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  • Female  (308)
  • *Ecosystem  (170)
  • 2010-2014  (471)
  • 1980-1984
  • 2010  (471)
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  • 2010-2014  (471)
  • 1980-1984
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  • 1
    Publication Date: 2010-12-24
    Description: Impulsivity, describing action without foresight, is an important feature of several psychiatric diseases, suicidality and violent behaviour. The complex origins of impulsivity hinder identification of the genes influencing it and the diseases with which it is associated. Here we perform exon-focused sequencing of impulsive individuals in a founder population, targeting fourteen genes belonging to the serotonin and dopamine domain. A stop codon in HTR2B was identified that is common (minor allele frequency 〉 1%) but exclusive to Finnish people. Expression of the gene in the human brain was assessed, as well as the molecular functionality of the stop codon, which was associated with psychiatric diseases marked by impulsivity in both population and family-based analyses. Knockout of Htr2b increased impulsive behaviours in mice, indicative of predictive validity. Our study shows the potential for identifying and tracing effects of rare alleles in complex behavioural phenotypes using founder populations, and indicates a role for HTR2B in impulsivity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183507/" 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/PMC3183507/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bevilacqua, Laura -- Doly, Stephane -- Kaprio, Jaakko -- Yuan, Qiaoping -- Tikkanen, Roope -- Paunio, Tiina -- Zhou, Zhifeng -- Wedenoja, Juho -- Maroteaux, Luc -- Diaz, Silvina -- Belmer, Arnaud -- Hodgkinson, Colin A -- Dell'osso, Liliana -- Suvisaari, Jaana -- Coccaro, Emil -- Rose, Richard J -- Peltonen, Leena -- Virkkunen, Matti -- Goldman, David -- AA-09203/AA/NIAAA NIH HHS/ -- AA-12502/AA/NIAAA NIH HHS/ -- Z01 AA000301-09/Intramural NIH HHS/ -- Z01 AA000301-10/Intramural NIH HHS/ -- Z99 AA999999/Intramural NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1061-6. doi: 10.1038/nature09629.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, NIH, Rockville, Maryland 20852, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179162" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Case-Control Studies ; Cell Line ; Female ; Finland ; Founder Effect ; Gene Expression Regulation ; Gene Knockout Techniques ; Genotype ; Humans ; Impulsive Behavior/*genetics ; Male ; Mental Disorders/genetics ; Mice ; Mice, 129 Strain ; Mice, Knockout ; Pedigree ; Polymorphism, Single Nucleotide/genetics ; Receptor, Serotonin, 5-HT2B/*genetics/*metabolism ; Testosterone/blood/cerebrospinal fluid
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Nature Publishing Group (NPG)
    Publication Date: 2010-12-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ahmed, Farooq -- England -- Nature. 2010 Dec 23;468(7327):S20. doi: 10.1038/468S20a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179081" target="_blank"〉PubMed〈/a〉
    Keywords: *Epigenomics ; Female ; Fetal Nutrition Disorders ; Humans ; *Maternal Nutritional Physiological Phenomena ; Obesity ; Pregnancy ; *Prenatal Exposure Delayed Effects ; Starvation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Nature Publishing Group (NPG)
    Publication Date: 2010-12-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Callaway, Ewen -- England -- Nature. 2010 Dec 23;468(7327):1012. doi: 10.1038/4681012a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179140" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Female ; *Fossils ; Genome/*genetics ; Hominidae/classification/*genetics ; Humans
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2010-12-24
    Description: Drosophila melanogaster is one of the most well studied genetic model organisms; nonetheless, its genome still contains unannotated coding and non-coding genes, transcripts, exons and RNA editing sites. Full discovery and annotation are pre-requisites for understanding how the regulation of transcription, splicing and RNA editing directs the development of this complex organism. Here we used RNA-Seq, tiling microarrays and cDNA sequencing to explore the transcriptome in 30 distinct developmental stages. We identified 111,195 new elements, including thousands of genes, coding and non-coding transcripts, exons, splicing and editing events, and inferred protein isoforms that previously