulate pro-longevity pathways. Thus, mitochondrial dysfunction plays a complex role in regulating longevity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Ying -- Hekimi, Siegfried -- MOP-114891/Canadian Institutes of Health Research/Canada -- MOP-123295/Canadian Institutes of Health Research/Canada -- MOP-97869/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1204-7. doi: 10.1126/science.aac4357.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada. ; Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada. siegfried.hekimi@mcgill.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785479" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Animals ; Caenorhabditis elegans Proteins/genetics ; Electron Transport/genetics ; Electron Transport Complex III/genetics ; Longevity/genetics/*physiology ; Mice ; Mice, Knockout ; Mitochondria/genetics/*metabolism ; Point Mutation ; Reactive Oxygen Species/*metabolism
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  • 11
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1186-7. doi: 10.1126/science.350.6265.1186.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785474" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/genetics/physiology ; Caenorhabditis elegans Proteins/genetics/physiology ; Caloric Restriction ; Death ; Humans ; Hydra/genetics/physiology ; Longevity/genetics/*physiology ; Mice ; Mutation ; Phosphatidylinositol 3-Kinases/genetics/physiology
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  • 12
    Publication Date: 2016-01-20
    Description: Migratory species depend on a suite of interconnected sites. Threats to unprotected links in these chains of sites are driving rapid population declines of migrants around the world, yet the extent to which different parts of the annual cycle are protected remains unknown. We show that just 9% of 1451 migratory birds are adequately covered by protected areas across all stages of their annual cycle, in comparison with 45% of nonmigratory birds. This discrepancy is driven by protected area placement that does not cover the full annual cycle of migratory species, indicating that global efforts toward coordinated conservation planning for migrants are yet to bear fruit. Better-targeted investment and enhanced coordination among countries are needed to conserve migratory species throughout their migratory cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Runge, Claire A -- Watson, James E M -- Butchart, Stuart H M -- Hanson, Jeffrey O -- Possingham, Hugh P -- Fuller, Richard A -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1255-8. doi: 10.1126/science.aac9180.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Geography, Planning and Environmental Management, University of Queensland, Brisbane, QLD, 4072, Australia. National Center for Ecological Analysis and Synthesis (NCEAS), University of California, Santa Barbara, Santa Barbara, CA 93101, USA. claire.runge@uqconnect.edu.au. ; School of Geography, Planning and Environmental Management, University of Queensland, Brisbane, QLD, 4072, Australia. Global Conservation Program, Wildlife Conservation Society, New York, NY, USA. ; BirdLife International, Wellbrook Court, Cambridge CB3 0NA, UK. ; School of Biological Sciences, University of Queensland, Brisbane, QLD 4072, Australia. ; School of Biological Sciences, University of Queensland, Brisbane, QLD 4072, Australia. Department of Life Sciences, Imperial College London, Silwood Park, Ascot, Berkshire SL5 7PY, England, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785490" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Migration ; Animals ; *Birds ; Breeding ; *Conservation of Natural Resources ; Population Dynamics ; Seasons
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  • 13
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cleary, Allison S -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1174-5. doi: 10.1126/science.aad7103.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pennsylvania State University College of Medicine, Hershey PA 17078, USA. acleary@hmc.psu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785463" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/genetics/metabolism/*pathology ; Clone Cells/metabolism/pathology ; Female ; Mammary Neoplasms, Experimental/genetics/metabolism/*pathology ; Mice ; Neoplasms, Basal Cell/genetics/metabolism/pathology ; Wnt1 Protein/genetics/*metabolism ; ras Proteins/genetics/metabolism
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  • 14
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Currie, Janet -- Grenfell, Bryan -- Farrar, Jeremy -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):815-6. doi: 10.1126/science.aad8521.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Princeton University, Woodrow Wilson School, Princeton, NJ 08540, USA. jcurrie@princeton.edu. ; Princeton University, Woodrow Wilson School, Princeton, NJ 08540, USA. ; Wellcome Trust, 215 Euston Road, London NW1 2BE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912880" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Communicable Disease Control/*methods/*organization & administration ; Delivery of Health Care ; Disease Reservoirs ; Epidemics/*prevention & control ; *Global Health ; Hemorrhagic Fever, Ebola/epidemiology/prevention & control ; Humans ; International Cooperation ; Zika Virus Infection/epidemiology/prevention & control ; Zoonoses/prevention & control/transmission
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Loreto, Elgion Lucio Silva -- Wallau, Gabriel Luz -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1273. doi: 10.1126/science.351.6279.1273-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departamento de Bioquimica e Biologia Molecular, Universidade Federal de Santa Maria, Rio Grande do Sul, Brazil. ; Departamento de Entomologia, Centro de Pesquisas Aggeu Magalhaes-FIOCRUZ-CPqAM, Recife, PE, Brazil. gabriel.wallau@cpqam.fiocruz.br.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989241" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Culicidae/drug effects/*microbiology ; Dengue/*prevention & control/transmission ; Insecticides/pharmacology ; Mosquito Control/*methods ; Risk ; *Wolbachia
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  • 16
    Publication Date: 2016-01-02
    Description: CRISPR/Cas9-mediated genome editing holds clinical potential for treating genetic diseases, such as Duchenne muscular dystrophy (DMD), which is caused by mutations in the dystrophin gene. To correct DMD by skipping mutant dystrophin exons in postnatal muscle tissue in vivo, we used adeno-associated virus-9 (AAV9) to deliver gene-editing components to postnatal mdx mice, a model of DMD. Different modes of AAV9 delivery were systematically tested, including intraperitoneal at postnatal day 1 (P1), intramuscular at P12, and retro-orbital at P18. Each of these methods restored dystrophin protein expression in cardiac and skeletal muscle to varying degrees, and expression increased from 3 to 12 weeks after injection. Postnatal gene editing also enhanced skeletal muscle function, as measured by grip strength tests 4 weeks after injection. This method provides a potential means of correcting mutations responsible for DMD and other monogenic disorders after birth.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760628/" 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/PMC4760628/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Long, Chengzu -- Amoasii, Leonela -- Mireault, Alex A -- McAnally, John R -- Li, Hui -- Sanchez-Ortiz, Efrain -- Bhattacharyya, Samadrita -- Shelton, John M -- Bassel-Duby, Rhonda -- Olson, Eric N -- DK-099653/DK/NIDDK NIH HHS/ -- HL-077439/HL/NHLBI NIH HHS/ -- HL-093039/HL/NHLBI NIH HHS/ -- HL-111665/HL/NHLBI NIH HHS/ -- R01 DK099653/DK/NIDDK NIH HHS/ -- R01 HL077439/HL/NHLBI NIH HHS/ -- R01 HL093039/HL/NHLBI NIH HHS/ -- R01 HL111665/HL/NHLBI NIH HHS/ -- U01 HL100401/HL/NHLBI NIH HHS/ -- U01-HL-100401/HL/NHLBI NIH HHS/ -- U54 HD 087351/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):400-3. doi: 10.1126/science.aad5725. Epub 2015 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Sen. Paul D. Wellstone Muscular Dystrophy Cooperative Research Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Sen. Paul D. Wellstone Muscular Dystrophy Cooperative Research Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. eric.olson@utsouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721683" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *CRISPR-Cas Systems ; Dependovirus ; Disease Models, Animal ; Dystrophin/*genetics ; Exons/genetics ; Female ; Forelimb/physiopathology ; Genetic Therapy/*methods ; Genome/genetics ; Hand Strength ; Male ; Mice ; Mice, Inbred mdx ; Muscle, Skeletal/metabolism ; Muscular Dystrophy, Duchenne/genetics/*therapy ; Myocardium/metabolism
