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  • Humans  (6,557)
  • Chemical Engineering  (3,544)
  • 2005-2009  (4,616)
  • 1985-1989  (5,485)
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  • 1
    Publication Date: 2022-05-25
    Description: The primary objective of this publication is to share with a wider audience the valuable information and extensive dialogue that took place amongst over 140 individuals who attended the second in a series of planned workshops on the science and management of coastal landforms in Massachusetts. This workshop took place at the Woods Hole Oceanographic Institution on January 24, 2001. The individuals who attended this workshop are actively engaged in planning, managing, regulating, engineering, educating, and studying coastal landforms and their beneficial functions. This workshop titled, Can Humans & Coastal Landforms Co-exist?’, was a natural follow-up to a previous workshop, Coastal Landform Management in Massachusetts, held at WHOI October 9-10, 1997 (proceedings published as WHOI Technical Report #WHOI-98-16). The workshop had a very practical, applied focus, providing state-of-the-art scientific understanding of coastal landform function, case history management and regulation of human activities proposed on coastal landforms, a multi-faceted mock conservation commission hearing presented by practicing technical consultants and attorneys that involved all attendees acting as regulators in breakout sessions, and, at the conclusion of the workshop, an open discussion on all issues related to the science and management of coastal landforms, including future research needs.
    Description: Funding for these proceedings was provided by WHOI Sea Grant and the NOAA National Sea Grant College Program Office, Department of Commerce, under NOAA Grant No. M10-2, Woods Hole Oceanographic Institution Sea Grant Project No. NA86R60075.
    Keywords: Coastal ; Landforms ; Humans
    Repository Name: Woods Hole Open Access Server
    Type: Technical Report
    Format: 1574993 bytes
    Format: application/pdf
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  • 2
    Publication Date: 2009-12-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kayani, Saheeb Ahmed -- England -- Nature. 2009 Dec 24;462(7276):984. doi: 10.1038/462984b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033020" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; History, 20th Century ; History, 21st Century ; Humans ; Pakistan ; *Religion and Science ; Science/history
    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: 2009-12-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buchen, Lizzie -- England -- Nature. 2009 Dec 24;462(7276):962-3. doi: 10.1038/462962a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033008" target="_blank"〉PubMed〈/a〉
    Keywords: Climate Change ; Economic Recession ; Humans ; Influenza A Virus, H1N1 Subtype ; Influenza, Human/epidemiology ; Moon ; *Research/economics/legislation & jurisprudence
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Nature Publishing Group (NPG)
    Publication Date: 2009-12-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mitchinson, Andrew -- England -- Nature. 2009 Dec 24;462(7276):992. doi: 10.1038/462992a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033032" target="_blank"〉PubMed〈/a〉
    Keywords: Alcohol Drinking/*metabolism ; Alcoholic Beverages/adverse effects/*analysis ; Humans
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Nature Publishing Group (NPG)
    Publication Date: 2009-12-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kool, Richard -- England -- Nature. 2009 Dec 24;462(7276):984. doi: 10.1038/462984a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033021" target="_blank"〉PubMed〈/a〉
    Keywords: History, 19th Century ; Humans ; *Periodicals as Topic ; Science/*history ; Selection, Genetic
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  • 6
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    Nature Publishing Group (NPG)
    Publication Date: 2009-12-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schiermeier, Quirin -- Witze, Alexandra -- England -- Nature. 2009 Dec 24;462(7276):968-9. doi: 10.1038/462968a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033012" target="_blank"〉PubMed〈/a〉
    Keywords: Disaster Planning/economics/methods ; Education/trends ; Humans ; Indian Ocean Islands ; *Tsunamis
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2009-12-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blanke, Olaf -- Forcucci, Luca -- Dieguez, Sebastian -- England -- Nature. 2009 Dec 24;462(7276):984. doi: 10.1038/462984d.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033017" target="_blank"〉PubMed〈/a〉
    Keywords: *Art ; Humans ; Neurosciences/*methods/standards ; Visual Perception/*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
    Publication Date: 2009-12-25
    Description: The ATP-dependent chromatin assembly and remodelling factor (ACF) functions to generate regularly spaced nucleosomes, which are required for heritable gene silencing. The mechanism by which ACF mobilizes nucleosomes remains poorly understood. Here we report a single-molecule FRET study that monitors the remodelling of individual nucleosomes by ACF in real time, revealing previously unknown remodelling intermediates and dynamics. In the presence of ACF and ATP, the nucleosomes exhibit gradual translocation along DNA interrupted by well-defined kinetic pauses that occurred after approximately seven or three to four base pairs of translocation. The binding of ACF, translocation of DNA and exiting of translocation pauses are all ATP-dependent, revealing three distinct functional roles of ATP during remodelling. At equilibrium, a continuously bound ACF complex can move the nucleosome back-and-forth many times before dissociation, indicating that ACF is a highly processive and bidirectional nucleosome translocase.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835771/" 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/PMC2835771/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blosser, Timothy R -- Yang, Janet G -- Stone, Michael D -- Narlikar, Geeta J -- Zhuang, Xiaowei -- GM073767/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Dec 24;462(7276):1022-7. doi: 10.1038/nature08627.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Massachusetts 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033040" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; *Chromatin Assembly and Disassembly ; Fluorescence Resonance Energy Transfer ; Humans ; *Models, Molecular ; Nucleosomes/*chemistry ; Protein Structure, Tertiary ; Transcription Factors/*chemistry/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    Nature Publishing Group (NPG)
    Publication Date: 2009-12-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Borrell, Brendan -- England -- Nature. 2009 Dec 24;462(7276):970. doi: 10.1038/462970a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033014" target="_blank"〉PubMed〈/a〉
    Keywords: Complement C3b/chemistry ; Crystallography, X-Ray/ethics ; *Databases, Protein/ethics/standards ; Humans ; *Scientific Misconduct
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  • 10
    Publication Date: 2009-12-25
    Description: Multiple somatic rearrangements are often found in cancer genomes; however, the underlying processes of rearrangement and their contribution to cancer development are poorly characterized. Here we use a paired-end sequencing strategy to identify somatic rearrangements in breast cancer genomes. There are more rearrangements in some breast cancers than previously appreciated. Rearrangements are more frequent over gene footprints and most are intrachromosomal. Multiple rearrangement architectures are present, but tandem duplications are particularly common in some cancers, perhaps reflecting a specific defect in DNA maintenance. Short overlapping sequences at most rearrangement junctions indicate that these have been mediated by non-homologous end-joining DNA repair, although varying sequence patterns indicate that multiple processes of this type are operative. Several expressed in-frame fusion genes were identified but none was recurrent. The study provides a new perspective on cancer genomes, highlighting the diversity of somatic rearrangements and their potential contribution to cancer development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3398135/" 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/PMC3398135/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stephens, Philip J -- McBride, David J -- Lin, Meng-Lay -- Varela, Ignacio -- Pleasance, Erin D -- Simpson, Jared T -- Stebbings, Lucy A -- Leroy, Catherine -- Edkins, Sarah -- Mudie, Laura J -- Greenman, Chris D -- Jia, Mingming -- Latimer, Calli -- Teague, Jon W -- Lau, King Wai -- Burton, John -- Quail, Michael A -- Swerdlow, Harold -- Churcher, Carol -- Natrajan, Rachael -- Sieuwerts, Anieta M -- Martens, John W M -- Silver, Daniel P -- Langerod, Anita -- Russnes, Hege E G -- Foekens, John A -- Reis-Filho, Jorge S -- van 't Veer, Laura -- Richardson, Andrea L -- Borresen-Dale, Anne-Lise -- Campbell, Peter J -- Futreal, P Andrew -- Stratton, Michael R -- 077012/Z/05/Z/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- CA089393/CA/NCI NIH HHS/ -- England -- Nature. 2009 Dec 24;462(7276):1005-10. doi: 10.1038/nature08645.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033038" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics ; Cell Line, Tumor ; Cells, Cultured ; *Chromosome Aberrations ; DNA Breaks ; Female ; Gene Rearrangement/*genetics ; Genome, Human/*genetics ; Genomic Library ; Humans ; Sequence Analysis, DNA
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  • 11
    Publication Date: 2009-12-25
    Description: Evenly spaced nucleosomes directly correlate with condensed chromatin and gene silencing. The ATP-dependent chromatin assembly factor (ACF) forms such structures in vitro and is required for silencing in vivo. ACF generates and maintains nucleosome spacing by constantly moving a nucleosome towards the longer flanking DNA faster than the shorter flanking DNA. How the enzyme rapidly moves back and forth between both sides of a nucleosome to accomplish bidirectional movement is unknown. Here we show that nucleosome movement depends cooperatively on two ACF molecules, indicating that ACF functions as a dimer of ATPases. Further, the nucleotide state determines whether the dimer closely engages one or both sides of the nucleosome. Three-dimensional reconstruction by single-particle electron microscopy of the ATPase-nucleosome complex in an activated ATP state reveals a dimer architecture in which the two ATPases face each other. Our results indicate a model in which the two ATPases work in a coordinated manner, taking turns to engage either side of a nucleosome, thereby allowing processive bidirectional movement. This novel dimeric motor mechanism differs from that of dimeric motors such as kinesin and dimeric helicases that processively translocate unidirectionally and reflects the unique challenges faced by motors that move nucleosomes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2869534/" 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/PMC2869534/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Racki, Lisa R -- Yang, Janet G -- Naber, Nariman -- Partensky, Peretz D -- Acevedo, Ashley -- Purcell, Thomas J -- Cooke, Roger -- Cheng, Yifan -- Narlikar, Geeta J -- R01 GM073767/GM/NIGMS NIH HHS/ -- R01 GM073767-01/GM/NIGMS NIH HHS/ -- R01 GM073767-02/GM/NIGMS NIH HHS/ -- R01 GM073767-03/GM/NIGMS NIH HHS/ -- R01 GM073767-03S1/GM/NIGMS NIH HHS/ -- R01 GM073767-04/GM/NIGMS NIH HHS/ -- R01 GM073767-05/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Dec 24;462(7276):1016-21. doi: 10.1038/nature08621.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco, California 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033039" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Cell Line ; Chromatin Assembly and Disassembly/*physiology ; Dimerization ; Gene Silencing/physiology ; Histones/metabolism ; Humans ; Microscopy, Electron, Transmission ; *Models, Molecular ; Multiprotein Complexes/*metabolism ; Nucleosomes/chemistry/*metabolism ; Protein Binding ; Protein Structure, Tertiary ; Transcription Factors/chemistry/metabolism
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  • 12
    Publication Date: 2009-12-25