eluded discovery using established experimental, prediction and conservation-based approaches. These data substantially expand the number of known transcribed elements in the Drosophila genome and provide a high-resolution view of transcriptome dynamics throughout development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075879/" 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/PMC3075879/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graveley, Brenton R -- Brooks, Angela N -- Carlson, Joseph W -- Duff, Michael O -- Landolin, Jane M -- Yang, Li -- Artieri, Carlo G -- van Baren, Marijke J -- Boley, Nathan -- Booth, Benjamin W -- Brown, James B -- Cherbas, Lucy -- Davis, Carrie A -- Dobin, Alex -- Li, Renhua -- Lin, Wei -- Malone, John H -- Mattiuzzo, Nicolas R -- Miller, David -- Sturgill, David -- Tuch, Brian B -- Zaleski, Chris -- Zhang, Dayu -- Blanchette, Marco -- Dudoit, Sandrine -- Eads, Brian -- Green, Richard E -- Hammonds, Ann -- Jiang, Lichun -- Kapranov, Phil -- Langton, Laura -- Perrimon, Norbert -- Sandler, Jeremy E -- Wan, Kenneth H -- Willingham, Aarron -- Zhang, Yu -- Zou, Yi -- Andrews, Justen -- Bickel, Peter J -- Brenner, Steven E -- Brent, Michael R -- Cherbas, Peter -- Gingeras, Thomas R -- Hoskins, Roger A -- Kaufman, Thomas C -- Oliver, Brian -- Celniker, Susan E -- U01 HB004271/HB/NHLBI NIH HHS/ -- U01 HG004271/HG/NHGRI NIH HHS/ -- U01 HG004271-01/HG/NHGRI NIH HHS/ -- ZIA DK015600-14/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Mar 24;471(7339):473-9. doi: 10.1038/nature09715. Epub 2010 Dec 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Developmental Biology, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, Connecticut 06030-6403, USA. graveley@neuron.uchc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179090" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing/genetics ; Animals ; Base Sequence ; Drosophila Proteins/genetics ; Drosophila melanogaster/embryology/*genetics/*growth & development ; Exons/genetics ; Female ; *Gene Expression Profiling ; Gene Expression Regulation, Developmental/*genetics ; Genes, Insect/genetics ; Genome, Insect/genetics ; Male ; MicroRNAs/genetics ; Oligonucleotide Array Sequence Analysis ; Protein Isoforms/genetics ; RNA Editing/genetics ; RNA, Messenger/analysis/genetics ; RNA, Small Untranslated/analysis/genetics ; Sequence Analysis ; Sex Characteristics ; Transcription, Genetic/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2010-12-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petherick, Anna -- England -- Nature. 2010 Dec 23;468(7327):S5-7. doi: 10.1038/468S5a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179083" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Suckling ; Body Weight/physiology ; Breast Feeding ; Female ; Humans ; Infant ; Infant, Newborn ; Intelligence/physiology ; Macropodidae/growth & development/physiology ; Milk/chemistry/immunology ; Milk, Human/*chemistry/microbiology/parasitology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2010-12-21
    Description: Spatial asymmetries in neural connectivity have an important role in creating basic building blocks of neuronal processing. A key circuit module of directionally selective (DS) retinal ganglion cells is a spatially asymmetric inhibitory input from starburst amacrine cells. It is not known how and when this circuit asymmetry is established during development. Here we photostimulate mouse starburst cells targeted with channelrhodopsin-2 (refs 6-8) while recording from a single genetically labelled type of DS cell. We follow the spatial distribution of synaptic strengths between starburst and DS cells during early postnatal development before these neurons can respond to a physiological light stimulus, and confirm connectivity by monosynaptically restricted trans-synaptic rabies viral tracing. We show that asymmetry develops rapidly over a 2-day period through an intermediate state in which random or symmetric synaptic connections have been established. The development of asymmetry involves the spatially selective reorganization of inhibitory synaptic inputs. Intriguingly, the spatial distribution of excitatory synaptic inputs from starburst cells is significantly more symmetric than that of the inhibitory inputs at the end of this developmental period. Our work demonstrates a rapid developmental switch from a symmetric to asymmetric input distribution for inhibition in the neural circuit of a principal cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yonehara, Keisuke -- Balint, Kamill -- Noda, Masaharu -- Nagel, Georg -- Bamberg, Ernst -- Roska, Botond -- England -- Nature. 