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  • 17
    Publication Date: 2016-01-23
    Description: Differentiated macrophages can self-renew in tissues and expand long term in culture, but the gene regulatory mechanisms that accomplish self-renewal in the differentiated state have remained unknown. Here we show that in mice, the transcription factors MafB and c-Maf repress a macrophage-specific enhancer repertoire associated with a gene network that controls self-renewal. Single-cell analysis revealed that, in vivo, proliferating resident macrophages can access this network by transient down-regulation of Maf transcription factors. The network also controls embryonic stem cell self-renewal but is associated with distinct embryonic stem cell-specific enhancers. This indicates that distinct lineage-specific enhancer platforms regulate a shared network of genes that control self-renewal potential in both stem and mature cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soucie, Erinn L -- Weng, Ziming -- Geirsdottir, Laufey -- Molawi, Kaaweh -- Maurizio, Julien -- Fenouil, Romain -- Mossadegh-Keller, Noushine -- Gimenez, Gregory -- VanHille, Laurent -- Beniazza, Meryam -- Favret, Jeremy -- Berruyer, Carole -- Perrin, Pierre -- Hacohen, Nir -- Andrau, J-C -- Ferrier, Pierre -- Dubreuil, Patrice -- Sidow, Arend -- Sieweke, Michael H -- P01AG036695/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):aad5510. doi: 10.1126/science.aad5510. Epub 2016 Jan 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Centre de Recherche en Cancerologie de Marseille, INSERM (U1068), CNRS (U7258), Universite Aix-Marseille (UM105), Marseille, France. sieweke@ciml.univ-mrs.fr erinn.soucie@inserm.fr arend@stanford.edu. ; Department of Pathology, Stanford University, Stanford, CA 94305-5324, USA. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Max-Delbruck-Centrum fur Molekulare Medizin in der Helmholtz-Gemeinschaft, 10 Robert-Rossle-Strasse, 13125 Berlin, Germany. ; Broad Institute of Harvard University and MIT, Cambridge, MA 02142, USA. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Institut de Genetique Moleculaire de Montpellier, CNRS UMR 5535, 1919 Route de Mende, 34293 Montpellier, France. ; Centre de Recherche en Cancerologie de Marseille, INSERM (U1068), CNRS (U7258), Universite Aix-Marseille (UM105), Marseille, France. ; Department of Pathology, Stanford University, Stanford, CA 94305-5324, USA. Department of Genetics, Stanford University, Stanford, CA 94305, USA. sieweke@ciml.univ-mrs.fr erinn.soucie@inserm.fr arend@stanford.edu. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Max-Delbruck-Centrum fur Molekulare Medizin in der Helmholtz-Gemeinschaft, 10 Robert-Rossle-Strasse, 13125 Berlin, Germany. sieweke@ciml.univ-mrs.fr erinn.soucie@inserm.fr arend@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26797145" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/*genetics ; Cell Lineage/*genetics ; Cell Proliferation ; Cells, Cultured ; Down-Regulation ; Embryonic Stem Cells/*cytology ; Enhancer Elements, Genetic/*physiology ; *Gene Expression Regulation ; Gene Regulatory Networks ; Macrophages/*cytology ; MafB Transcription Factor/metabolism ; Mice ; Proto-Oncogene Proteins c-maf/metabolism ; Single-Cell Analysis ; Transcriptional Activation
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  • 18
    Publication Date: 2016-04-02
    Description: Global climate change is a major threat to biodiversity. Large-scale analyses have generally focused on the impacts of climate change on the geographic ranges of species and on phenology, the timing of ecological phenomena. We used long-term monitoring of the abundance of breeding birds across Europe and the United States to produce, for both regions, composite population indices for two groups of species: those for which climate suitability has been either improving or declining since 1980. The ratio of these composite indices, the climate impact indicator (CII), reflects the divergent fates of species favored or disadvantaged by climate change. The trend in CII is positive and similar in the two regions. On both continents, interspecific and spatial variation in population abundance trends are well predicted by climate suitability trends.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stephens, Philip A -- Mason, Lucy R -- Green, Rhys E -- Gregory, Richard D -- Sauer, John R -- Alison, Jamie -- Aunins, Ainars -- Brotons, Lluis -- Butchart, Stuart H M -- Campedelli, Tommaso -- Chodkiewicz, Tomasz -- Chylarecki, Przemyslaw -- Crowe, Olivia -- Elts, Jaanus -- Escandell, Virginia -- Foppen, Ruud P B -- Heldbjerg, Henning -- Herrando, Sergi -- Husby, Magne -- Jiguet, Frederic -- Lehikoinen, Aleksi -- Lindstrom, Ake -- Noble, David G -- Paquet, Jean-Yves -- Reif, Jiri -- Sattler, Thomas -- Szep, Tibor -- Teufelbauer, Norbert -- Trautmann, Sven -- van Strien, Arco J -- van Turnhout, Chris A M -- Vorisek, Petr -- Willis, Stephen G -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):84-7. doi: 10.1126/science.aac4858.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Conservation Ecology Group, School of Biological and Biomedical Sciences, Durham University, South Road, Durham DH1 3LE, UK. ; Royal Society for the Protection of Birds, Centre for Conservation Science, The Lodge, Sandy, Bedfordshire SG19 2DL, UK. ; Royal Society for the Protection of Birds, Centre for Conservation Science, The Lodge, Sandy, Bedfordshire SG19 2DL, UK. Conservation Science Group, Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, UK. ; United States Geological Survey, Patuxent Wildlife Research Center, 12100 Beech Forest Road, Laurel, MD 20708, USA. ; Institute of Integrative Biology, University of Liverpool, Crown Street, Liverpool L69 3BX, UK. ; Faculty of Biology, University of Latvia, Jelgavas iela 1, Riga, LV-1004, Latvia. ; Center for Mediterranean Forest Research, Centre Tecnologic Forestal de Catalunya, InForest JRU, Solsona 25280, Spain. REAF, Cerdanyola del Valles 08193, Catalonia, Spain. CSIC, Cerdanyola del Valles 08193, Catalonia, Spain. ; Conservation Science Group, Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, UK. BirdLife International, The David Attenborough Building, Pembroke Street, Cambridge CB2 3QZ, UK. ; MITO2000 National Committee; c/o Dream Italia, Via Garibaldi 3, 52015, Pratovecchio-Stia, Arezzo, Italy. ; Ogolnopolskie Towarzystwo Ochrony Ptakow, Odrowaza 24,05-270 Marki, Poland. ; Museum and Institute of Zoology, Polish Academy of Sciences, Wilcza 64, 00-679 Warszawa, Poland. ; BirdWatch Ireland, Unit 20 Block D Bullford Business Campus, Kilcoole, County Wicklow, Ireland. ; Institute of Ecology and Earth Sciences, University of Tartu, Vanemuise Street 46, 51014 Tartu, Estonia. Estonian Ornithological Society, Veski 4, 51005 Tartu, Estonia. ; Sociedad Espanola de Ornitologia/BirdLife Melquiades Biencinto, 34, 28053 Madrid. Spain. ; European Bird Census Council, Post Office Box 6521, 6503 GA Nijmegen, Netherlands. Sovon Dutch Centre for Field Ornithology, Post Office Box 6521, 6503 GA Nijmegen, Netherlands. Department of Animal Ecology and Ecophysiology, Institute for Water and Wetland Research, Radboud University, Post Office Box 9010, 6500 GL Nijmegen, Netherlands. ; Dansk Ornitologisk Forening-BirdLife Denmark and University of Aarhus, Vesterbrogade 140, 1620 Kobenhavn V, Denmark. ; European Bird Census Council-Catalan Ornithological Institute, Natural History Museum of Barcelona, Placa Leonardo da Vinci 4-5, 08019 Barcelona, Catalonia, Spain. ; Section for Science, Nord University, 7600 Levanger, Norway. ; UMR7204 Sorbonne Universites-MNHN-CNRS-UPMC, CESCO, CRBPO, CP 