    Description: The inference of transcriptional networks that regulate transitions into physiological or pathological cellular states remains a central challenge in systems biology. A mesenchymal phenotype is the hallmark of tumour aggressiveness in human malignant glioma, but the regulatory programs responsible for implementing the associated molecular signature are largely unknown. Here we show that reverse-engineering and an unbiased interrogation of a glioma-specific regulatory network reveal the transcriptional module that activates expression of mesenchymal genes in malignant glioma. Two transcription factors (C/EBPbeta and STAT3) emerge as synergistic initiators and master regulators of mesenchymal transformation. Ectopic co-expression of C/EBPbeta and STAT3 reprograms neural stem cells along the aberrant mesenchymal lineage, whereas elimination of the two factors in glioma cells leads to collapse of the mesenchymal signature and reduces tumour aggressiveness. In human glioma, expression of C/EBPbeta and STAT3 correlates with mesenchymal differentiation and predicts poor clinical outcome. These results show that the activation of a small regulatory module is necessary and sufficient to initiate and maintain an aberrant phenotypic state in cancer cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4011561/" 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/PMC4011561/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carro, Maria Stella -- Lim, Wei Keat -- Alvarez, Mariano Javier -- Bollo, Robert J -- Zhao, Xudong -- Snyder, Evan Y -- Sulman, Erik P -- Anne, Sandrine L -- Doetsch, Fiona -- Colman, Howard -- Lasorella, Anna -- Aldape, Ken -- Califano, Andrea -- Iavarone, Antonio -- 1RC2CA148308-01/CA/NCI NIH HHS/ -- P20 GM075059/GM/NIGMS NIH HHS/ -- P20GM075059/GM/NIGMS NIH HHS/ -- R01 CA085628/CA/NCI NIH HHS/ -- R01 CA101644/CA/NCI NIH HHS/ -- R01 CA109755/CA/NCI NIH HHS/ -- R01 CA127643/CA/NCI NIH HHS/ -- R01 NS061776/NS/NINDS NIH HHS/ -- R01 NS061776-01A2/NS/NINDS NIH HHS/ -- R01 NS061776-02/NS/NINDS NIH HHS/ -- R01CA085628/CA/NCI NIH HHS/ -- R01CA101644/CA/NCI NIH HHS/ -- R01CA109755/CA/NCI NIH HHS/ -- R01NS061776/NS/NINDS NIH HHS/ -- RC2 CA148308/CA/NCI NIH HHS/ -- U01 CA168426/CA/NCI NIH HHS/ -- U54 CA121852/CA/NCI NIH HHS/ -- U54CA121852/CA/NCI NIH HHS/ -- England -- Nature. 2010 Jan 21;463(7279):318-25. doi: 10.1038/nature08712. Epub 2009 Dec 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Genetics, Columbia University Medical Center, New York, New York 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20032975" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Neoplasms/diagnosis/*genetics/*pathology ; CCAAT-Enhancer-Binding Protein-beta/genetics/metabolism ; Cell Differentiation/genetics ; Cell Line, Tumor ; Cell Transformation, Neoplastic/genetics/metabolism/pathology ; Cellular Reprogramming/genetics ; Computational Biology ; *Gene Expression Regulation, Neoplastic ; *Gene Regulatory Networks ; Glioma/diagnosis/genetics/pathology ; Humans ; Mesenchymal Stromal Cells/metabolism/pathology ; Mesoderm/*metabolism/*pathology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Neoplasm Invasiveness/genetics/pathology ; Neurons/metabolism/pathology ; Prognosis ; Reproducibility of Results ; STAT3 Transcription Factor/genetics/metabolism ; *Transcription, Genetic
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  • 13
    Publication Date: 2009-12-23
    Description: Reprogramming of somatic cell nuclei to yield induced pluripotent stem (iPS) cells makes possible derivation of patient-specific stem cells for regenerative medicine. However, iPS cell generation is asynchronous and slow (2-3 weeks), the frequency is low (〈0.1%), and DNA demethylation constitutes a bottleneck. To determine regulatory mechanisms involved in reprogramming, we generated interspecies heterokaryons (fused mouse embryonic stem (ES) cells and human fibroblasts) that induce reprogramming synchronously, frequently and fast. Here we show that reprogramming towards pluripotency in single heterokaryons is initiated without cell division or DNA replication, rapidly (1 day) and efficiently (70%). Short interfering RNA (siRNA)-mediated knockdown showed that activation-induced cytidine deaminase (AID, also known as AICDA) is required for promoter demethylation and induction of OCT4 (also known as POU5F1) and NANOG gene expression. AID protein bound silent methylated OCT4 and NANOG promoters in fibroblasts, but not active demethylated promoters in ES cells. These data provide new evidence that mammalian AID is required for active DNA demethylation and initiation of nuclear reprogramming towards pluripotency in human somatic cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2906123/" 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/PMC2906123/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhutani, Nidhi -- Brady, Jennifer J -- Damian, Mara -- Sacco, Alessandra -- Corbel, Stephane Y -- Blau, Helen M -- AG009521/AG/NIA NIH HHS/ -- AG024987/AG/NIA NIH HHS/ -- AI007328/AI/NIAID NIH HHS/ -- R01 AG009521/AG/NIA NIH HHS/ -- R01 AG009521-25/AG/NIA NIH HHS/ -- R01 AG024987/AG/NIA NIH HHS/ -- R01 AG024987-05/AG/NIA NIH HHS/ -- T32 AI007328/AI/NIAID NIH HHS/ -- U01 HL100397/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Feb 25;463(7284):1042-7. doi: 10.1038/nature08752.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Baxter Laboratory for Stem Cell Biology, Institute for Stem Cell Biology and Regenerative Medicine, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305-5175, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20027182" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Fusion ; Cell Line ; Cells, Cultured ; Cellular Reprogramming/genetics/*physiology ; Chromatin Immunoprecipitation ; Cytidine Deaminase/deficiency/genetics/*metabolism ; DNA/chemistry/genetics/metabolism ; *DNA Methylation ; DNA Replication ; Embryonic Stem Cells/cytology/metabolism ; Fibroblasts/cytology/metabolism ; Gene Expression Regulation ; Gene Knockdown Techniques ; Homeodomain Proteins/genetics ; Humans ; Induced Pluripotent Stem Cells/*cytology/enzymology/*metabolism ; Lung/cytology/embryology ; Mice ; Models, Biological ; Octamer Transcription Factor-3/genetics ; Promoter Regions, Genetic/genetics ; Time Factors
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  • 14
    Publication Date: 2009-12-23
    Description: Influenza A virus is an RNA virus that encodes up to 11 proteins and this small coding capacity demands that the virus use the host cellular machinery for many aspects of its life cycle. Knowledge of these host cell requirements not only informs us of the molecular pathways exploited by the virus but also provides further targets that could be pursued for antiviral drug development. Here we use an integrative systems approach, based on genome-wide RNA interference screening, to identify 295 cellular cofactors required for early-stage influenza virus replication. Within this group, those involved in kinase-regulated signalling, ubiquitination and phosphatase activity are the most highly enriched, and 181 factors assemble into a highly significant host-pathogen interaction network. Moreover, 219 of the 295 factors were confirmed to be required for efficient wild-type influenza virus growth, and further analysis of a subset of genes showed 23 factors necessary for viral entry, including members of the vacuolar ATPase (vATPase) and COPI-protein families, fibroblast growth factor receptor (FGFR) proteins, and glycogen synthase kinase 3 (GSK3)-beta. Furthermore, 10 proteins were confirmed to be involved in post-entry steps of influenza virus replication. These include nuclear import components, proteases, and the calcium/calmodulin-dependent protein kinase (CaM kinase) IIbeta (CAMK2B). Notably, growth of swine-origin H1N1 influenza virus is also dependent on the identified host factors, and we show that small molecule inhibitors of several factors, including vATPase and CAMK2B, antagonize influenza virus replication.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862546/" 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/PMC2862546/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Konig, Renate -- Stertz, Silke -- Zhou, Yingyao -- Inoue, Atsushi -- Hoffmann, H-Heinrich -- Bhattacharyya, Suchita -- Alamares, Judith G -- Tscherne, Donna M -- Ortigoza, Mila B -- Liang, Yuhong -- Gao, Qinshan -- Andrews, Shane E -- Bandyopadhyay, Sourav -- De Jesus, Paul -- Tu, Buu P -- Pache, Lars -- Shih, Crystal -- Orth, Anthony -- Bonamy, Ghislain -- Miraglia, Loren -- Ideker, Trey -- Garcia-Sastre, Adolfo -- Young, John A T -- Palese, Peter -- Shaw, Megan L -- Chanda, Sumit K -- 1 P01 AI058113/AI/NIAID NIH HHS/ -- 1 S10 RR0 9145-01/RR/NCRR NIH HHS/ -- 1 T32 AI07647/AI/NIAID NIH HHS/ -- 1F32AI081428/AI/NIAID NIH HHS/ -- 1R21AI083673/AI/NIAID NIH HHS/ -- 5R24 CA095823-04/CA/NCI NIH HHS/ -- HHSN266200700010C/PHS HHS/ -- HHSN272200900032C/PHS HHS/ -- P01 AI058113/AI/NIAID NIH HHS/ -- P01 AI058113-010004/AI/NIAID NIH HHS/ -- P01 AI058113-020004/AI/NIAID NIH HHS/ -- P01 AI058113-030004/AI/NIAID NIH HHS/ -- P01 AI058113-040004/AI/NIAID NIH HHS/ -- P01 AI058113-050004/AI/NIAID NIH HHS/ -- T32 AI007647/AI/NIAID NIH HHS/ -- T32 AI007647-01/AI/NIAID NIH HHS/ -- T32 AI007647-02/AI/NIAID NIH HHS/ -- T32 AI007647-03/AI/NIAID NIH HHS/ -- T32 AI007647-04/AI/NIAID NIH HHS/ -- T32 AI007647-05/AI/NIAID NIH HHS/ -- T32 AI007647-06/AI/NIAID NIH HHS/ -- T32 AI007647-07/AI/NIAID NIH HHS/ -- T32 AI007647-08/AI/NIAID NIH HHS/ -- T32 AI007647-09/AI/NIAID NIH HHS/ -- T32 AI007647-10/AI/NIAID NIH HHS/ -- T32 GM007280/GM/NIGMS NIH HHS/ -- U01 AI074539/AI/NIAID NIH HHS/ -- U01 AI074539-01/AI/NIAID NIH HHS/ -- U01 AI074539-02/AI/NIAID NIH HHS/ -- U01 AI074539-03/AI/NIAID NIH HHS/ -- U01 AI1074539/AI/NIAID NIH HHS/ -- U54 AI057158/AI/NIAID NIH HHS/ -- U54 AI057158-065713/AI/NIAID NIH HHS/ -- U54 AI057159/AI/NIAID NIH HHS/ -- England -- Nature. 2010 Feb 11;463(7282):813-7. doi: 10.1038/nature08699.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Infectious and Inflammatory Disease Center, Burnham Institute for Medical Research.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20027183" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Factors/*genetics/*physiology ; Cell Line ; Cercopithecus aethiops ; Gene Library ; Genome, Human/genetics ; Host-Pathogen Interactions/genetics/*physiology ; Humans ; Influenza A Virus, H1N1 Subtype/classification/growth & development ; Influenza A virus/classification/*growth & development ; Influenza, Human/*genetics/*virology ; RNA Interference ; Vero Cells ; Virus Internalization ; Virus Replication/*physiology
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    Electronic ISSN: 1476-4687
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  • 15
    Publication Date: 2009-12-22
    Description: Broken chromosomes arising from DNA double-strand breaks result from endogenous events such as the production of reactive oxygen species during cellular metabolism, as well as from exogenous sources such as ionizing radiation. Left unrepaired or incorrectly repaired they can lead to genomic changes that may result in cell death or cancer. DNA-dependent protein kinase (DNA-PK), a holoenzyme that comprises the DNA-PK catalytic subunit (DNA-PKcs) and the heterodimer Ku70/Ku80, has a major role in non-homologous end joining-the main pathway in mammals used to repair double-strand breaks. DNA-PKcs is a serine/threonine protein kinase comprising a single polypeptide chain of 4,128 amino acids and belonging to the phosphatidylinositol-3-OH kinase (PI(3)K)-related protein family. DNA-PKcs is involved in the sensing and transmission of DNA damage signals to proteins such as p53, setting off events that lead to cell cycle arrest. It phosphorylates a wide range of substrates in vitro, including Ku70/Ku80, which is translocated along DNA. Here we present the crystal structure of human DNA-PKcs at 6.6 A resolution, in which the overall fold is clearly visible, to our knowledge, for the first time. The many alpha-helical HEAT repeats (helix-turn-helix motifs) facilitate bending and allow the polypeptide chain to fold into a hollow circular structure. The carboxy-terminal kinase domain is located on top of this structure, and a small HEAT repeat domain that probably binds DNA is inside. The structure provides a flexible cradle to promote DNA double-strand-break repair.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811870/" 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/PMC2811870/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sibanda, Bancinyane L -- Chirgadze, Dimitri Y -- Blundell, Tom L -- 079281/Wellcome Trust/United Kingdom -- A3846/Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2010 Jan 7;463(7277):118-21. doi: 10.1038/nature08648. Epub 2009 Dec 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Cambridge, Old Addenbrooke's site, 80 Tennis Court Road, Cambridge CB2 1GA, UK. lynn@cryst.bioc.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20023628" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Nuclear/chemistry ; Catalytic Domain ; Crystallography, X-Ray ; DNA/metabolism ; DNA Breaks, Double-Stranded ; DNA-Activated Protein Kinase/*chemistry/metabolism ; DNA-Binding Proteins/chemistry ; HeLa Cells ; *Helix-Turn-Helix Motifs ; Humans ; Models, Molecular ; Nuclear Proteins/*chemistry/metabolism ; Protein Folding ; Protein Structure, Secondary
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  • 16
    Publication Date: 2009-12-22