2011 Jan 20;469(7330):407-10. doi: 10.1038/nature09711. Epub 2010 Dec 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neural Circuit Laboratories, Friedrich Miescher Institute for Biomedical Research, 4058 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21170022" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/physiology ; Amacrine Cells/metabolism/physiology/radiation effects ; Animals ; Female ; Light ; Male ; Mice ; *Models, Neurological ; *Motion ; Motion Perception/*physiology ; Neural Inhibition/*physiology ; Neural Pathways/*physiology ; Neuroanatomical Tract-Tracing Techniques ; Photic Stimulation ; Rabies virus/genetics/isolation & purification/physiology ; Retina/cytology/growth & development/*physiology ; Retinal Ganglion Cells/physiology ; Rhodopsin/genetics/metabolism ; Synapses/metabolism
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2010-12-18
    Description: On the basis of projected losses of their essential sea-ice habitats, a United States Geological Survey research team concluded in 2007 that two-thirds of the world's polar bears (Ursus maritimus) could disappear by mid-century if business-as-usual greenhouse gas emissions continue. That projection, however, did not consider the possible benefits of greenhouse gas mitigation. A key question is whether temperature increases lead to proportional losses of sea-ice habitat, or whether sea-ice cover crosses a tipping point and irreversibly collapses when temperature reaches a critical threshold. Such a tipping point would mean future greenhouse gas mitigation would confer no conservation benefits to polar bears. Here we show, using a general circulation model, that substantially more sea-ice habitat would be retained if greenhouse gas rise is mitigated. We also show, with Bayesian network model outcomes, that increased habitat retention under greenhouse gas mitigation means that polar bears could persist throughout the century in greater numbers and more areas than in the business-as-usual case. Our general circulation model outcomes did not reveal thresholds leading to irreversible loss of ice; instead, a linear relationship between global mean surface air temperature and sea-ice habitat substantiated the hypothesis that sea-ice thermodynamics can overcome albedo feedbacks proposed to cause sea-ice tipping points. Our outcomes indicate that rapid summer ice losses in models and observations represent increased volatility of a thinning sea-ice cover, rather than tipping-point behaviour. Mitigation-driven Bayesian network outcomes show that previously predicted declines in polar bear distribution and numbers are not unavoidable. Because polar bears are sentinels of the Arctic marine ecosystem and trends in their sea-ice habitats foreshadow future global changes, mitigating greenhouse gas emissions to improve polar bear status would have conservation benefits throughout and beyond the Arctic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amstrup, Steven C -- Deweaver, Eric T -- Douglas, David C -- Marcot, Bruce G -- Durner, George M -- Bitz, Cecilia M -- Bailey, David A -- England -- Nature. 2010 Dec 16;468(7326):955-8. doi: 10.1038/nature09653.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉US Geological Survey, Alaska Science Center, 4210 University Drive, Anchorage, Alaska 99508, USA. samstrup@pbears.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21164484" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aquatic Organisms ; Arctic Regions ; Bayes Theorem ; Carbon Dioxide/analysis ; *Ecosystem ; Endangered Species/statistics & numerical data/*trends ; Environmental Monitoring ; Gases/analysis ; Global Warming/prevention & control/statistics & numerical data ; Greenhouse Effect/*prevention & control/statistics & numerical data ; *Ice Cover ; Models, Theoretical ; Population Density ; Predatory Behavior ; Seasons ; Seawater/analysis/chemistry ; Temperature ; Thermodynamics ; Time Factors ; Ursidae/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Nature Publishing Group (NPG)
    Publication Date: 2010-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbott, Alison -- England -- Nature. 2010 Dec 16;468(7326):886-8. doi: 10.1038/468886a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21164459" target="_blank"〉PubMed〈/a〉