135, 43 Rue Buffon, 75005 Paris, France. ; The Helsinki Lab of Ornithology, Finnish Museum of Natural History, Post Office Box 17, 00014 University of Helsinki, Finland. ; Biodiversity Unit, Department of Biology, Lund University, Ecology Building, S-223 62 Lund, Sweden. ; The British Trust for Ornithology, The Nunnery, Thetford, Norfolk IP24 2PU, UK. ; Natagora, Departement Etudes, Rue Nanon 98, B-5000 Namur, Belgium. ; Institute for Environmental Studies, Faculty of Science, Charles University in Prague, Czech Republic. Department of Zoology and Laboratory of Ornithology, Faculty of Science, Palacky University Olomouc, 17 Listopadu 50, 771 43 Olomouc, Czech Republic. ; Swiss Ornithological Institute, Seerose 1, 6204 Sempach, Switzerland. ; Institute of Environmental Sciences, University of Nyiregyhaza, Sostoi ut 31/b, 4400 Nyiregyhaza, Hungary. ; BirdLife Austria, Museumsplatz 1/10/8, A-1070 Vienna, Austria. ; Dachverband Deutscher Avifaunisten e.V. (Federation of German Avifaunists), An den Speichern 6, D-48157 Munster, Germany. ; Statistics Netherlands, Post Office Box 24500, 2490 HA The Hague, Netherlands. ; Sovon Dutch Centre for Field Ornithology, Post Office Box 6521, 6503 GA Nijmegen, Netherlands. Department of Animal Ecology and Ecophysiology, Institute for Water and Wetland Research, Radboud University, Post Office Box 9010, 6500 GL Nijmegen, Netherlands. ; Department of Zoology and Laboratory of Ornithology, Faculty of Science, Palacky University Olomouc, 17 Listopadu 50, 771 43 Olomouc, Czech Republic. Pan-European Common Bird Monitoring Scheme, Czech Society for Ornithology, Na Belidle 252/34, CZ-15000 Prague 5, Czech Republic.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034371" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Migration ; Animals ; Biodiversity ; *Birds ; Breeding ; *Climate Change ; Ecological Parameter Monitoring ; Europe ; Population Dynamics ; United States
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  • 19
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ma, Eric H -- Jones, Russell G -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):670-1. doi: 10.1126/science.aaf1929.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Goodman Cancer Research Centre, Department of Physiology, McGill University, Montreal, QC, H3A 1A3, Canada. Department of Physiology, McGill University, Montreal, QC, H3G 1Y6, Canada. ; Goodman Cancer Research Centre, Department of Physiology, McGill University, Montreal, QC, H3A 1A3, Canada. Department of Physiology, McGill University, Montreal, QC, H3G 1Y6, Canada. russell.jones@mcgill.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Mitochondria/*metabolism ; Multiprotein Complexes/*metabolism ; Purines/*biosynthesis/*metabolism ; TOR Serine-Threonine Kinases/*metabolism ; Tetrahydrofolates/*metabolism
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  • 20
    Publication Date: 2016-01-28
    Description: Hydroxymethylcytosine, well described in DNA, occurs also in RNA. Here, we show that hydroxymethylcytosine preferentially marks polyadenylated RNAs and is deposited by Tet in Drosophila. We map the transcriptome-wide hydroxymethylation landscape, revealing hydroxymethylcytosine in the transcripts of many genes, notably in coding sequences, and identify consensus sites for hydroxymethylation. We found that RNA hydroxymethylation can favor mRNA translation. Tet and hydroxymethylated RNA are found to be most abundant in the Drosophila brain, and Tet-deficient fruitflies suffer impaired brain development, accompanied by decreased RNA hydroxymethylation. This study highlights the distribution, localization, and function of cytosine hydroxymethylation and identifies central roles for this modification in Drosophila.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delatte, Benjamin -- Wang, Fei -- Ngoc, Long Vo -- Collignon, Evelyne -- Bonvin, Elise -- Deplus, Rachel -- Calonne, Emilie -- Hassabi, Bouchra -- Putmans, Pascale -- Awe, Stephan -- Wetzel, Collin -- Kreher, Judith -- Soin, Romuald -- Creppe, Catherine -- Limbach, Patrick A -- Gueydan, Cyril -- Kruys, Veronique -- Brehm, Alexander -- Minakhina, Svetlana -- Defrance, Matthieu -- Steward, Ruth -- Fuks, Francois -- R01 GM089992/GM/NIGMS NIH HHS/ -- T32 CA117846/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):282-5. doi: 10.1126/science.aac5253.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cancer Epigenetics, Faculty of Medicine, ULB Cancer Research Center (U-CRC), Universite Libre de Bruxelles (ULB), Brussels, Belgium. ; Waksman Institute, Department of Molecular Biology and Biochemistry, Cancer Institute of New Jersey, Rutgers University, Piscataway, NJ, USA. ; Laboratory of Molecular Biology of the Gene, Faculty of Sciences, Universite Libre de Bruxelles, Gosselies, Belgium. ; Institut fur Molekularbiologie und Tumorforschung, Philipps-Universitat Marburg, Marburg, Germany. ; Department of Chemistry, University of Cincinnati, Cincinnati, OH, USA. ; Laboratory of Cancer Epigenetics, Faculty of Medicine, ULB Cancer Research Center (U-CRC), Universite Libre de Bruxelles (ULB), Brussels, Belgium. ffuks@ulb.ac.be.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816380" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*abnormalities/metabolism ; Cell Line ; Cytosine/*analogs & derivatives/metabolism ; Dioxygenases/genetics/metabolism ; Drosophila melanogaster/genetics/*growth & development/metabolism ; Methylation ; RNA, Messenger/genetics/*metabolism ; Transcriptome
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  • 21
    Publication Date: 2016-02-26
    Description: T cell-mediated destruction of insulin-producing beta cells in the pancreas causes type 1 diabetes (T1D). CD4 T cell responses play a central role in beta cell destruction, but the identity of the epitopes recognized by pathogenic CD4 T cells remains unknown. We found that diabetes-inducing CD4 T cell clones isolated from nonobese diabetic mice recognize epitopes formed by covalent cross-linking of proinsulin peptides to other peptides present in beta cell secretory granules. These hybrid insulin peptides (HIPs) are antigenic for CD4 T cells and can be detected by mass spectrometry in beta cells. CD4 T cells from the residual pancreatic islets of two organ donors who had T1D also recognize HIPs. Autoreactive T cells targeting hybrid peptides may explain how immune tolerance is broken in T1D.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delong, Thomas -- Wiles, Timothy A -- Baker, Rocky L -- Bradley, Brenda -- Barbour, Gene -- Reisdorph, Richard -- Armstrong, Michael -- Powell, Roger L -- Reisdorph, Nichole -- Kumar, Nitesh -- Elso, Colleen M -- DeNicola, Megan -- Bottino, Rita -- Powers, Alvin C -- Harlan, David M -- Kent, Sally C -- Mannering, Stuart I -- Haskins, Kathryn -- 1K01DK094941/DK/NIDDK NIH HHS/ -- 1R01DK081166/DK/NIDDK NIH HHS/ -- 5U01DK89572/DK/NIDDK NIH HHS/ -- DK104211/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):711-4. doi: 10.1126/science.aad2791.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Microbiology, University of Colorado School of Medicine, Denver, Anschutz Medical Campus, Aurora, CO 80045, USA. thomas.delong@ucdenver.edu katie.haskins@ucdenver.edu. ; Department of Immunology and Microbiology, University of Colorado School of Medicine, Denver, Anschutz Medical Campus, Aurora, CO 80045, USA. ; Pharmaceutical Sciences, University of Colorado School of Medicine, Aurora, CO 80045, USA. ; Immunology and Diabetes Unit, St. Vincent's Institute of Medical Research, 9 Princes Street, Fitzroy, Victoria 3065, Australia. ; Department of Medicine, Diabetes Division, Diabetes Center of Excellence, University of Massachusetts Medical School, Worcester, MA, USA. ; Institute of Cellular Therapeutics, Allegheny-Singer Research Institute, Allegheny Health Network, Pittsburgh, PA, USA. ; Division of Diabetes, Endocrinology, and Metabolism, Department of Medicine, and Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN, USA. VA Tennessee Valley Healthcare System, Nashville, TN, USA. ; Immunology and Diabetes Unit, St. Vincent's Institute of Medical Research, 9 Princes Street, Fitzroy, Victoria 3065, Australia. University of Melbourne, Department of Medicine, St. Vincent's Hospital, Fitzroy, Victoria 3065, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912858" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; C-Peptide/chemistry/*immunology ; CD4-Positive T-Lymphocytes/*immunology ; Clone Cells ; Diabetes Mellitus, Experimental/*immunology/pathology ; Diabetes Mellitus, Type 1/*immunology/pathology ; Epitopes/*immunology ; Immune Tolerance ; Insulin-Secreting Cells/*immunology/pathology ; Mice ; Mice, Inbred NOD ; Molecular Sequence Data ; Peptides/chemistry/immunology