    Description: MCL1 is essential for the survival of stem and progenitor cells of multiple lineages, and is unique among pro-survival BCL2 family members in that it is rapidly turned over through the action of ubiquitin ligases. B- and mantle-cell lymphomas, chronic myeloid leukaemia, and multiple myeloma, however, express abnormally high levels of MCL1, contributing to chemoresistance and disease relapse. The mechanism of MCL1 overexpression in cancer is not well understood. Here we show that the deubiquitinase USP9X stabilizes MCL1 and thereby promotes cell survival. USP9X binds MCL1 and removes the Lys 48-linked polyubiquitin chains that normally mark MCL1 for proteasomal degradation. Increased USP9X expression correlates with increased MCL1 protein in human follicular lymphomas and diffuse large B-cell lymphomas. Moreover, patients with multiple myeloma overexpressing USP9X have a poor prognosis. Knockdown of USP9X increases MCL1 polyubiquitination, which enhances MCL1 turnover and cell killing by the BH3 mimetic ABT-737. These results identify USP9X as a prognostic and therapeutic target, and they show that deubiquitinases may stabilize labile oncoproteins in human malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwickart, Martin -- Huang, Xiaodong -- Lill, Jennie R -- Liu, Jinfeng -- Ferrando, Ronald -- French, Dorothy M -- Maecker, Heather -- O'Rourke, Karen -- Bazan, Fernando -- Eastham-Anderson, Jeffrey -- Yue, Peng -- Dornan, David -- Huang, David C S -- Dixit, Vishva M -- England -- Nature. 2010 Jan 7;463(7277):103-7. doi: 10.1038/nature08646. Epub 2009 Dec 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20023629" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/drug effects ; Biphenyl Compounds/pharmacology ; Cell Line ; Cell Line, Tumor ; Cell Survival ; DNA Damage ; Etoposide/pharmacology ; Female ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Half-Life ; Humans ; Lysine/metabolism ; Mice ; Mice, SCID ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasms/diagnosis/*metabolism/*pathology ; Nitrophenols/pharmacology ; Phosphorylation/radiation effects ; Piperazines/pharmacology ; Polyubiquitin/*metabolism ; Prognosis ; Protein Binding/radiation effects ; Protein Stability ; Proto-Oncogene Proteins c-bcl-2/genetics/*metabolism ; RNA Interference ; Sulfonamides/pharmacology ; Taxoids/pharmacology ; Ubiquitin Thiolesterase/deficiency/genetics/*metabolism ; Ubiquitination ; Ultraviolet Rays ; Xenograft Model Antitumor Assays
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  • 17
    Publication Date: 2009-12-22
    Description: Innate immune responses are important in combating various microbes during the early phases of infection. Natural killer (NK) cells are innate lymphocytes that, unlike T and B lymphocytes, do not express antigen receptors but rapidly exhibit cytotoxic activities against virus-infected cells and produce various cytokines. Here we report a new type of innate lymphocyte present in a novel lymphoid structure associated with adipose tissues in the peritoneal cavity. These cells do not express lineage (Lin) markers but do express c-Kit, Sca-1 (also known as Ly6a), IL7R and IL33R. Similar lymphoid clusters were found in both human and mouse mesentery and we term this tissue 'FALC' (fat-associated lymphoid cluster). FALC Lin(-)c-Kit(+)Sca-1(+) cells are distinct from lymphoid progenitors and lymphoid tissue inducer cells. These cells proliferate in response to IL2 and produce large amounts of T(H)2 cytokines such as IL5, IL6 and IL13. IL5 and IL6 regulate B-cell antibody production and self-renewal of B1 cells. Indeed, FALC Lin(-)c-Kit(+)Sca-1(+) cells support the self-renewal of B1 cells and enhance IgA production. IL5 and IL13 mediate allergic inflammation and protection against helminth infection. After helminth infection and in response to IL33, FALC Lin(-)c-Kit(+)Sca-1(+) cells produce large amounts of IL13, which leads to goblet cell hyperplasia-a critical step for helminth expulsion. In mice devoid of FALC Lin(-)c-Kit(+)Sca-1(+) cells, such goblet cell hyperplasia was not induced. Thus, FALC Lin(-)c-Kit(+)Sca-1(+) cells are T(H)2-type innate lymphocytes, and we propose that these cells be called 'natural helper cells'.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moro, Kazuyo -- Yamada, Taketo -- Tanabe, Masanobu -- Takeuchi, Tsutomu -- Ikawa, Tomokatsu -- Kawamoto, Hiroshi -- Furusawa, Jun-Ichi -- Ohtani, Masashi -- Fujii, Hideki -- Koyasu, Shigeo -- England -- Nature. 2010 Jan 28;463(7280):540-4. doi: 10.1038/nature08636. Epub 2009 Dec 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20023630" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*cytology/*immunology ; Animals ; Antigens, Ly/genetics/*immunology/metabolism ; B-Lymphocytes/cytology/immunology ; Cell Proliferation ; Cytokines/*immunology ; *Gene Expression Regulation ; Humans ; Lymphocytes/*immunology ; Membrane Proteins/genetics/*immunology ; Mesentery/immunology ; Mice ; Mice, Inbred C57BL ; Nematoda/physiology ; Nematode Infections/immunology ; Proto-Oncogene Proteins c-kit/genetics/*immunology ; Th2 Cells/immunology
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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dovidio, John F -- New York, N.Y. -- Science. 2009 Dec 18;326(5960):1641-2. doi: 10.1126/science.1184231.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Yale University, New Haven, CT 06520-8205, USA. john.dovidio@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019277" target="_blank"〉PubMed〈/a〉
    Keywords: *African Continental Ancestry Group ; Cues ; *European Continental Ancestry Group ; Humans ; *Nonverbal Communication ; *Prejudice ; *Social Behavior ; *Television ; United States
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  • 19
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-19
    Description: The role of starchy plants in early hominin diets and when the culinary processing of starches began have been difficult to track archaeologically. Seed collecting is conventionally perceived to have been an irrelevant activity among the Pleistocene foragers of southern Africa, on the grounds of both technological difficulty in the processing of grains and the belief that roots, fruits, and nuts, not cereals, were the basis for subsistence for the past 100,000 years and further back in time. A large assemblage of starch granules has been retrieved from the surfaces of Middle Stone Age stone tools from Mozambique, showing that early Homo sapiens relied on grass seeds starting at least 105,000 years ago, including those of sorghum grasses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mercader, Julio -- New York, N.Y. -- Science. 2009 Dec 18;326(5960):1680-3. doi: 10.1126/science.1173966.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Archaeology, University of Calgary, Alberta, T2N 1N4, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019285" target="_blank"〉PubMed〈/a〉
    Keywords: *Archaeology ; Diet ; Edible Grain/*history ; History, Ancient ; Humans ; Mozambique ; *Poaceae ; *Seeds ; *Sorghum ; Starch
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  • 20
    Publication Date: 2009-12-19
    Description: Compared with more explicit racial slurs and statements, biased facial expressions and body language may resist conscious identification and thus produce a hidden social influence. In four studies, we show that race biases can be subtly transmitted via televised nonverbal behavior. Characters on 11 popular television shows exhibited more negative nonverbal behavior toward black than toward status-matched white characters. Critically, exposure to prowhite (versus problack) nonverbal bias increased viewers' bias even though patterns of nonverbal behavior could not be consciously reported. These findings suggest that hidden patterns of televised nonverbal behavior influence bias among viewers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3764987/" 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/PMC3764987/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weisbuch, Max -- Pauker, Kristin -- Ambady, Nalini -- F32 MH078350/MH/NIMH NIH HHS/ -- F32MH078350/MH/NIMH NIH HHS/ -- R01 MH070833/MH/NIMH NIH HHS/ -- R01 MH070833-02/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 Dec 18;326(5960):1711-4. doi: 10.1126/science.1178358.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Tufts University, 490 Boston Avenue, Medford, MA 02155, USA. max.weisbuch@tufts.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019288" target="_blank"〉PubMed〈/a〉
    Keywords: *African Continental Ancestry Group ; Cues ; *European Continental Ancestry Group ; Facial Expression ; Female ; Humans ; Kinesics ; Male ; *Nonverbal Communication ; *Prejudice ; *Television ; United States
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  • 21
    Publication Date: 2009-12-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fu, Alice C -- Raizen, Senta A -- Shavelson, Richard J -- New York, N.Y. -- Science. 2009 Dec 18;326(5960):1637-8. doi: 10.1126/science.1177780.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Education, Stanford University, Stanford, CA 94305, USA. alicefu@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019274" target="_blank"〉PubMed〈/a〉
    Keywords: Achievement ; Adolescent ; Biological Science Disciplines/*education ; Child ; Earth Sciences/*education ; *Educational Measurement ; Humans ; Natural Science Disciplines/*education ; United States
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  • 22
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mitchell, Tom M -- New York, N.Y. -- Science. 2009 Dec 18;326(5960):1644-5. doi: 10.1126/science.1174459.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Machine Learning Department, Carnegie Mellon University, Pittsburgh, PA 15213, USA. tom.mitchell@cs.cmu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019279" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; *Behavior ; *Data Mining ; Geographic Information Systems ; *Health ; Humans ; *Information Systems ; Interpersonal Relations ; *Privacy
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  • 23
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baron, Jonathan -- New York, N.Y. -- Science. 2009 Dec 18;326(5960):1632; author reply 1632-3. doi: 10.1126/science.326.5960.1632-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019273" target="_blank"〉PubMed〈/a〉
    Keywords: *Cooperative Behavior ; Games, Experimental ; Humans ; *Punishment ; *Reward
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  • 24
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2009 Dec 18;326(5960):1598-9. doi: 10.1126/science.326.5960.1598-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019252" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Bone and Bones/anatomy & histology ; Ethiopia ; Female ; *Fossils ; Geography ; *Hominidae/anatomy & histology/classification/physiology ; Humans ; Locomotion ; Posture ; Skeleton ; Walking
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  • 25
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2009 Dec 18;326(5960):1600-7. doi: 10.1126/science.326.5960.1600.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019253" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid/metabolism ; Animals ; Astronomical Phenomena ; Gamma Rays ; Genetic Therapy ; Graphite ; Humans ; Lasers ; Longevity/drug effects ; Membrane Transport Proteins/metabolism ; Physical Phenomena ; *Science ; Sirolimus/pharmacology ; X-Rays
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  • 26
    Publication Date: 2009-12-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krane, D E -- Bahn, V -- Balding, D -- Barlow, B -- Cash, H -- Desportes, B L -- D'Eustachio, P -- Devlin, K -- Doom, T E -- Dror, I -- Ford, S -- Funk, C -- Gilder, J -- Hampikian, G -- Inman, K -- Jamieson, A -- Kent, P E -- Koppl, R -- Kornfield, I -- Krimsky, S -- Mnookin, J -- Mueller, L -- Murphy, E -- Paoletti, D R -- Petrov, D A -- Raymer, M -- Risinger, D M -- Roth, A -- Rudin, N -- Shields, W -- Siegel, J A -- Slatkin, M -- Song, Y S -- Speed, T -- Spiegelman, C -- Sullivan, P -- Swienton, A R -- Tarpey, T -- Thompson, W C -- Ungvarsky, E -- Zabell, S -- New York, N.Y. -- Science. 2009 Dec 18;326(5960):1631-2. doi: 10.1126/science.326.5960.1631.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019271" target="_blank"〉PubMed〈/a〉
    Keywords: *Access to Information ; *Databases, Nucleic Acid ; Humans ; Privacy ; United States ; United States Government Agencies
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  • 27
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- Cohen, Jon -- New York, N.Y. -- Science. 2009 Dec 18;326(5960):1607. doi: 10.1126/science.326.5960.1607.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019257" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Disease Outbreaks ; Humans ; *Influenza A Virus, H1N1 Subtype/genetics/immunology/isolation & ; purification/pathogenicity ; Influenza Vaccines/adverse effects/supply & distribution ; Influenza, Human/*epidemiology/prevention & control/virology ; Mass Vaccination ; Orthomyxoviridae Infections/epidemiology/veterinary/virology ; Swine ; Swine Diseases/epidemiology/virology ; World Health Organization
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 28
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garber, Ken -- New York, N.Y. -- Science. 2009 Dec 18;326(5960):1619. doi: 10.1126/science.326.5960.1619.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019269" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/administration & dosage/metabolism/*therapeutic use ; Clinical Trials, Phase I as Topic ; Humans ; Melanoma/*drug therapy/genetics/metabolism/secondary ; Mutant Proteins/antagonists & inhibitors/genetics/metabolism ; Pharmaceutical Preparations/*administration & dosage/metabolism ; Proto-Oncogene Proteins B-raf/antagonists & inhibitors/genetics/*metabolism ; Signal Transduction/drug effects