    Keywords: Academies and Institutes/organization & administration ; Agriculture/methods/trends ; Animals ; *Ecosystem ; Gene Knockdown Techniques ; Genetic Engineering ; Germany ; Herbicides ; Insects/drug effects/physiology ; Pheromones/genetics/*metabolism/pharmacology/toxicity ; Plants/drug effects/genetics/*metabolism ; Plants, Genetically Modified ; Predatory Behavior/drug effects ; *Research/economics ; Seeds/genetics/metabolism ; Stimulation, Chemical ; Tobacco/drug effects/genetics/metabolism ; Utah
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2010-12-18
    Description: The adipose-derived hormone leptin maintains energy balance in part through central nervous system-mediated increases in sympathetic outflow that enhance fat burning. Triggering of beta-adrenergic receptors in adipocytes stimulates energy expenditure by cyclic AMP (cAMP)-dependent increases in lipolysis and fatty-acid oxidation. Although the mechanism is unclear, catecholamine signalling is thought to be disrupted in obesity, leading to the development of insulin resistance. Here we show that the cAMP response element binding (CREB) coactivator Crtc3 promotes obesity by attenuating beta-adrenergic receptor signalling in adipose tissue. Crtc3 was activated in response to catecholamine signals, when it reduced adenyl cyclase activity by upregulating the expression of Rgs2, a GTPase-activating protein that also inhibits adenyl cyclase activity. As a common human CRTC3 variant with increased transcriptional activity is associated with adiposity in two distinct Mexican-American cohorts, these results suggest that adipocyte CRTC3 may play a role in the development of obesity in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3025711/" 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/PMC3025711/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, Youngsup -- Altarejos, Judith -- Goodarzi, Mark O -- Inoue, Hiroshi -- Guo, Xiuqing -- Berdeaux, Rebecca -- Kim, Jeong-Ho -- Goode, Jason -- Igata, Motoyuki -- Paz, Jose C -- Hogan, Meghan F -- Singh, Pankaj K -- Goebel, Naomi -- Vera, Lili -- Miller, Nina -- Cui, Jinrui -- Jones, Michelle R -- CHARGE Consortium -- GIANT Consortium -- Chen, Yii-Der I -- Taylor, Kent D -- Hsueh, Willa A -- Rotter, Jerome I -- Montminy, Marc -- M01 RR000425-36/RR/NCRR NIH HHS/ -- M01-RR00425/RR/NCRR NIH HHS/ -- N01 HC095159/HC/NHLBI NIH HHS/ -- N01-HC95159/HC/NHLBI NIH HHS/ -- N02 HL64278/HL/NHLBI NIH HHS/ -- N02-HL64278/HL/NHLBI NIH HHS/ -- P30 DK063491/DK/NIDDK NIH HHS/ -- P30 DK063491-09/DK/NIDDK NIH HHS/ -- P30-DK063491/DK/NIDDK NIH HHS/ -- R01 DK033651/DK/NIDDK NIH HHS/ -- R01 DK049777/DK/NIDDK NIH HHS/ -- R01 DK049777-18/DK/NIDDK NIH HHS/ -- R01 DK079888/DK/NIDDK NIH HHS/ -- R01 DK079888-05/DK/NIDDK NIH HHS/ -- R01 HL071205/HL/NHLBI NIH HHS/ -- R01 HL071205-05/HL/NHLBI NIH HHS/ -- R01 HL088457/HL/NHLBI NIH HHS/ -- R01 HL088457-04/HL/NHLBI NIH HHS/ -- R01-DK049777/DK/NIDDK NIH HHS/ -- R01-DK083834/DK/NIDDK NIH HHS/ -- R01-DK79888/DK/NIDDK NIH HHS/ -- R01-HL088457/HL/NHLBI NIH HHS/ -- R01-L071205/PHS HHS/ -- R37 DK083834/DK/NIDDK NIH HHS/ -- R37 DK083834-26/DK/NIDDK NIH HHS/ -- R37 DK083834-27/DK/NIDDK NIH HHS/ -- England -- Nature. 2010 Dec 16;468(7326):933-9. doi: 10.1038/nature09564.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21164481" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/drug effects/metabolism ; Adipose Tissue/drug effects/metabolism ; Animals ; Body Temperature ; Catecholamines/*metabolism ; Cells, Cultured ; Cyclic AMP/metabolism ; Cyclic AMP Response Element-Binding Protein/antagonists & inhibitors/metabolism ; Dietary Fats/pharmacology ; *Energy Metabolism/genetics ; Female ; Genome-Wide Association Study ; Humans ; Insulin Resistance ; Mexican Americans/genetics ; Mice ; Obesity/chemically induced/genetics/metabolism ; Phosphorylation ; RGS Proteins/biosynthesis/genetics ; Receptors, Adrenergic, beta/metabolism ; Signal Transduction/drug effects/*physiology ; Transcription Factors/chemistry/deficiency/genetics/*metabolism
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , 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: 2010-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nathans, Jeremy -- New York, N.Y. -- Science. 2010 Dec 17;330(6011):1625. doi: 10.1126/science.330.6011.1625-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21163997" target="_blank"〉PubMed〈/a〉
    Keywords: China ; *Family Planning Policy ; Female ; Humans ; Male ; *Population Growth ; Sex Ratio
    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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