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  • 22
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dobson, Stephen L -- Bordenstein, Seth R -- Rose, Robert I -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):526-7. doi: 10.1126/science.352.6285.526-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Kentucky, Lexington, KY 40546, USA. MosquitoMate Inc., Lexington, KY 40503, USA. sdobson@uky.edu. ; Vanderbilt University, Nashville, TN, 37235, USA. ; Biotechnology Regulatory Consulting, Frederick, MD 21704, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126029" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Culicidae/*microbiology ; Dengue/*prevention & control ; Mosquito Control/*methods ; *Wolbachia
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  • 23
    Publication Date: 2016-04-30
    Description: Wakefulness is driven by the widespread release of neuromodulators by the ascending arousal system. Yet, it is unclear how these substances orchestrate state-dependent, global changes in neuronal activity. Here, we show that neuromodulators induce increases in the extracellular K(+) concentration ([K(+)]e) in cortical slices electrically silenced by tetrodotoxin. In vivo, arousal was linked to AMPA receptor-independent elevations of [K(+)]e concomitant with decreases in [Ca(2+)]e, [Mg(2+)]e, [H(+)]e, and the extracellular volume. Opposite, natural sleep and anesthesia reduced [K(+)]e while increasing [Ca(2+)]e, [Mg(2+)]e, and [H(+)]e as well as the extracellular volume. Local cortical activity of sleeping mice could be readily converted to the stereotypical electroencephalography pattern of wakefulness by simply imposing a change in the extracellular ion composition. Thus, extracellular ions control the state-dependent patterns of neural activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, Fengfei -- O'Donnell, John -- Xu, Qiwu -- Kang, Ning -- Goldman, Nanna -- Nedergaard, Maiken -- NS078167/NS/NINDS NIH HHS/ -- NS078304/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):550-5. doi: 10.1126/science.aad4821.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Translational Neuromedicine, University of Rochester Medical Center, Rochester, NY 14642, USA. Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. ; Center for Translational Neuromedicine, University of Rochester Medical Center, Rochester, NY 14642, USA. ; Center for Translational Neuromedicine, University of Rochester Medical Center, Rochester, NY 14642, USA. Center for Basic and Translational Neuroscience, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen 2200, Denmark. nedergaard@urmc.rochester.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126038" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/analysis/metabolism ; Cations/analysis/*metabolism ; Cerebral Cortex/chemistry/drug effects/*physiology ; Electroencephalography ; Magnesium/analysis/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Neurons/drug effects/metabolism/physiology ; Neurotransmitter Agents/metabolism/pharmacology ; Potassium/*metabolism ; Receptors, AMPA/metabolism ; Sleep/drug effects/*physiology ; Sodium Channel Blockers/pharmacology ; Tetrodotoxin/pharmacology ; Wakefulness/drug effects/*physiology
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  • 24
    Publication Date: 2016-03-19
    Description: Systemic inflammation, which results from the massive release of proinflammatory molecules into the circulatory system, is a major risk factor for severe illness, but the precise mechanisms underlying its control are not fully understood. We observed that prostaglandin E2 (PGE2), through its receptor EP4, is down-regulated in human systemic inflammatory disease. Mice with reduced PGE2 synthesis develop systemic inflammation, associated with translocation of gut bacteria, which can be prevented by treatment with EP4 agonists. Mechanistically, we demonstrate that PGE2-EP4 signaling acts directly on type 3 innate lymphoid cells (ILCs), promoting their homeostasis and driving them to produce interleukin-22 (IL-22). Disruption of the ILC-IL-22 axis impairs PGE2-mediated inhibition of systemic inflammation. Hence, the ILC-IL-22 axis is essential in protecting against gut barrier dysfunction, enabling PGE2-EP4 signaling to impede systemic inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841390/" 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/PMC4841390/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duffin, Rodger -- O'Connor, Richard A -- Crittenden, Siobhan -- Forster, Thorsten -- Yu, Cunjing -- Zheng, Xiaozhong -- Smyth, Danielle -- Robb, Calum T -- Rossi, Fiona -- Skouras, Christos -- Tang, Shaohui -- Richards, James -- Pellicoro, Antonella -- Weller, Richard B -- Breyer, Richard M -- Mole, Damian J -- Iredale, John P -- Anderton, Stephen M -- Narumiya, Shuh -- Maizels, Rick M -- Ghazal, Peter -- Howie, Sarah E -- Rossi, Adriano G -- Yao, Chengcan -- 106122/Wellcome Trust/United Kingdom -- BB/K091121/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- DK37097/DK/NIDDK NIH HHS/ -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1333-8. doi: 10.1126/science.aad9903.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh EH16 4TJ, UK. ; Division of Pathway Medicine, Edinburgh Infectious Diseases, The University of Edinburgh, Edinburgh EH16 4SB, UK. ; Institute for Immunology and Infection Research, The University of Edinburgh, Edinburgh EH9 3JT, UK. ; MRC Centre for Regenerative Medicine, The University of Edinburgh, Edinburgh EH16 4UU, UK. ; Department of Gastroenterology, First Affiliated Hospital of Jinan University, Guangzhou 510630, China. ; Department of Veterans Affairs, Tennessee Valley Health Authority, Nashville, TN 37212, USA. Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA. ; Center for Innovation in Immunoregulative Technology and Therapeutics (AK Project), Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan. Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST), Tokyo 102-0075, Japan. ; Division of Pathway Medicine, Edinburgh Infectious Diseases, The University of Edinburgh, Edinburgh EH16 4SB, UK. Centre for Synthetic and Systems Biology (SynthSys), The University of Edinburgh, Edinburgh EH9 3JD, UK. ; Medical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh EH16 4TJ, UK. chengcan.yao@ed.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Infections/genetics/immunology ; Dinoprostone/*immunology ; Gene Expression ; Humans ; Immunity, Innate ; Inflammation/drug therapy/*immunology/microbiology ; Interleukins/*immunology ; Intestines/*immunology/microbiology ; Lymphocytes/*immunology ; Mice ; Receptors, Prostaglandin E, EP4 Subtype/antagonists & ; inhibitors/genetics/*immunology ; Signal Transduction
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  • 25