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 29
    Publication Date: 2009-12-19
    Description: Many people incur costs to reward strangers who have been kind to others. Theoretical and experimental evidence suggests that such "indirect rewarding" sustains cooperation between unrelated humans. Its emergence is surprising, because rewarders incur costs but receive no immediate benefits. It can prevail in the long run only if rewarders earn higher payoffs than "defectors" who ignore strangers' kindness. We provide experimental evidence regarding the payoffs received by individuals who employ these and other strategies, such as "indirect punishment," by imposing costs on unkind strangers. We find that if unkind strangers cannot be punished, defection earns most. If they can be punished, however, then indirect rewarding earns most. Indirect punishment plays this important role, even if it gives a low payoff and is rarely implemented.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ule, Aljaz -- Schram, Arthur -- Riedl, Arno -- Cason, Timothy N -- New York, N.Y. -- Science. 2009 Dec 18;326(5960):1701-4. doi: 10.1126/science.1178883.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Research in Experimental Economics and Political Decision-Making (CREED), University of Amsterdam, Roetersstraat 11, 1018 WB Amsterdam, Netherlands. a.ule@uva.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019287" target="_blank"〉PubMed〈/a〉
    Keywords: Altruism ; *Cooperative Behavior ; Games, Experimental ; Humans ; *Punishment ; *Reward ; *Social Behavior
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  • 30
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2009 Dec 18;326(5960):1606. doi: 10.1126/science.326.5960.1606.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019256" target="_blank"〉PubMed〈/a〉
    Keywords: Forecasting ; Genome, Human ; Humans ; Induced Pluripotent Stem Cells ; Neoplasms/metabolism ; Proteins/genetics ; *Science ; Space Flight
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  • 31
    Publication Date: 2009-12-19
    Description: A huge research literature, across the behavioral and social sciences, uses information on individuals' subjective well-being. These are responses to questions--asked by survey interviewers or medical personnel--such as, "How happy do you feel on a scale from 1 to 4?" Yet there is little scientific evidence that such data are meaningful. This study examines a 2005-2008 Behavioral Risk Factor Surveillance System random sample of 1.3 million U.S. citizens. Life satisfaction in each U.S. state is measured. Across America, people's answers trace out the same pattern of quality of life as previously estimated, from solely nonsubjective data, in one branch of economics (so-called "compensating differentials" neoclassical theory, originally from Adam Smith). There is a state-by-state match (r = 0.6, P 〈 0.001) between subjective and objective well-being. This result has some potential to help to unify disciplines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oswald, Andrew J -- Wu, Stephen -- New York, N.Y. -- Science. 2010 Jan 29;327(5965):576-9. doi: 10.1126/science.1180606. Epub 2009 Dec 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Economics, University of Warwick, Coventry CV4 7AL, UK. andrew.oswald@warwick.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019249" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Economics ; Female ; *Happiness ; *Health Surveys ; Humans ; *Income ; Male ; Models, Economic ; *Personal Satisfaction ; *Quality of Life ; Regression Analysis ; *Socioeconomic Factors ; Surveys and Questionnaires ; United States
    Print ISSN: 0036-8075
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  • 32
    Publication Date: 2009-12-18
    Description: All cancers carry somatic mutations. A subset of these somatic alterations, termed driver mutations, confer selective growth advantage and are implicated in cancer development, whereas the remainder are passengers. Here we have sequenced the genomes of a malignant melanoma and a lymphoblastoid cell line from the same person, providing the first comprehensive catalogue of somatic mutations from an individual cancer. The catalogue provides remarkable insights into the forces that have shaped this cancer genome. The dominant mutational signature reflects DNA damage due to ultraviolet light exposure, a known risk factor for malignant melanoma, whereas the uneven distribution of mutations across the genome, with a lower prevalence in gene footprints, indicates that DNA repair has been preferentially deployed towards transcribed regions. The results illustrate the power of a cancer genome sequence to reveal traces of the DNA damage, repair, mutation and selection processes that were operative years before the cancer became symptomatic.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3145108/" 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/PMC3145108/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pleasance, Erin D -- Cheetham, R Keira -- Stephens, Philip J -- McBride, David J -- Humphray, Sean J -- Greenman, Chris D -- Varela, Ignacio -- Lin, Meng-Lay -- Ordonez, Gonzalo R -- Bignell, Graham R -- Ye, Kai -- Alipaz, Julie -- Bauer, Markus J -- Beare, David -- Butler, Adam -- Carter, Richard J -- Chen, Lina -- Cox, Anthony J -- Edkins, Sarah -- Kokko-Gonzales, Paula I -- Gormley, Niall A -- Grocock, Russell J -- Haudenschild, Christian D -- Hims, Matthew M -- James, Terena -- Jia, Mingming -- Kingsbury, Zoya -- Leroy, Catherine -- Marshall, John -- Menzies, Andrew -- Mudie, Laura J -- Ning, Zemin -- Royce, Tom -- Schulz-Trieglaff, Ole B -- Spiridou, Anastassia -- Stebbings, Lucy A -- Szajkowski, Lukasz -- Teague, Jon -- Williamson, David -- Chin, Lynda -- Ross, Mark T -- Campbell, Peter J -- Bentley, David R -- Futreal, P Andrew -- Stratton, Michael R -- 077012/Z/05/Z/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- 093867/Wellcome Trust/United Kingdom -- England -- Nature. 2010 Jan 14;463(7278):191-6. doi: 10.1038/nature08658. Epub 2009 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016485" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Cell Line, Tumor ; DNA Damage/genetics ; DNA Mutational Analysis ; DNA Repair/genetics ; Gene Dosage/genetics ; Genes, Neoplasm/*genetics ; Genome, Human/*genetics ; Humans ; Loss of Heterozygosity/genetics ; Male ; Melanoma/etiology/genetics ; MicroRNAs/genetics ; Mutagenesis, Insertional/genetics ; Mutation/*genetics ; Neoplasms/etiology/*genetics ; Polymorphism, Single Nucleotide/genetics ; Precision Medicine ; Sequence Deletion/genetics ; Ultraviolet Rays
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  • 33
    Publication Date: 2009-12-18
    Description: Effects of susceptibility variants may depend on from which parent they are inherited. Although many associations between sequence variants and human traits have been discovered through genome-wide associations, the impact of parental origin has largely been ignored. Here we show that for 38,167 Icelanders genotyped using single nucleotide polymorphism (SNP) chips, the parental origin of most alleles can be determined. For this we used a combination of genealogy and long-range phasing. We then focused on SNPs that associate with diseases and are within 500 kilobases of known imprinted genes. Seven independent SNP associations were examined. Five-one with breast cancer, one with basal-cell carcinoma and three with type 2 diabetes-have parental-origin-specific associations. These variants are located in two genomic regions, 11p15 and 7q32, each harbouring a cluster of imprinted genes. Furthermore, we observed a novel association between the SNP rs2334499 at 11p15 and type 2 diabetes. Here the allele that confers risk when paternally inherited is protective when maternally transmitted. We identified a differentially methylated CTCF-binding site at 11p15 and demonstrated correlation of rs2334499 with decreased methylation of that site.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3746295/" 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/PMC3746295/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kong, Augustine -- Steinthorsdottir, Valgerdur -- Masson, Gisli -- Thorleifsson, Gudmar -- Sulem, Patrick -- Besenbacher, Soren -- Jonasdottir, Aslaug -- Sigurdsson, Asgeir -- Kristinsson, Kari Th -- Jonasdottir, Adalbjorg -- Frigge, Michael L -- Gylfason, Arnaldur -- Olason, Pall I -- Gudjonsson, Sigurjon A -- Sverrisson, Sverrir -- Stacey, Simon N -- Sigurgeirsson, Bardur -- Benediktsdottir, Kristrun R -- Sigurdsson, Helgi -- Jonsson, Thorvaldur -- Benediktsson, Rafn -- Olafsson, Jon H -- Johannsson, Oskar Th -- Hreidarsson, Astradur B -- Sigurdsson, Gunnar -- DIAGRAM Consortium -- Ferguson-Smith, Anne C -- Gudbjartsson, Daniel F -- Thorsteinsdottir, Unnur -- Stefansson, Kari -- 077016/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- G9723500/Medical Research Council/United Kingdom -- K08 AR055688/AR/NIAMS NIH HHS/ -- MC_U106179471/Medical Research Council/United Kingdom -- MC_U106179474/Medical Research Council/United Kingdom -- MC_U127592696/Medical Research Council/United Kingdom -- R01 DK029867/DK/NIDDK NIH HHS/ -- England -- Nature. 2009 Dec 17;462(7275):868-74. doi: 10.1038/nature08625.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉deCODE genetics, Sturlugata 8, 101 Reykjavik, Iceland. kong@decode.is〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016592" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Binding Sites ; Breast Neoplasms/genetics ; Carcinoma, Basal Cell/genetics ; Chromosomes, Human, Pair 11/genetics ; Chromosomes, Human, Pair 7/genetics ; DNA Methylation/genetics ; Diabetes Mellitus, Type 2/genetics ; *Fathers ; Female ; Genetic Predisposition to Disease/*genetics ; Genome, Human/genetics ; Genomic Imprinting/genetics ; Haplotypes ; Humans ; Iceland ; Male ; *Mothers ; Pedigree ; Polymorphism, Single Nucleotide/*genetics ; Repressor Proteins/metabolism
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  • 34
    Publication Date: 2009-12-18
    Description: Mutations in BRCA1 are associated with a high risk of breast and ovarian cancer. BRCA1 participates in the DNA damage response and acts as a ubiquitin ligase. However, its regulation remains poorly understood. Here we report that BRCA1 is modified by small ubiquitin-like modifier (SUMO) in response to genotoxic stress, and co-localizes at sites of DNA damage with SUMO1, SUMO2/3 and the SUMO-conjugating enzyme Ubc9. PIAS SUMO E3 ligases co-localize with and modulate SUMO modification of BRCA1, and are required for BRCA1 ubiquitin ligase activity in cells. In vitro SUMO modification of the BRCA1/BARD1 heterodimer greatly increases its ligase activity, identifying it as a SUMO-regulated ubiquitin ligase (SRUbL). Further, PIAS SUMO ligases are required for complete accumulation of double-stranded DNA (dsDNA) damage-repair proteins subsequent to RNF8 accrual, and for proficient double-strand break repair. These data demonstrate that the SUMOylation pathway plays a significant role in mammalian DNA damage response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morris, Joanna R -- Boutell, Chris -- Keppler, Melanie -- Densham, Ruth -- Weekes, Daniel -- Alamshah, Amin -- Butler, Laura -- Galanty, Yaron -- Pangon, Laurent -- Kiuchi, Tai -- Ng, Tony -- Solomon, Ellen -- 10331/Cancer Research UK/United Kingdom -- 6900577/Medical Research Council/United Kingdom -- C8820/A9494/Cancer Research UK/United Kingdom -- G0100152 #56891/Medical Research Council/United Kingdom -- G9600577/Medical Research Council/United Kingdom -- MC_UP_A550_1030/Medical Research Council/United Kingdom -- England -- Nature. 2009 Dec 17;462(7275):886-90. doi: 10.1038/nature08593.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical and Molecular Genetics, King's College London, Guy's Medical School Campus, London SE1 9RT, UK. jo.morris@genetics.kcl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016594" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/*metabolism ; COS Cells ; Cell Line ; Cercopithecus aethiops ; DNA Breaks, Double-Stranded ; *DNA Damage ; DNA Repair ; HeLa Cells ; Histones/metabolism ; Humans ; Protein Inhibitors of Activated STAT/metabolism ; Small Ubiquitin-Related Modifier Proteins/*metabolism ; Ubiquitin-Conjugating Enzymes/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination
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  • 35
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    Nature Publishing Group (NPG)
    Publication Date: 2009-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dolgin, Elie -- England -- Nature. 2009 Dec 17;462(7275):843-5. doi: 10.1038/462843a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016572" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Genome, Human/*genetics ; History, 20th Century ; History, 21st Century ; *Human Genome Project/history ; Humans ; Male ; Reproducibility of Results ; Research Design ; *Research Personnel ; Research Subjects