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: Transposable elements (TEs) are both a boon and a bane to eukaryotic organisms, depending on where they integrate into the genome and how their sequences function once integrated. We focus on two types of TEs: long interspersed elements (LINEs) and short interspersed elements (SINEs). LINEs and SINEs are retrotransposons; that is, they transpose via an RNA intermediate. We discuss how LINEs and SINEs have expanded in eukaryotic genomes and contribute to genome evolution. An emerging body of evidence indicates that LINEs and SINEs function to regulate gene expression by affecting chromatin structure, gene transcription, pre-mRNA processing, or aspects of mRNA metabolism. We also describe how adenosine-to-inosine editing influences SINE function and how ongoing retrotransposition is countered by the body's defense mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elbarbary, Reyad A -- Lucas, Bronwyn A -- Maquat, Lynne E -- P30 AR061307/AR/NIAMS NIH HHS/ -- R37 GM074593/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):aac7247. doi: 10.1126/science.aac7247. Epub 2016 Feb 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA. Center for RNA Biology, University of Rochester, Rochester, NY, USA. ; Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA. Center for RNA Biology, University of Rochester, Rochester, NY, USA. Department of Oncology, Wilmot Cancer Institute, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA. lynne_maquat@urmc.rochester.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912865" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/ultrastructure ; Disease/genetics ; Evolution, Molecular ; *Gene Expression Regulation ; Humans ; Long Interspersed Nucleotide Elements/genetics/*physiology ; Mice ; Protein Biosynthesis ; RNA Precursors/metabolism ; RNA Processing, Post-Transcriptional ; RNA Stability ; RNA, Messenger/metabolism ; Short Interspersed Nucleotide Elements/genetics/*physiology ; Transcription, Genetic
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  • 26
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tuting, Thomas -- de Visser, Karin E -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):145-6. doi: 10.1126/science.aaf7300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, University Hospital Magdeburg, Magdeburg, Germany. ; Division of Immunology, The Netherlands Cancer Institute, Amsterdam, Netherlands. k.d.visser@nki.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124439" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bystander Effect ; Humans ; Immunotherapy/methods ; Leukocyte Count ; Mice ; Mice, Transgenic ; Neoplasm Metastasis/*immunology/*therapy ; Neoplasms, Experimental/immunology/pathology/therapy ; Neutrophils/*immunology/*pathology
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  • 27
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):799-800. doi: 10.1126/science.351.6275.799.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912871" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Brain Mapping/economics/*methods ; DNA/*analysis ; Financing, Organized ; Fluorescence ; Mice ; Nerve Net/physiology ; Neurons/*chemistry ; Neurosciences/economics/trends ; RNA/*analysis ; Synapses/*physiology
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  • 28
    Publication Date: 2016-01-28
    Description: Muscle contraction depends on release of Ca(2+) from the sarcoplasmic reticulum (SR) and reuptake by the Ca(2+)adenosine triphosphatase SERCA. We discovered a putative muscle-specific long noncoding RNA that encodes a peptide of 34 amino acids and that we named dwarf open reading frame (DWORF). DWORF localizes to the SR membrane, where it enhances SERCA activity by displacing the SERCA inhibitors, phospholamban, sarcolipin, and myoregulin. In mice, overexpression of DWORF in cardiomyocytes increases peak Ca(2+) transient amplitude and SR Ca(2+) load while reducing the time constant of cytosolic Ca(2+) decay during each cycle of contraction-relaxation. Conversely, slow skeletal muscle lacking DWORF exhibits delayed Ca(2+) clearance and relaxation and reduced SERCA activity. DWORF is the only endogenous peptide known to activate the SERCA pump by physical interaction and provides a means for enhancing muscle contractility.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, Benjamin R -- Makarewich, Catherine A -- Anderson, Douglas M -- Winders, Benjamin R -- Troupes, Constantine D -- Wu, Fenfen -- Reese, Austin L -- McAnally, John R -- Chen, Xiongwen -- Kavalali, Ege T -- Cannon, Stephen C -- Houser, Steven R -- Bassel-Duby, Rhonda -- Olson, Eric N -- AR-063182/AR/NIAMS NIH HHS/ -- DK-099653/DK/NIDDK NIH HHS/ -- F30AR 067094/AR/NIAMS NIH HHS/ -- HL-077439,/HL/NHLBI NIH HHS/ -- HL-093039/HL/NHLBI NIH HHS/ -- HL-111665/HL/NHLBI NIH HHS/ -- R01 AR063182/AR/NIAMS NIH HHS/ -- U01-HL-100401/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):271-5. doi: 10.1126/science.aad4076.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Physiology, Temple University School of Medicine, Philadelphia, PA 19140, USA. Department of Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA 19140, USA. ; Department of Neurology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Department of Physiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. eric.olson@utsouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816378" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Binding Proteins/metabolism ; Humans ; Mice ; Mice, Knockout ; *Muscle Contraction ; Muscle Proteins/metabolism ; Muscle, Skeletal/*metabolism ; Myocardial Contraction ; Myocytes, Cardiac/*metabolism ; Peptides/genetics/*metabolism ; Proteolipids/metabolism ; RNA, Long Noncoding/genetics/metabolism ; Sarcoplasmic Reticulum/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/*metabolism ; Transcription, Genetic
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  • 29
    Publication Date: 2016-01-02
    Description: Duchenne muscular dystrophy (DMD) is a devastating disease affecting about 1 out of 5000 male births and caused by mutations in the dystrophin gene. Genome editing has the potential to restore expression of a modified dystrophin gene from the native locus to modulate disease progression. In this study, adeno-associated virus was used to deliver the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 system to the mdx mouse model of DMD to remove the mutated exon 23 from the dystrophin gene. This includes local and systemic delivery to adult mice and systemic delivery to neonatal mice. Exon 23 deletion by CRISPR-Cas9 resulted in expression of the modified dystrophin gene, partial recovery of functional dystrophin protein in skeletal myofibers and cardiac muscle, improvement of muscle biochemistry, and significant enhancement of muscle force. This work establishes CRISPR-Cas9-based genome editing as a potential therapy to treat DMD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, Christopher E -- Hakim, Chady H -- Ousterout, David G -- Thakore, Pratiksha I -- Moreb, Eirik A -- Castellanos Rivera, Ruth M -- Madhavan, Sarina -- Pan, Xiufang -- Ran, F Ann -- Yan, Winston X -- Asokan, Aravind -- Zhang, Feng -- Duan, Dongsheng -- Gersbach, Charles A -- DP1-MH100706/DP/NCCDPHP CDC HHS/ -- DP2-OD008586/OD/NIH HHS/ -- P01HL112761/HL/NHLBI NIH HHS/ -- R01DK097768/DK/NIDDK NIH HHS/ -- R01HL089221/HL/NHLBI NIH HHS/ -- R01NS90634/NS/NINDS NIH HHS/ -- T32GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):403-7. doi: 10.1126/science.aad5143. Epub 2015 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Engineering, Duke University, Durham, NC, USA. Center for Genomic and Computational Biology, Duke University, Durham, NC, USA. ; Department of Molecular Microbiology and Immunology, University of Missouri, Columbia, MO, USA. ; Gene Therapy Center, Departments of Genetics, Biochemistry and Biophysics, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. Society of Fellows, Harvard University, Cambridge, MA, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. Graduate Program in Biophysics, Harvard Medical School, Boston, MA, USA. Harvard-MIT Division of Health Sciences and Technology, Harvard Medical School, Boston, MA, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. McGovern Institute for Brain Research, Massachusetts Institute of Technology, Cambridge, MA, USA. Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA. Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA. ; Department of Molecular Microbiology and Immunology, University of Missouri, Columbia, MO, USA. Department of Neurology, University of Missouri, Columbia, MO, USA. ; Department of Biomedical Engineering, Duke University, Durham, NC, USA. Center for Genomic and Computational Biology, Duke University, Durham, NC, USA. Department of Orthopaedic Surgery, Duke University Medical Center, Durham, NC, USA. charles.gersbach@duke.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721684" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *CRISPR-Cas Systems ; Clustered Regularly Interspaced Short Palindromic Repeats ; Dependovirus ; Disease Models, Animal ; Dystrophin/*genetics ; Exons/*genetics ; Genetic Therapy/*methods ; Male ; Mice ; Mice, Inbred mdx ; Muscle, Skeletal/*metabolism ; Muscular Dystrophy, Duchenne/genetics/*therapy ; Sequence Deletion
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  • 30
    Publication Date: 2016-04-23
    Description: The general view that only adaptive immunity can build immunological memory has recently been challenged. In organisms lacking adaptive immunity, as well as in mammals, the innate immune system can mount resistance to reinfection, a phenomenon termed "trained immunity" or "innate immune memory." Trained immunity is orchestrated by epigenetic reprogramming, broadly defined as sustained changes in gene expression and cell physiology that do not involve permanent genetic changes such as mutations and recombination, which are essential for adaptive immunity. The discovery of trained immunity may open the door for novel vaccine approaches, new therapeutic strategies for the treatment of immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Netea, Mihai G -- Joosten, Leo A B -- Latz, Eicke -- Mills, Kingston H G -- Natoli, Gioacchino -- Stunnenberg, Hendrik G -- O'Neill, Luke A J -- Xavier, Ramnik J -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):aaf1098. doi: 10.1126/science.aaf1098. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, Netherlands. mihai.netea@radboudumc.nl. ; Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, Netherlands. ; Institute of Innate Immunity, Bonn University, Bonn, Germany. Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA. German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany. ; School of Biochemistry and Immunology, Trinity College, Dublin, Ireland. ; Department of Experimental Oncology, European Institute of Oncology, Milan, Italy. ; Department of Molecular Biology, Faculties of Science and Medicine, Radboud Institute of Molecular Life Sciences, Radboud University, Nijmegen, Netherlands. ; The Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Center for Computational and Integrative Biology and Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102489" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Methylation ; Epigenesis, Genetic ; Histones/metabolism ; Humans ; Immunity, Innate/genetics/*immunology ; Immunologic Memory/genetics/*immunology ; Infection/*immunology ; Inflammation/immunology ; Invertebrates/immunology ; Plants/immunology ; Transcription, Genetic ; Vaccination ; Vaccines/*immunology
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  • 31
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Neill, Scott L -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):526. doi: 10.1126/science.352.6285.526-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Eliminate Dengue Program, School of Biological Sciences, Monash University, Clayton, Victoria 3800, Australia. scott.oneill@monash.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126028" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Culicidae/*microbiology ; Dengue/*prevention & control ; Mosquito Control/*methods ; *Wolbachia
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  • 32
    Publication Date: 2016-03-19
    Description: Expansions of a hexanucleotide repeat (GGGGCC) in the noncoding region of the C9orf72 gene are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. Decreased expression of C9orf72 is seen in expansion carriers, suggesting that loss of function may play a role in disease. We found that two independent mouse lines lacking the C9orf72 ortholog (3110043O21Rik) in all tissues developed normally and aged without motor neuron disease. Instead, C9orf72 null mice developed progressive splenomegaly and lymphadenopathy with accumulation of engorged macrophage-like cells. C9orf72 expression was highest in myeloid cells, and the loss of C9orf72 led to lysosomal accumulation and altered immune responses in macrophages and microglia, with age-related neuroinflammation similar to C9orf72 ALS but not sporadic ALS human patient tissue. Thus, C9orf72 is required for the normal function of myeloid cells, and altered microglial function may contribute to neurodegeneration in C9orf72 expansion carriers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Rourke, J G -- Bogdanik, L -- Yanez, A -- Lall, D -- Wolf, A J -- Muhammad, A K M G -- Ho, R -- Carmona, S -- Vit, J P -- Zarrow, J -- Kim, K J -- Bell, S -- Harms, M B -- Miller, T M -- Dangler, C A -- Underhill, D M -- Goodridge, H S -- Lutz, C M -- Baloh, R H -- GM085796/GM/NIGMS NIH HHS/ -- NS069669/NS/NINDS NIH HHS/ -- NS078398/NS/NINDS NIH HHS/ -- NS087351/NS/NINDS NIH HHS/ -- UL1TR000124/TR/NCATS NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1324-9. doi: 10.1126/science.aaf1064.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Board of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. ; The Jackson Laboratory, Bar Harbor, ME, USA. ; Division of Biomedical Sciences, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. ; Department of Neurology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA. ; Board of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. Department of Neurology, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989253" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/immunology ; Amyotrophic Lateral Sclerosis/genetics/*immunology ; Animals ; Frontotemporal Dementia/genetics/*immunology ; Gene Knockdown Techniques ; Guanine Nucleotide Exchange Factors/genetics/*physiology ; Heterozygote ; Humans ; Lymphatic Diseases/genetics/immunology ; Macrophages/*immunology ; Mice ; Mice, Knockout ; Microglia/*immunology ; Myeloid Cells/*immunology ; Proteins/genetics/*physiology ; Rats ; Splenomegaly/genetics/immunology
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  • 33
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1250-1. doi: 10.1126/science.351.6279.1250. Epub 2016 Mar 17.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989228" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asia ; Biological Evolution ; Bone and Bones ; DNA/genetics ; Europe ; Female ; Fossils ; Humans ; Male ; *Mating Preference, Animal ; Neanderthals/*genetics/*psychology ; *Sexual Behavior
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  • 34
    Publication Date: 2016-04-30
    Description: Recent studies in human populations and mouse models reveal notable congruences in gut microbial taxa whose abundances are partly regulated by host genotype. Host genes associating with these taxa are related to diet sensing, metabolism, and immunity. These broad patterns are further validated in similar studies of nonmammalian microbiomes. The next generation of genome-wide association studies will expand the size of the data sets and refine the microbial phenotypes to fully capture these intriguing signatures of host-microbiome coevolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodrich, Julia K -- Davenport, Emily R -- Waters, Jillian L -- Clark, Andrew G -- Ley, Ruth E -- R01 DK093595/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):532-5. doi: 10.1126/science.aad9379.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Cornell University, Ithaca NY, USA. ; Department of Molecular Biology and Genetics, Cornell University, Ithaca NY, USA. Department of Microbiome Science, Max Planck Institute for Developmental Biology, Tubingen, Germany. ; Department of Molecular Biology and Genetics, Cornell University, Ithaca NY, USA. Department of Microbiology, Cornell University, Ithaca NY, USA. Department of Microbiome Science, Max Planck Institute for Developmental Biology, Tubingen, Germany. rel222@cornell.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126034" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/*classification/genetics ; Diet ; *Genome-Wide Association Study ; Genotype ; Humans ; Mice ; Microbiota/genetics/*physiology ; Phenotype ; *Quantitative Trait Loci ; Species Specificity
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  • 35
    Publication Date: 2016-03-26