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  • 36
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    Nature Publishing Group (NPG)
    Publication Date: 2009-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuper, Adam -- England -- Nature. 2009 Dec 17;462(7275):862. doi: 10.1038/462862a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anthropology, Yale University, New Haven, Connecticut 06520, USA. adam.kuper@googlemail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016590" target="_blank"〉PubMed〈/a〉
    Keywords: Anthropology/*history ; Brazil ; France ; History, 20th Century ; Humans ; Indians, South American
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  • 37
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    Nature Publishing Group (NPG)
    Publication Date: 2009-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wadman, Meredith -- England -- Nature. 2009 Dec 17;462(7275):837. doi: 10.1038/462837a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016569" target="_blank"〉PubMed〈/a〉
    Keywords: Embryo Research/economics/ethics/*legislation & jurisprudence ; *Embryonic Stem Cells ; Humans ; *Informed Consent ; National Institutes of Health (U.S.)/legislation & jurisprudence ; United States
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  • 38
    Publication Date: 2009-12-18
    Description: DNA double-strand breaks (DSBs) are highly cytotoxic lesions that are generated by ionizing radiation and various DNA-damaging chemicals. Following DSB formation, cells activate the DNA-damage response (DDR) protein kinases ATM, ATR and DNA-PK (also known as PRKDC). These then trigger histone H2AX (also known as H2AFX) phosphorylation and the accumulation of proteins such as MDC1, 53BP1 (also known as TP53BP1), BRCA1, CtIP (also known as RBBP8), RNF8 and RNF168/RIDDLIN into ionizing radiation-induced foci (IRIF) that amplify DSB signalling and promote DSB repair. Attachment of small ubiquitin-related modifier (SUMO) to target proteins controls diverse cellular functions. Here, we show that SUMO1, SUMO2 and SUMO3 accumulate at DSB sites in mammalian cells, with SUMO1 and SUMO2/3 accrual requiring the E3 ligase enzymes PIAS4 and PIAS1. We also establish that PIAS1 and PIAS4 are recruited to damage sites via mechanisms requiring their SAP domains, and are needed for the productive association of 53BP1, BRCA1 and RNF168 with such regions. Furthermore, we show that PIAS1 and PIAS4 promote DSB repair and confer ionizing radiation resistance. Finally, we establish that PIAS1 and PIAS4 are required for effective ubiquitin-adduct formation mediated by RNF8, RNF168 and BRCA1 at sites of DNA damage. These findings thus identify PIAS1 and PIAS4 as components of the DDR and reveal how protein recruitment to DSB sites is controlled by coordinated SUMOylation and ubiquitylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2904806/" 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/PMC2904806/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galanty, Yaron -- Belotserkovskaya, Rimma -- Coates, Julia -- Polo, Sophie -- Miller, Kyle M -- Jackson, Stephen P -- 086861/Wellcome Trust/United Kingdom -- 11224/Cancer Research UK/United Kingdom -- A5290/Cancer Research UK/United Kingdom -- Cancer Research UK/United Kingdom -- England -- Nature. 2009 Dec 17;462(7275):935-9. doi: 10.1038/nature08657.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Wellcome Trust and Cancer Research UK Gurdon Institute, and Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016603" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/metabolism ; Cell Line ; Cell Line, Tumor ; *DNA Breaks, Double-Stranded ; *DNA Repair ; DNA-Binding Proteins/genetics/metabolism ; Fluorescence Recovery After Photobleaching ; Humans ; Intracellular Signaling Peptides and Proteins/genetics/metabolism ; Models, Biological ; Phosphorylation ; Protein Inhibitors of Activated STAT/chemistry/genetics/*metabolism ; Protein Structure, Tertiary ; Replication Protein A/metabolism ; Small Ubiquitin-Related Modifier Proteins/genetics/*metabolism ; Ubiquitin-Conjugating Enzymes/genetics/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination
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  • 39
    Publication Date: 2009-12-18
    Description: Many collective human activities, including violence, have been shown to exhibit universal patterns. The size distributions of casualties both in whole wars from 1816 to 1980 and terrorist attacks have separately been shown to follow approximate power-law distributions. However, the possibility of universal patterns ranging across wars in the size distribution or timing of within-conflict events has barely been explored. Here we show that the sizes and timing of violent events within different insurgent conflicts exhibit remarkable similarities. We propose a unified model of human insurgency that reproduces these commonalities, and explains conflict-specific variations quantitatively in terms of underlying rules of engagement. Our model treats each insurgent population as an ecology of dynamically evolving, self-organized groups following common decision-making processes. Our model is consistent with several recent hypotheses about modern insurgency, is robust to many generalizations, and establishes a quantitative connection between human insurgency, global terrorism and ecology. Its similarity to financial market models provides a surprising link between violent and non-violent forms of human behaviour.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bohorquez, Juan Camilo -- Gourley, Sean -- Dixon, Alexander R -- Spagat, Michael -- Johnson, Neil F -- England -- Nature. 2009 Dec 17;462(7275):911-4. doi: 10.1038/nature08631.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Industrial Engineering and CEIBA Complex Systems Research Center, Universidad de Los Andes, Bogota, Colombia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016600" target="_blank"〉PubMed〈/a〉
    Keywords: Afghanistan ; Colombia ; *Conflict (Psychology) ; Decision Making ; *Ecology ; Group Processes ; Humans ; Iraq ; Models, Economic ; Terrorism ; Time Factors ; *Violence ; *Warfare
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  • 40
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    Nature Publishing Group (NPG)
    Publication Date: 2009-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boulton, Simon J -- England -- Nature. 2009 Dec 17;462(7275):857-8. doi: 10.1038/462857a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016586" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Breaks, Double-Stranded ; DNA Repair/*physiology ; Humans ; Protein Inhibitors of Activated STAT/*metabolism ; Small Ubiquitin-Related Modifier Proteins/*metabolism ; Ubiquitination
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  • 41
    Publication Date: 2009-12-18
    Description: Cancer is driven by mutation. Worldwide, tobacco smoking is the principal lifestyle exposure that causes cancer, exerting carcinogenicity through 〉60 chemicals that bind and mutate DNA. Using massively parallel sequencing technology, we sequenced a small-cell lung cancer cell line, NCI-H209, to explore the mutational burden associated with tobacco smoking. A total of 22,910 somatic substitutions were identified, including 134 in coding exons. Multiple mutation signatures testify to the cocktail of carcinogens in tobacco smoke and their proclivities for particular bases and surrounding sequence context. Effects of transcription-coupled repair and a second, more general, expression-linked repair pathway were evident. We identified a tandem duplication that duplicates exons 3-8 of CHD7 in frame, and another two lines carrying PVT1-CHD7 fusion genes, indicating that CHD7 may be recurrently rearranged in this disease. These findings illustrate the potential for next-generation sequencing to provide unprecedented insights into mutational processes, cellular repair pathways and gene networks associated with cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2880489/" 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/PMC2880489/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pleasance, Erin D -- Stephens, Philip J -- O'Meara, Sarah -- McBride, David J -- Meynert, Alison -- Jones, David -- Lin, Meng-Lay -- Beare, David -- Lau, King Wai -- Greenman, Chris -- Varela, Ignacio -- Nik-Zainal, Serena -- Davies, Helen R -- Ordonez, Gonzalo R -- Mudie, Laura J -- Latimer, Calli -- Edkins, Sarah -- Stebbings, Lucy -- Chen, Lina -- Jia, Mingming -- Leroy, Catherine -- Marshall, John -- Menzies, Andrew -- Butler, Adam -- Teague, Jon W -- Mangion, Jonathon -- Sun, Yongming A -- McLaughlin, Stephen F -- Peckham, Heather E -- Tsung, Eric F -- Costa, Gina L -- Lee, Clarence C -- Minna, John D -- Gazdar, Adi -- Birney, Ewan -- Rhodes, Michael D -- McKernan, Kevin J -- Stratton, Michael R -- Futreal, P Andrew -- Campbell, Peter J -- 077012/Wellcome Trust/United Kingdom -- 077012/Z/05/Z/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- 093867/Wellcome Trust/United Kingdom -- P50 CA070907/CA/NCI NIH HHS/ -- P50CA70907/CA/NCI NIH HHS/ -- England -- Nature. 2010 Jan 14;463(7278):184-90. doi: 10.1038/nature08629. Epub 2009 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016488" target="_blank"〉PubMed〈/a〉
    Keywords: Carcinogens/toxicity ; Cell Line, Tumor ; DNA Copy Number Variations/drug effects/genetics ; DNA Damage/genetics ; DNA Helicases/genetics ; DNA Mutational Analysis ; DNA Repair/genetics ; DNA-Binding Proteins/genetics ; Exons/genetics ; Gene Expression Regulation, Neoplastic/drug effects ; Genome, Human/drug effects/genetics ; Humans ; Lung Neoplasms/*etiology/*genetics ; Mutagenesis, Insertional/drug effects/genetics ; Mutation/drug effects/*genetics ; Promoter Regions, Genetic/genetics ; Sequence Deletion/genetics ; Small Cell Lung Carcinoma/*etiology/*genetics ; Smoking/*adverse effects ; Tobacco/*adverse effects
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  • 42
    Publication Date: 2009-12-17
    Description: Using next-generation sequencing technology alone, we have successfully generated and assembled a draft sequence of the giant panda genome. The assembled contigs (2.25 gigabases (Gb)) cover approximately 94% of the whole genome, and the remaining gaps (0.05 Gb) seem to contain carnivore-specific repeats and tandem repeats. Comparisons with the dog and human showed that the panda genome has a lower divergence rate. The assessment of panda genes potentially underlying some of its unique traits indicated that its bamboo diet might be more dependent on its gut microbiome than its own genetic composition. We also identified more than 2.7 million heterozygous single nucleotide polymorphisms in the diploid genome. Our data and analyses provide a foundation for promoting mammalian genetic research, and demonstrate the feasibility for using next-generation sequencing technologies for accurate, cost-effective and rapid de novo assembly of large eukaryotic genomes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3951497/" 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/PMC3951497/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Ruiqiang -- Fan, Wei -- Tian, Geng -- Zhu, Hongmei -- He, Lin -- Cai, Jing -- Huang, Quanfei -- Cai, Qingle -- Li, Bo -- Bai, Yinqi -- Zhang, Zhihe -- Zhang, Yaping -- Wang, Wen -- Li, Jun -- Wei, Fuwen -- Li, Heng -- Jian, Min -- Li, Jianwen -- Zhang, Zhaolei -- Nielsen, Rasmus -- Li, Dawei -- Gu, Wanjun -- Yang, Zhentao -- Xuan, Zhaoling -- Ryder, Oliver A -- Leung, Frederick Chi-Ching -- Zhou, Yan -- Cao, Jianjun -- Sun, Xiao -- Fu, Yonggui -- Fang, Xiaodong -- Guo, Xiaosen -- Wang, Bo -- Hou, Rong -- Shen, Fujun -- Mu, Bo -- Ni, Peixiang -- Lin, Runmao -- Qian, Wubin -- Wang, Guodong -- Yu, Chang -- Nie, Wenhui -- Wang, Jinhuan -- Wu, Zhigang -- Liang, Huiqing -- Min, Jiumeng -- Wu, Qi -- Cheng, Shifeng -- Ruan, Jue -- Wang, Mingwei -- Shi, Zhongbin -- Wen, Ming -- Liu, Binghang -- Ren, Xiaoli -- Zheng, Huisong -- Dong, Dong -- Cook, Kathleen -- Shan, Gao -- Zhang, Hao -- Kosiol, Carolin -- Xie, Xueying -- Lu, Zuhong -- Zheng, Hancheng -- Li, Yingrui -- Steiner, Cynthia C -- Lam, Tommy Tsan-Yuk -- Lin, Siyuan -- Zhang, Qinghui -- Li, Guoqing -- Tian, Jing -- Gong, Timing -- Liu, Hongde -- Zhang, Dejin -- Fang, Lin -- Ye, Chen -- Zhang, Juanbin -- Hu, Wenbo -- Xu, Anlong -- Ren, Yuanyuan -- Zhang, Guojie -- Bruford, Michael W -- Li, Qibin -- Ma, Lijia -- Guo, Yiran -- An, Na -- Hu, Yujie -- Zheng, Yang -- Shi, Yongyong -- Li, Zhiqiang -- Liu, Qing -- Chen, Yanling -- Zhao, Jing -- Qu, Ning -- Zhao, Shancen -- Tian, Feng -- Wang, Xiaoling -- Wang, Haiyin -- Xu, Lizhi -- Liu, Xiao -- Vinar, Tomas -- Wang, Yajun -- Lam, Tak-Wah -- Yiu, Siu-Ming -- Liu, Shiping -- Zhang, Hemin -- Li, Desheng -- Huang, Yan -- Wang, Xia -- Yang, Guohua -- Jiang, Zhi -- Wang, Junyi -- Qin, Nan -- Li, Li -- Li, Jingxiang -- Bolund, Lars -- Kristiansen, Karsten -- Wong, Gane Ka-Shu -- Olson, Maynard -- Zhang, Xiuqing -- Li, Songgang -- Yang, Huanming -- Wang, Jian -- Wang, Jun -- R01 HG003229/HG/NHGRI NIH HHS/ -- R01 HG003229-05/HG/NHGRI NIH HHS/ -- England -- Nature. 2010 Jan 21;463(7279):311-7. doi: 10.1038/nature08696. Epub 2009 Dec 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BGI-Shenzhen, Shenzhen 518083, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20010809" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; China ; Conserved Sequence/genetics ; Contig Mapping ; Diet/veterinary ; Dogs ; Evolution, Molecular ; Female ; Fertility/genetics/physiology ; Genome/*genetics ; *Genomics ; Heterozygote ; Humans ; Multigene Family/genetics ; Polymorphism, Single Nucleotide/genetics ; Receptors, G-Protein-Coupled/genetics ; Sequence Alignment ; Sequence Analysis, DNA ; Synteny/genetics ; Ursidae/classification/*genetics/physiology