    Description: Cell assembly sequences during learning are "replayed" during hippocampal ripples and contribute to the consolidation of episodic memories. However, neuronal sequences may also reflect preexisting dynamics. We report that sequences of place-cell firing in a novel environment are formed from a combination of the contributions of a rigid, predominantly fast-firing subset of pyramidal neurons with low spatial specificity and limited change across sleep-experience-sleep and a slow-firing plastic subset. Slow-firing cells, rather than fast-firing cells, gained high place specificity during exploration, elevated their association with ripples, and showed increased bursting and temporal coactivation during postexperience sleep. Thus, slow- and fast-firing neurons, although forming a continuous distribution, have different coding and plastic properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grosmark, Andres D -- Buzsaki, Gyorgy -- MH102840/MH/NIMH NIH HHS/ -- MH54671/MH/NIMH NIH HHS/ -- NS075015/NS/NINDS NIH HHS/ -- R01 MH107396/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1440-3. doi: 10.1126/science.aad1935.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Columbia University Medical Center, New York, NY 10019, USA. The Neuroscience Institute, School of Medicine, New York University, New York, NY 10016, USA. ; The Neuroscience Institute, School of Medicine, New York University, New York, NY 10016, USA. Center for Neural Science, New York University, New York, NY 10016, USA. gyorgy.buzsaki@nyumc.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013730" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Hippocampus/cytology/*physiopathology ; Learning/*physiology ; Male ; Maze Learning ; Neuronal Plasticity ; Pyramidal Cells/*physiology ; Rats ; Rats, Inbred LEC ; Sleep/physiology
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  • 36
    Publication Date: 2016-01-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Winemiller, K O -- McIntyre, P B -- Castello, L -- Fluet-Chouinard, E -- Giarrizzo, T -- Nam, S -- Baird, I G -- Darwall, W -- Lujan, N K -- Harrison, I -- Stiassny, M L J -- Silvano, R A M -- Fitzgerald, D B -- Pelicice, F M -- Agostinho, A A -- Gomes, L C -- Albert, J S -- Baran, E -- Petrere, M Jr -- Zarfl, C -- Mulligan, M -- Sullivan, J P -- Arantes, C C -- Sousa, L M -- Koning, A A -- Hoeinghaus, D J -- Sabaj, M -- Lundberg, J G -- Armbruster, J -- Thieme, M L -- Petry, P -- Zuanon, J -- Torrente Vilara, G -- Snoeks, J -- Ou, C -- Rainboth, W -- Pavanelli, C S -- Akama, A -- van Soesbergen, A -- Saenz, L -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):128-9. doi: 10.1126/science.aac7082.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉See supplementary materials for author affiliations. k-winemiller@tamu.edu. ; See supplementary materials for author affiliations.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744397" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; Congo ; Conservation of Natural Resources ; Fisheries ; *Fishes ; Fresh Water ; Mekong Valley ; *Power Plants ; Risk ; *Rivers
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  • 37
    Publication Date: 2016-04-16
    Description: Coral bleaching events threaten the sustainability of the Great Barrier Reef (GBR). Here we show that bleaching events of the past three decades have been mitigated by induced thermal tolerance of reef-building corals, and this protective mechanism is likely to be lost under near-future climate change scenarios. We show that 75% of past thermal stress events have been characterized by a temperature trajectory that subjects corals to a protective, sub-bleaching stress, before reaching temperatures that cause bleaching. Such conditions confer thermal tolerance, decreasing coral cell mortality and symbiont loss during bleaching by over 50%. We find that near-future increases in local temperature of as little as 0.5 degrees C result in this protective mechanism being lost, which may increase the rate of degradation of the GBR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ainsworth, Tracy D -- Heron, Scott F -- Ortiz, Juan Carlos -- Mumby, Peter J -- Grech, Alana -- Ogawa, Daisie -- Eakin, C Mark -- Leggat, William -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):338-42. doi: 10.1126/science.aac7125.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Australian Research Council Centre of Excellence for Coral Reef Studies, James Cook University, Townsville 4810, Australia. ; Coral Reef Watch, U.S. National Oceanic and Atmospheric Administration (NOAA), College Park, MD 20740, USA. Marine Geophysical Laboratory, College of Science, Technology and Engineering, James Cook University, Townsville 4811, Australia. ; Marine Spatial Ecology Lab, School of Biological Sciences, University of Queensland, Brisbane 4072, Australia. Australian Research Council Centre of Excellence for Coral Reef Studies, University of Queensland, Brisbane 4072, Australia. ; Department of Environmental Sciences, Macquarie University, Sydney 2109, Australia. ; Australian Research Council Centre of Excellence for Coral Reef Studies, James Cook University, Townsville 4810, Australia. The College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville 4810, Australia. ; Coral Reef Watch, U.S. National Oceanic and Atmospheric Administration (NOAA), College Park, MD 20740, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081069" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthozoa/cytology/*physiology ; Cell Count ; Cell Death ; *Climate Change ; *Coral Reefs ; Dinoflagellida/cytology/physiology ; *Heat-Shock Response ; Hot Temperature ; Photosynthesis ; Pigments, Biological/*physiology ; Symbiosis
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  • 38
    Publication Date: 2016-02-26
    Description: Bruns and Taylor argue that our finding of widespread distribution among Glomeromycota "virtual taxa" is undermined by the species definition applied. Although identifying appropriate species concepts and accessing taxonomically informative traits are challenges for microorganism biogeography, the virtual taxa represent a pragmatic classification that corresponds approximately to the species rank of classical Glomeromycota taxonomy, yet is applicable to environmental DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Opik, Maarja -- Davison, John -- Moora, Mari -- Partel, Meelis -- Zobel, Martin -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):826. doi: 10.1126/science.aad5495.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Botany, University of Tartu, 40 Lai Street, 51005 Tartu, Estonia. maarja.opik@ut.ee. ; Department of Botany, University of Tartu, 40 Lai Street, 51005 Tartu, Estonia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912890" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Ecosystem ; Humans ; *Mycorrhizae ; Plant Roots/*microbiology ; *Symbiosis
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  • 39
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Payre, Francois -- Desplan, Claude -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):226-7. doi: 10.1126/science.aad9873.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre de Biologie du Developpement, CNRS UMR5547, Universite Paul Sabatier, Toulouse, France. ; Department of Biology, New York University, New York, NY, USA. claude.desplan@nyu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816363" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; *Muscle Contraction ; Muscle, Skeletal/*metabolism ; Myocytes, Cardiac/*metabolism ; Peptides/*metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/*metabolism
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  • 40
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):802. doi: 10.1126/science.351.6275.802.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912873" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Child Development ; Child, Preschool ; *Gastrointestinal Microbiome ; Germ-Free Life ; Growth Disorders/*microbiology/*therapy ; Humans ; Infant ; Malnutrition/*therapy ; Mice ; Muscle Development ; Osteogenesis ; Translational Medical Research
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  • 41
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):433. doi: 10.1126/science.351.6272.433.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823406" target="_blank"〉PubMed〈/a〉
    Keywords: Anaerobiosis/genetics/physiology ; Animals ; Anoxia/*physiopathology ; Fundulidae/genetics/*physiology ; Humans ; MicroRNAs/genetics/metabolism ; Oxygen/*metabolism ; Stroke/*physiopathology ; gamma-Aminobutyric Acid/metabolism
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  • 42
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):647. doi: 10.1126/science.351.6274.647.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912835" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Shells/*anatomy & histology ; Animals ; Bees ; Biomechanical Phenomena ; Cockroaches/*anatomy & histology ; Robotics/*trends ; Wasps
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  • 43
    Publication Date: 2016-03-12
    Description: Scavenger receptor BI (SR-BI) is the major receptor for high-density lipoprotein (HDL) cholesterol (HDL-C). In humans, high amounts of HDL-C in plasma are associated with a lower risk of coronary heart disease (CHD). Mice that have depleted Scarb1 (SR-BI knockout mice) have markedly elevated HDL-C levels but, paradoxically, increased atherosclerosis. The impact of SR-BI on HDL metabolism and CHD risk in humans remains unclear. Through targeted sequencing of coding regions of lipid-modifying genes in 328 individuals with extremely high plasma HDL-C levels, we identified a homozygote for a loss-of-function variant, in which leucine replaces proline 376 (P376L), in SCARB1, the gene encoding SR-BI. The P376L variant impairs posttranslational processing of SR-BI and abrogates selective HDL cholesterol uptake in transfected cells, in hepatocyte-like cells derived from induced pluripotent stem cells from the homozygous subject, and in mice. Large population-based studies revealed that subjects who are heterozygous carriers of the P376L variant have significantly increased levels of plasma HDL-C. P376L carriers have a profound HDL-related phenotype and an increased risk of CHD (odds ratio = 1.79, which is statistically significant).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zanoni, Paolo -- Khetarpal, Sumeet A -- Larach, Daniel B -- Hancock-Cerutti, William F -- Millar, John S -- Cuchel, Marina -- DerOhannessian, Stephanie -- Kontush, Anatol -- Surendran, Praveen -- Saleheen, Danish -- Trompet, Stella -- Jukema, J Wouter -- De Craen, Anton -- Deloukas, Panos -- Sattar, Naveed -- Ford, Ian -- Packard, Chris -- Majumder, Abdullah al Shafi -- Alam, Dewan S -- Di Angelantonio, Emanuele -- Abecasis, Goncalo -- Chowdhury, Rajiv -- Erdmann, Jeanette -- Nordestgaard, Borge G -- Nielsen, Sune F -- Tybjaerg-Hansen, Anne -- Schmidt, Ruth Frikke -- Kuulasmaa, Kari -- Liu, Dajiang J -- Perola, Markus -- Blankenberg, Stefan -- Salomaa, Veikko -- Mannisto, Satu -- Amouyel, Philippe -- Arveiler, Dominique -- Ferrieres, Jean -- Muller-Nurasyid, Martina -- Ferrario, Marco -- Kee, Frank -- Willer, Cristen J -- Samani, Nilesh -- Schunkert, Heribert -- Butterworth, Adam S -- Howson, Joanna M M -- Peloso, Gina M -- Stitziel, Nathan O -- Danesh, John -- Kathiresan, Sekar -- Rader, Daniel J -- CHD Exome+ Consortium -- CARDIoGRAM Exome Consortium -- Global Lipids Genetics Consortium -- R01 DK089256/DK/NIDDK NIH HHS/ -- R01 HL117078/HL/NHLBI NIH HHS/ -- TL1 RR024133/RR/NCRR NIH HHS/ -- TL1R000138/PHS HHS/ -- TL1RR024133/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1166-71. doi: 10.1126/science.aad3517.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Genetics and Medicine, Division of Translational Medicine and Human Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Departments of Genetics and Medicine, Division of Translational Medicine and Human Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. INSERM UMR 1166 ICAN, Universite Pierre et Marie Curie Paris 6, Hopital de la Pitie, Paris, France. ; INSERM UMR 1166 ICAN, Universite Pierre et Marie Curie Paris 6, Hopital de la Pitie, Paris, France. ; Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. ; Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. Department of Biostatistics and Epidemiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Centre for Non-Communicable Diseases, Karachi, Pakistan. ; Department of Gerontology and Geriatrics, Leiden University Medical Center, Leiden, Netherlands. Department of Cardiology, Leiden University Medical Center, Leiden, Netherlands. ; Department of Cardiology, Leiden University Medical Center, Leiden, Netherlands. The Interuniversity Cardiology Institute of the Netherlands, Utrecht, Netherlands. ; Department of Gerontology and Geriatrics, Leiden University Medical Center, Leiden, Netherlands. ; Wellcome Trust Sanger Institute, Genome Campus, Hinxton, UK. ; Institute of Cardiovascular and Medical Sciences, British Heart Foundation, Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, UK. ; Robertson Center for Biostatistics, University of Glasgow, Glasgow, UK. ; Glasgow Clinical Research Facility, Western Infirmary, Glasgow, UK. ; National Institute of Cardiovascular Diseases, Sher-e-Bangla Nagar, Dhaka, Bangladesh. ; International Centre for Diarrhoeal Disease Research, Mohakhali, Dhaka, Bangladesh. ; Center for Statistical Genetics, Department of Biostatistics, University of Michigan School of Public Health, Ann Arbor, MI 48109, USA. ; Institute for Integrative and Experimental Genomics, University of Lubeck, Lubeck 23562, Germany. ; Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, Herlev, Denmark. ; Copenhagen University Hospital, University of Copenhagen, Copenhagen, Denmark. ; Department of Clinical Biochemistry, Rigshospitalet, Copenhagen University Hospitals, Copenhagen, Denmark. ; Department of Health, National Institute for Health and Welfare, Helsinki, Finland. ; Department of Public Health Sciences, College of Medicine, Pennsylvania State University, Hershey, PA 17033, USA. ; Department of Health, National Institute for Health and Welfare, Helsinki, Finland. Institute of Molecular Medicine FIMM, University of Helsinki, Helsinki, Finland. ; Department of General and Interventional Cardiology, University Heart Center Hamburg, Hamburg, Germany. University Medical Center Hamburg-Eppendorf, Hamburg, Germany. ; Department of Epidemiology and Public Health, Institut Pasteur de Lille, Lille, France. ; Department of Epidemiology and Public Health, University of Strasbourg, Strasbourg, France. ; Department of Epidemiology, Toulouse University-CHU Toulouse, Toulouse, France. ; Institute of Genetic Epidemiology, Helmholtz Zentrum Munchen-German Research Center for Environmental Health, Neuherberg, Germany. Department of Medicine I, Ludwig-Maximilians-University Munich, Munich, Germany. ; Research Centre in Epidemiology and Preventive Medicine, Department of Clinical and Experimental Medicine, University of Insubria, Varese, Italy. ; UKCRC Centre of Excellence for Public Health, Queens University, Belfast, Northern Ireland. ; Department of Computational Medicine and Bioinformatics, Department of Human Genetics, and Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA. ; Department of Cardiovascular Sciences, University of Leicester, Leicester, UK. National Institute for Health Research (NIHR) Leicester Cardiovascular Biomedical Research Unit, Glenfield Hotel, Leicester, UK. ; Deutsches Herzzentrum Munchen, Technische Universitat Munchen, Munich, Germany. ; Broad Institute and Center for Human Genetic Research, Massachusetts General Hospital, Boston, MA 02114, USA. ; Department of Medicine, Division of Cardiology, Department of Genetics, and the McDonnell Genome Institute, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. Wellcome Trust Sanger Institute, Genome Campus, Hinxton, UK. ; Departments of Genetics and Medicine, Division of Translational Medicine and Human Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. rader@mail.med.upenn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965621" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Amino Acid Substitution ; Animals ; Cholesterol, HDL/*blood ; Coronary Disease/*blood/*genetics ; DNA Mutational Analysis ; Female ; Genetic Variation ; Heterozygote ; Homozygote ; Humans ; Leucine/genetics ; Male ; Mice ; Middle Aged ; Proline/genetics ; Protein Processing, Post-Translational ; Risk ; Scavenger Receptors, Class B/*genetics/metabolism
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