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  • 43
    Publication Date: 2009-12-17
    Description: Recent research on changing fears has examined targeting reconsolidation. During reconsolidation, stored information is rendered labile after being retrieved. Pharmacological manipulations at this stage result in an inability to retrieve the memories at later times, suggesting that they are erased or persistently inhibited. Unfortunately, the use of these pharmacological manipulations in humans can be problematic. Here we introduce a non-invasive technique to target the reconsolidation of fear memories in humans. We provide evidence that old fear memories can be updated with non-fearful information provided during the reconsolidation window. As a consequence, fear responses are no longer expressed, an effect that lasted at least a year and was selective only to reactivated memories without affecting others. These findings demonstrate the adaptive role of reconsolidation as a window of opportunity to rewrite emotional memories, and suggest a non-invasive technique that can be used safely in humans to prevent the return of fear.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3640262/" 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/PMC3640262/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schiller, Daniela -- Monfils, Marie-H -- Raio, Candace M -- Johnson, David C -- Ledoux, Joseph E -- Phelps, Elizabeth A -- K05 MH067048/MH/NIMH NIH HHS/ -- P50 MH058911/MH/NIMH NIH HHS/ -- R01 MH038774/MH/NIMH NIH HHS/ -- R01 MH046516/MH/NIMH NIH HHS/ -- R21 MH072279/MH/NIMH NIH HHS/ -- R37 MH038774/MH/NIMH NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2010 Jan 7;463(7277):49-53. doi: 10.1038/nature08637. Epub 2009 Dec 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neural Science, New York University, New York, New York 10003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20010606" target="_blank"〉PubMed〈/a〉
    Keywords: Conditioning, Classical/*physiology ; Cues ; Electrodes ; Electroshock ; Extinction, Psychological/*physiology ; Fear/*physiology/*psychology ; Humans ; Memory/*physiology ; Models, Neurological ; Models, Psychological ; Neuronal Plasticity/*physiology ; Photic Stimulation ; Time Factors
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  • 44
    Publication Date: 2009-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knepper, Mark A -- Mindell, Joseph A -- England -- Nature. 2009 Dec 10;462(7274):733-4. doi: 10.1038/462733a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20010678" target="_blank"〉PubMed〈/a〉
    Keywords: Crystallography, X-Ray ; Desulfovibrio vulgaris/*chemistry ; Humans ; Kidney/metabolism ; Membrane Transport Proteins/*chemistry/*metabolism ; Protein Structure, Quaternary ; Structure-Activity Relationship ; Urea/chemistry/*metabolism
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  • 45
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    Nature Publishing Group (NPG)
    Publication Date: 2009-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nayar, Anjali -- England -- Nature. 2009 Dec 10;462(7274):717-9. doi: 10.1038/462717a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20010663" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cameroon/epidemiology ; Communicable Diseases, Emerging/epidemiology/prevention & ; control/*transmission/*virology ; Disease Outbreaks/prevention & control/veterinary ; History, 20th Century ; History, 21st Century ; Humans ; Population Surveillance/*methods ; Zoonoses/epidemiology/*transmission/*virology
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  • 46
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    Nature Publishing Group (NPG)
    Publication Date: 2009-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wadman, Meredith -- England -- Nature. 2009 Dec 10;462(7274):711. doi: 10.1038/462711a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20010660" target="_blank"〉PubMed〈/a〉
    Keywords: Clinical Trials as Topic ; Complementary Therapies/*trends ; Evidence-Based Medicine/*trends ; Humans ; National Institutes of Health (U.S.)/*trends ; Pain/prevention & control ; Pain Management ; United States
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  • 47
    Publication Date: 2009-12-17
    Description: Techniques to detect and quantify DNA and RNA molecules in biological samples have had a central role in genomics research. Over the past decade, several techniques have been developed to improve detection performance and reduce the cost of genetic analysis. In particular, significant advances in label-free methods have been reported. Yet detection of DNA molecules at concentrations below the femtomolar level requires amplified detection schemes. Here we report a unique nanomechanical response of hybridized DNA and RNA molecules that serves as an intrinsic molecular label. Nanomechanical measurements on a microarray surface have sufficient background signal rejection to allow direct detection and counting of hybridized molecules. The digital response of the sensor provides a large dynamic range that is critical for gene expression profiling. We have measured differential expressions of microRNAs in tumour samples; such measurements have been shown to help discriminate between the tissue origins of metastatic tumours. Two hundred picograms of total RNA is found to be sufficient for this analysis. In addition, the limit of detection in pure samples is found to be one attomolar. These results suggest that nanomechanical read-out of microarrays promises attomolar-level sensitivity and large dynamic range for the analysis of gene expression, while eliminating biochemical manipulations, amplification and labelling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2966338/" 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/PMC2966338/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Husale, Sudhir -- Persson, Henrik H J -- Sahin, Ozgur -- HG000205/HG/NHGRI NIH HHS/ -- P01 HG000205/HG/NHGRI NIH HHS/ -- P01 HG000205-20/HG/NHGRI NIH HHS/ -- England -- Nature. 2009 Dec 24;462(7276):1075-8. doi: 10.1038/nature08626. Epub 2009 Dec 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Rowland Institute at Harvard, Harvard University, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20010806" target="_blank"〉PubMed〈/a〉
    Keywords: DNA, Complementary/*genetics ; Gene Expression Profiling/economics/*methods ; Humans ; *Mechanical Phenomena ; MicroRNAs/*genetics ; Nucleic Acid Hybridization ; Oligonucleotide Array Sequence Analysis/economics/*methods ; Sensitivity and Specificity
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  • 48
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1468-9. doi: 10.1126/science.326.5959.1468-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007873" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Proliferation ; Clinical Trials as Topic ; *Genetic Therapy ; Genetic Vectors ; HMGA2 Protein/genetics ; Hemoglobins/analysis ; Humans ; Male ; United States ; Young Adult ; beta-Globins/biosynthesis/*genetics ; beta-Thalassemia/genetics/*therapy
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  • 49
    Publication Date: 2009-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1478-9. doi: 10.1126/science.326.5959.1478.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007881" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Animals ; *Biological Evolution ; Diabetes Mellitus/epidemiology/etiology ; *Diet/history ; Dietary Carbohydrates ; Energy Intake ; Ethnic Groups ; Fossils ; History, Ancient ; Hominidae ; Humans ; Hypertension/epidemiology/etiology ; Meat ; Obesity/epidemiology/etiology
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  • 50
    Publication Date: 2009-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1476-7. doi: 10.1126/science.326.5959.1476.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007880" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines ; CD4-Positive T-Lymphocytes/*immunology/virology ; Female ; Genes ; HIV/immunology/physiology ; HIV Infections/*immunology ; Hemophilia A ; Homosexuality, Male ; Humans ; *Immunity, Innate ; Killer Cells, Natural/immunology ; Lymphocyte Activation ; Male ; Prostitution ; T-Lymphocytes, Regulatory/immunology
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  • 51
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mann, Charles C -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1466. doi: 10.1126/science.326.5959.1466.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007870" target="_blank"〉PubMed〈/a〉
    Keywords: *Anthropology/ethics ; Brazil ; Humans ; *Indians, South American ; *Societies, Scientific ; United States ; Venezuela
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  • 52
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1467. doi: 10.1126/science.326.5959.1467-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007872" target="_blank"〉PubMed〈/a〉
    Keywords: *Cell Line ; *Embryo Research/economics ; *Embryonic Stem Cells ; Financing, Government ; Humans ; *National Institutes of Health (U.S.)/economics ; Research Support as Topic ; United States
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  • 53
    Publication Date: 2009-12-17
    Description: Metabotropic glutamate receptor 5 (mGluR5) is highly expressed in the mammalian central nervous system (CNS). It is involved in multiple physiological functions and is a target for treatment of various CNS disorders, including schizophrenia. We report that Norbin, a neuron-specific protein, physically interacts with mGluR5 in vivo, increases the cell surface localization of the receptor, and positively regulates mGluR5 signaling. Genetic deletion of Norbin attenuates mGluR5-dependent stable changes in synaptic function measured as long-term depression or long-term potentiation of synaptic transmission in the hippocampus. As with mGluR5 knockout mice or mice treated with mGluR5-selective antagonists, Norbin knockout mice showed a behavioral phenotype associated with a rodent model of schizophrenia, as indexed by alterations both in sensorimotor gating and psychotomimetic-induced locomotor activity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796550/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796550/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Hong -- Westin, Linda -- Nong, Yi -- Birnbaum, Shari -- Bendor, Jacob -- Brismar, Hjalmar -- Nestler, Eric -- Aperia, Anita -- Flajolet, Marc -- Greengard, Paul -- DA 10044/DA/NIDA NIH HHS/ -- MH074866/MH/NIMH NIH HHS/ -- MH66172/MH/NIMH NIH HHS/ -- P01 DA010044/DA/NIDA NIH HHS/ -- P01 DA010044-020002/DA/NIDA NIH HHS/ -- P01 DA010044-030002/DA/NIDA NIH HHS/ -- P01 DA010044-04/DA/NIDA NIH HHS/ -- P01 DA010044-040002/DA/NIDA NIH HHS/ -- P01 DA010044-05/DA/NIDA NIH HHS/ -- P01 DA010044-050002/DA/NIDA NIH HHS/ -- P01 DA010044-06/DA/NIDA NIH HHS/ -- P01 DA010044-060002/DA/NIDA NIH HHS/ -- P01 DA010044-07/DA/NIDA NIH HHS/ -- P01 DA010044-070002/DA/NIDA NIH HHS/ -- P01 DA010044-08/DA/NIDA NIH HHS/ -- P01 DA010044-080002/DA/NIDA NIH HHS/ -- P01 DA010044-09/DA/NIDA NIH HHS/ -- P01 DA010044-090002/DA/NIDA NIH HHS/ -- P01 DA010044-10/DA/NIDA NIH HHS/ -- P01 DA010044-100002/DA/NIDA NIH HHS/ -- P01 DA010044-11/DA/NIDA NIH HHS/ -- P01 DA010044-110005/DA/NIDA NIH HHS/ -- P01 DA010044-12/DA/NIDA NIH HHS/ -- P01 DA010044-120005/DA/NIDA NIH HHS/ -- P01 DA010044-129002/DA/NIDA NIH HHS/ -- P01 DA010044-13/DA/NIDA NIH HHS/ -- P01 DA010044-130005/DA/NIDA NIH HHS/ -- P01 DA010044-139002/DA/NIDA NIH HHS/ -- P01 DA010044-14/DA/NIDA NIH HHS/ -- P01 DA010044-140005/DA/NIDA NIH HHS/ -- P01 DA010044-149002/DA/NIDA NIH HHS/ -- P01 DA010044-14S1/DA/NIDA NIH HHS/ -- P01 DA010044-14S10005/DA/NIDA NIH HHS/ -- P01 DA010044-14S19002/DA/NIDA NIH HHS/ -- P50 MH074866/MH/NIMH NIH HHS/ -- P50 MH074866-010001/MH/NIMH NIH HHS/ -- P50 MH074866-020001/MH/NIMH NIH HHS/ -- P50 MH074866-030001/MH/NIMH NIH HHS/ -- P50 MH074866-039001/MH/NIMH NIH HHS/ -- P50 MH074866-040001/MH/NIMH NIH HHS/ -- P50 MH074866-050001/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1554-7. doi: 10.1126/science.1178496.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007903" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Calcium/metabolism ; Calcium Signaling ; Cell Line ; Cell Membrane/metabolism ; Humans ; Mice ; Mice, Knockout ; Motor Activity ; Nerve Tissue Proteins/genetics/*metabolism ; Neuronal Plasticity ; Protein Binding ; Rats ; Receptor, Metabotropic Glutamate 5 ; Receptors, Metabotropic Glutamate/genetics/*metabolism ; Reflex, Startle ; Schizophrenia/physiopathology ; *Signal Transduction ; Synaptic Transmission ; Transfection
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  • 54
    Publication Date: 2009-12-17
    Description: Cells have self-organizing properties that control their behavior in complex tissues. Contact between cells expressing either B-type Eph receptors or their transmembrane ephrin ligands initiates bidirectional signals that regulate cell positioning. However, simultaneously investigating how information is processed in two interacting cell types remains a challenge. We implemented a proteomic strategy to systematically determine cell-specific signaling networks underlying EphB2- and ephrin-B1-controlled cell sorting. Quantitative mass spectrometric analysis of mixed populations of EphB2- and ephrin-B1-expressing cells that were labeled with different isotopes revealed cell-specific tyrosine phosphorylation events. Functional associations between these phosphotyrosine signaling networks and cell sorting were established with small interfering RNA screening. Data-driven network modeling revealed that signaling between mixed EphB2- and ephrin-B1-expressing cells is asymmetric and that the distinct cell types use different tyrosine kinases and targets to process signals induced by cell-cell contact. We provide systems- and cell-specific network models of contact-initiated signaling between two distinct cell types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jorgensen, Claus -- Sherman, Andrew -- Chen, Ginny I -- Pasculescu, Adrian -- Poliakov, Alexei -- Hsiung, Marilyn -- Larsen, Brett -- Wilkinson, David G -- Linding, Rune -- Pawson, Tony -- MC_U117532048/Medical Research Council/United Kingdom -- MOP-6849/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1502-9. doi: 10.1126/science.1176615.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute (SLRI), Mount Sinai Hospital, Toronto M5G 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007894" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Algorithms ; Cell Line ; Ephrin-B1/genetics/*metabolism ; Humans ; Ligands ; Mass Spectrometry ; Models, Biological ; PDZ Domains ; Phosphorylation ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein-Tyrosine Kinases/metabolism ; Proteomics ; RNA, Small Interfering ; Receptor, EphB2/genetics/*metabolism ; *Signal Transduction ; Tyrosine/metabolism ; src Homology Domains
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  • 55
    Publication Date: 2009-12-17
    Description: Glucose-6-phosphate dehydrogenase (G6PD) deficiency--the most common known enzymopathy--is associated with neonatal jaundice and hemolytic anemia usually after exposure to certain infections, foods, or medications. Although G6PD-deficient alleles appear to confer a protective effect against malaria, the link with clinical protection from Plasmodium infection remains unclear. We investigated the effect of a common G6PD deficiency variant in Southeast Asia--the G6PD-Mahidol(487A) variant--on human survival related to vivax and falciparum malaria. Our results show that strong and recent positive selection has targeted the Mahidol variant over the past 1500 years. We found that the G6PD-Mahidol(487A) variant reduces vivax, but not falciparum, parasite density in humans, which indicates that Plasmodium vivax has been a driving force behind the strong selective advantage conferred by this mutation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Louicharoen, Chalisa -- Patin, Etienne -- Paul, Richard -- Nuchprayoon, Issarang -- Witoonpanich, Bhee -- Peerapittayamongkol, Chayanon -- Casademont, Isabelle -- Sura, Thanyachai -- Laird, Nan M -- Singhasivanon, Pratap -- Quintana-Murci, Lluis -- Sakuntabhai, Anavaj -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1546-9. doi: 10.1126/science.1178849.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Pasteur, Laboratoire de la Genetique de la reponse aux infections chez l'homme, 75724 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007901" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Erythrocytes/metabolism/parasitology ; Female ; Gene Dosage ; Genetic Association Studies ; Genetic Predisposition to Disease ; Genotype ; Glucosephosphate Dehydrogenase/*genetics ; Glucosephosphate Dehydrogenase Deficiency/blood/complications/*genetics ; Haplotypes ; Humans ; Immunity, Innate ; Malaria, Falciparum/complications/genetics/parasitology ; Malaria, Vivax/complications/genetics/*parasitology ; Male ; *Mutation ; Plasmodium falciparum/physiology ; Plasmodium vivax/*physiology ; Polymorphism, Single Nucleotide ; *Selection, Genetic ; Thailand
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  • 56
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Normile, Dennis -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1470. doi: 10.1126/science.326.5959.1470.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007876" target="_blank"〉PubMed〈/a〉
    Keywords: Asia ; Asian Continental Ancestry Group/*genetics/history ; *Emigration and Immigration/history ; Ethnic Groups/*genetics/history ; Haplotypes ; History, Ancient ; Humans ; *Polymorphism, Single Nucleotide ; Population Dynamics
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  • 57
    Publication Date: 2009-12-17
    Description: Asia harbors substantial cultural and linguistic diversity, but the geographic structure of genetic variation across the continent remains enigmatic. Here we report a large-scale survey of autosomal variation from a broad geographic sample of Asian human populations. Our results show that genetic ancestry is strongly correlated with linguistic affiliations as well as geography. Most populations show relatedness within ethnic/linguistic groups, despite prevalent gene flow among populations. More than 90% of East Asian (EA) haplotypes could be found in either Southeast Asian (SEA) or Central-South Asian (CSA) populations and show clinal structure with haplotype diversity decreasing from south to north. Furthermore, 50% of EA haplotypes were found in SEA only and 5% were found in CSA only, indicating that SEA was a major geographic source of EA populations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉HUGO Pan-Asian SNP Consortium -- Abdulla, Mahmood Ameen -- Ahmed, Ikhlak -- Assawamakin, Anunchai -- Bhak, Jong -- Brahmachari, Samir K -- Calacal, Gayvelline C -- Chaurasia, Amit -- Chen, Chien-Hsiun -- Chen, Jieming -- Chen, Yuan-Tsong -- Chu, Jiayou -- Cutiongco-de la Paz, Eva Maria C -- De Ungria, Maria Corazon A -- Delfin, Frederick C -- Edo, Juli -- Fuchareon, Suthat -- Ghang, Ho -- Gojobori, Takashi -- Han, Junsong -- Ho, Sheng-Feng -- Hoh, Boon Peng -- Huang, Wei -- Inoko, Hidetoshi -- Jha, Pankaj -- Jinam, Timothy A -- Jin, Li -- Jung, Jongsun -- Kangwanpong, Daoroong -- Kampuansai, Jatupol -- Kennedy, Giulia C -- Khurana, Preeti -- Kim, Hyung-Lae -- Kim, Kwangjoong -- Kim, Sangsoo -- Kim, Woo-Yeon -- Kimm, Kuchan -- Kimura, Ryosuke -- Koike, Tomohiro -- Kulawonganunchai, Supasak -- Kumar, Vikrant -- Lai, Poh San -- Lee, Jong-Young -- Lee, Sunghoon -- Liu, Edison T -- Majumder, Partha P -- Mandapati, Kiran Kumar -- Marzuki, Sangkot -- Mitchell, Wayne -- Mukerji, Mitali -- Naritomi, Kenji -- Ngamphiw, Chumpol -- Niikawa, Norio -- Nishida, Nao -- Oh, Bermseok -- Oh, Sangho -- Ohashi, Jun -- Oka, Akira -- Ong, Rick -- Padilla, Carmencita D -- Palittapongarnpim, Prasit -- Perdigon, Henry B -- Phipps, Maude Elvira -- Png, Eileen -- Sakaki, Yoshiyuki -- Salvador, Jazelyn M -- Sandraling, Yuliana -- Scaria, Vinod -- Seielstad, Mark -- Sidek, Mohd Ros -- Sinha, Amit -- Srikummool, Metawee -- Sudoyo, Herawati -- Sugano, Sumio -- Suryadi, Helena -- Suzuki, Yoshiyuki -- Tabbada, Kristina A -- Tan, Adrian -- Tokunaga, Katsushi -- Tongsima, Sissades -- Villamor, Lilian P -- Wang, Eric -- Wang, Ying -- Wang, Haifeng -- Wu, Jer-Yuarn -- Xiao, Huasheng -- Xu, Shuhua -- Yang, Jin Ok -- Shugart, Yin Yao -- Yoo, Hyang-Sook -- Yuan, Wentao -- Zhao, Guoping -- Zilfalil, Bin Alwi -- Indian Genome Variation Consortium -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1541-5. doi: 10.1126/science.1177074.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007900" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Asia ; Asian Continental Ancestry Group/*genetics/history ; Bayes Theorem ; Cluster Analysis ; *Emigration and Immigration/history ; Ethnic Groups/*genetics/history ; Gene Flow ; Genotype ; Geography ; *Haplotypes ; History, Ancient ; Humans ; Language ; Linguistics ; Oligonucleotide Array Sequence Analysis ; Phylogeny ; *Polymorphism, Single Nucleotide ; Principal Component Analysis
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  • 58
    Publication Date: 2009-12-17
    Description: When oxygen is abundant, quiescent cells efficiently extract energy from glucose primarily by oxidative phosphorylation, whereas under the same conditions tumour cells consume glucose more avidly, converting it to lactate. This long-observed phenomenon is known as aerobic glycolysis, and is important for cell growth. Because aerobic glycolysis is only useful to growing cells, it is tightly regulated in a proliferation-linked manner. In mammals, this is partly achieved through control of pyruvate kinase isoform expression. The embryonic pyruvate kinase isoform, PKM2, is almost universally re-expressed in cancer, and promotes aerobic glycolysis, whereas the adult isoform, PKM1, promotes oxidative phosphorylation. These two isoforms result from mutually exclusive alternative splicing of the PKM pre-mRNA, reflecting inclusion of either exon 9 (PKM1) or exon 10 (PKM2). Here we show that three heterogeneous nuclear ribonucleoprotein (hnRNP) proteins, polypyrimidine tract binding protein (PTB, also known as hnRNPI), hnRNPA1 and hnRNPA2, bind repressively to sequences flanking exon 9, resulting in exon 10 inclusion. We also demonstrate that the oncogenic transcription factor c-Myc upregulates transcription of PTB, hnRNPA1 and hnRNPA2, ensuring a high PKM2/PKM1 ratio. Establishing a relevance to cancer, we show that human gliomas overexpress c-Myc, PTB, hnRNPA1 and hnRNPA2 in a manner that correlates with PKM2 expression. Our results thus define a pathway that regulates an alternative splicing event required for tumour cell proliferation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950088/" 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/PMC2950088/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉David, Charles J -- Chen, Mo -- Assanah, Marcela -- Canoll, Peter -- Manley, James L -- R01 GM048259/GM/NIGMS NIH HHS/ -- R01 GM048259-25/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Jan 21;463(7279):364-8. doi: 10.1038/nature08697. Epub 2009 Dec 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Columbia University, New York, New York 10027, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20010808" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing/*genetics ; Animals ; Cell Line, Tumor ; Exons/genetics ; Genes, myc ; Glycolysis ; Heterogeneous-Nuclear Ribonucleoprotein Group A-B/*metabolism ; Humans ; Mice ; NIH 3T3 Cells ; Neoplasms/enzymology/*genetics/*metabolism/pathology ; Oxidative Phosphorylation ; Polypyrimidine Tract-Binding Protein/*metabolism ; Protein Binding ; Proto-Oncogene Proteins c-myc/genetics/*metabolism ; Pyruvate Kinase/*genetics/metabolism ; RNA, Messenger/genetics/metabolism
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  • 59
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    Nature Publishing Group (NPG)
    Publication Date: 2009-12-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Russo, Gene -- England -- Nature. 2009 Oct 29;461(7268):1308-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19998548" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Science Disciplines/*economics/education/manpower/*trends ; Biotechnology/economics/manpower/organization & administration/trends ; Brazil ; Emigration and Immigration/statistics & numerical data ; Financing, Government ; Humans ; Research Personnel/economics/statistics & numerical data ; Research Support as Topic
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  • 60
    Publication Date: 2009-12-10
    Description: Both biosociological and psychological models, as well as animal research, suggest that testosterone has a key role in social interactions. Evidence from animal studies in rodents shows that testosterone causes aggressive behaviour towards conspecifics. Folk wisdom generalizes and adapts these findings to humans, suggesting that testosterone induces antisocial, egoistic, or even aggressive human behaviours. However, many researchers have questioned this folk hypothesis, arguing that testosterone is primarily involved in status-related behaviours in challenging social interactions, but causal evidence that discriminates between these views is sparse. Here we show that the sublingual administration of a single dose of testosterone in women causes a substantial increase in fair bargaining behaviour, thereby reducing bargaining conflicts and increasing the efficiency of social interactions. However, subjects who believed that they received testosterone-regardless of whether they actually received it or not-behaved much more unfairly than those who believed that they were treated with placebo. Thus, the folk hypothesis seems to generate a strong negative association between subjects' beliefs and the fairness of their offers, even though testosterone administration actually causes a substantial increase in the frequency of fair bargaining offers in our experiment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eisenegger, C -- Naef, M -- Snozzi, R -- Heinrichs, M -- Fehr, E -- England -- Nature. 2010 Jan 21;463(7279):356-9. doi: 10.1038/nature08711.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Empirical Research in Economics, Laboratory for Social and Neural Systems Research, University of Zurich, 8006 Zurich, Switzerland. eisenegger@iew.uzh.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19997098" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Sublingual ; Adult ; Aggression/drug effects/physiology/psychology ; Cooperative Behavior ; Double-Blind Method ; Female ; *Game Theory ; Humans ; Models, Biological ; Placebos ; *Prejudice ; Reproducibility of Results ; *Social Behavior ; Social Class ; Testosterone/administration & dosage/*pharmacology
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  • 61
    Publication Date: 2009-12-08
    Description: Obesity is a highly heritable and genetically heterogeneous disorder. Here we investigated the contribution of copy number variation to obesity in 300 Caucasian patients with severe early-onset obesity, 143 of whom also had developmental delay. Large (〉500 kilobases), rare (〈1%) deletions were significantly enriched in patients compared to 7,366 controls (P 〈 0.001). We identified several rare copy number variants that were recurrent in patients but absent or at much lower prevalence in controls. We identified five patients with overlapping deletions on chromosome 16p11.2 that were found in 2 out of 7,366 controls (P 〈 5 x 10(-5)). In three patients the deletion co-segregated with severe obesity. Two patients harboured a larger de novo 16p11.2 deletion, extending through a 593-kilobase region previously associated with autism and mental retardation; both of these patients had mild developmental delay in addition to severe obesity. In an independent sample of 1,062 patients with severe obesity alone, the smaller 16p11.2 deletion was found in an additional two patients. All 16p11.2 deletions encompass several genes but include SH2B1, which is known to be involved in leptin and insulin signalling. Deletion carriers exhibited hyperphagia and severe insulin resistance disproportionate for the degree of obesity. We show that copy number variation contributes significantly to the genetic architecture of human obesity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3108883/" 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/PMC3108883/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bochukova, Elena G -- Huang, Ni -- Keogh, Julia -- Henning, Elana -- Purmann, Carolin -- Blaszczyk, Kasia -- Saeed, Sadia -- Hamilton-Shield, Julian -- Clayton-Smith, Jill -- O'Rahilly, Stephen -- Hurles, Matthew E -- Farooqi, I Sadaf -- 077014/Wellcome Trust/United Kingdom -- 077014/Z/05/0Z/Wellcome Trust/United Kingdom -- 082390/Wellcome Trust/United Kingdom -- 082390/Z/07/Z)/Wellcome Trust/United Kingdom -- 085475/Wellcome Trust/United Kingdom -- G0900554/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2010 Feb 4;463(7281):666-70. doi: 10.1038/nature08689. Epub 2009 Dec 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19966786" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics ; Age of Onset ; Child ; *Chromosome Deletion ; Chromosomes, Human, Pair 16/*genetics ; Cohort Studies ; DNA Copy Number Variations/genetics ; Developmental Disabilities/complications/genetics ; European Continental Ancestry Group ; Genome-Wide Association Study ; Great Britain/epidemiology ; Heterozygote ; Humans ; Hyperphagia/genetics ; Inheritance Patterns/genetics ; Insulin Resistance/genetics ; Mutation/genetics ; Obesity/complications/epidemiology/*genetics/*physiopathology
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  • 62
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alberts, Bruce -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):916. doi: 10.1126/science.1184202.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965482" target="_blank"〉PubMed〈/a〉
    Keywords: *Education, Graduate ; Humans ; *Mentors ; *Research/education ; Research Personnel/*education ; Science/*education
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  • 63
    Publication Date: 2009-12-08
    Description: Loss-of-function genetic screens in model organisms have elucidated numerous biological processes, but the diploid genome of mammalian cells has precluded large-scale gene disruption. We used insertional mutagenesis to develop a screening method to generate null alleles in a human cell line haploid for all chromosomes except chromosome 8. Using this approach, we identified host factors essential for infection with influenza and genes encoding important elements of the biosynthetic pathway of diphthamide, which are required for the cytotoxic effects of diphtheria toxin and exotoxin A. We also identified genes needed for the action of cytolethal distending toxin, including a cell-surface protein that interacts with the toxin. This approach has both conceptual and practical parallels with genetic approaches in haploid yeast.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carette, Jan E -- Guimaraes, Carla P -- Varadarajan, Malini -- Park, Annie S -- Wuethrich, Irene -- Godarova, Alzbeta -- Kotecki, Maciej -- Cochran, Brent H -- Spooner, Eric -- Ploegh, Hidde L -- Brummelkamp, Thijn R -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1231-5. doi: 10.1126/science.1178955.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965467" target="_blank"〉PubMed〈/a〉
    Keywords: ADP Ribose Transferases/metabolism/toxicity ; Adenosine Diphosphate Ribose/metabolism ; Amino Acid Sequence ; Antigens, Bacterial/metabolism/toxicity ; Bacterial Toxins/*metabolism/toxicity ; Biosynthetic Pathways ; Cell Line, Tumor ; Diphtheria Toxin/metabolism/toxicity ; Exotoxins/metabolism/toxicity ; Genes ; *Genetic Testing ; *Haploidy ; Histidine/analogs & derivatives/biosynthesis ; *Host-Pathogen Interactions ; Humans ; Influenza A Virus, H1N1 Subtype/*pathogenicity ; Molecular Sequence Data ; Monosaccharide Transport Proteins/genetics/metabolism ; Mutagenesis, Insertional ; N-Acylneuraminate Cytidylyltransferase/genetics/metabolism ; Peptide Elongation Factor 2/metabolism ; Proteins/chemistry/genetics/metabolism ; Virulence Factors/metabolism/toxicity
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  • 64
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1173. doi: 10.1126/science.326.5957.1173.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965440" target="_blank"〉PubMed〈/a〉
    Keywords: *Agrochemicals/chemistry/pharmacology ; Antifungal Agents/chemistry/*pharmacology/therapeutic use ; Aspergillosis/drug therapy/*microbiology ; Aspergillus fumigatus/*drug effects/genetics ; Azoles/chemistry/pharmacology ; Cytochrome P-450 Enzyme System/genetics ; *Drug Resistance, Fungal ; Europe ; Fungal Proteins/genetics ; *Fungicides, Industrial/chemistry/pharmacology ; Humans ; Point Mutation ; Pulmonary Aspergillosis/drug therapy/*microbiology ; Soil Microbiology ; Tandem Repeat Sequences
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  • 65
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koenig, Robert -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):920-1. doi: 10.1126/science.326.5955.920.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965483" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; *International Cooperation ; *Islam ; Middle East ; *Science ; United States
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  • 66
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eisenberg, Joseph N S -- Aiello, Allison E -- Spicknall, Ian H -- Monto, Arnold S -- Reingold, Arthur -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):934; author reply 934. doi: 10.1126/science.326.5955.934-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965495" target="_blank"〉PubMed〈/a〉
    Keywords: Centers for Disease Control and Prevention (U.S.) ; Child ; Disease Susceptibility ; Humans ; *Immunity, Herd ; Influenza A Virus, H1N1 Subtype/*immunology ; Influenza Vaccines/*administration & dosage ; Influenza, Human/*prevention & control/transmission ; *Mass Vaccination ; Risk ; United States/epidemiology
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  • 67
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lahiri, Debomoy K -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):935-6. doi: 10.1126/science.326.5955.935-c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965496" target="_blank"〉PubMed〈/a〉
    Keywords: Faculty ; Financing, Government ; Humans ; *Mentors ; National Institutes of Health (U.S.)/*economics ; *Research Support as Topic/standards ; *Training Support ; United States
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  • 68
    Publication Date: 2009-12-08
    Description: We tested whether classroom activities that encourage students to connect course materials to their lives will increase student motivation and learning. We hypothesized that this effect will be stronger for students who have low expectations of success. In a randomized field experiment with high school students, we found that a relevance intervention, which encouraged students to make connections between their lives and what they were learning in their science courses, increased interest in science and course grades for students with low success expectations. The results have implications for the development of science curricula and theories of motivation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hulleman, Chris S -- Harackiewicz, Judith M -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1410-2. doi: 10.1126/science.1177067.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Graduate Psychology, James Madison University, Harrisonburg, VA 22807, USA. hullemcs@jmu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965759" target="_blank"〉PubMed〈/a〉
    Keywords: *Achievement ; Adolescent ; Biology/*education ; Curriculum ; Educational Measurement ; Female ; Humans ; *Learning ; Male ; *Motivation ; Natural Science Disciplines/*education ; Regression Analysis ; Science/*education
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  • 69
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: The extracellular matrix (ECM) and ECM proteins are important in phenomena as diverse as developmental patterning, stem cell niches, cancer, and genetic diseases. The ECM has many effects beyond providing structural support. ECM proteins typically include multiple, independently folded domains whose sequences and arrangement are highly conserved. Some of these domains bind adhesion receptors such as integrins that mediate cell-matrix adhesion and also transduce signals into cells. However, ECM proteins also bind soluble growth factors and regulate their distribution, activation, and presentation to cells. As organized, solid-phase ligands, ECM proteins can integrate complex, multivalent signals to cells in a spatially patterned and regulated fashion. These properties need to be incorporated into considerations of the functions of the ECM.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3536535/" 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/PMC3536535/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hynes, Richard O -- P01 HL066105/HL/NHLBI NIH HHS/ -- R01 CA017007/CA/NCI NIH HHS/ -- U54 CA126515/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1216-9. doi: 10.1126/science.1176009.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. rohynes@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965464" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion ; *Cell Physiological Processes ; Extracellular Matrix/*physiology ; Extracellular Matrix Proteins/chemistry/*metabolism ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Models, Biological ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Structure, Tertiary ; Signal Transduction ; Transforming Growth Factor beta/metabolism
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  • 70
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):921. doi: 10.1126/science.326.5955.921.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965484" target="_blank"〉PubMed〈/a〉
    Keywords: *Biomedical Research ; Fellowships and Scholarships ; *Financing, Organized ; Foundations/*economics ; Great Britain ; Humans ; Research Personnel/*economics ; *Research Support as Topic
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  • 71
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zimmer, Carl -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1334-6. doi: 10.1126/science.326.5958.1334.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965730" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodiversity ; *Biological Evolution ; Climate Change ; Cultural Evolution ; Ecosystem ; Evolution, Planetary ; Extinction, Biological ; Genetic Engineering ; *Genome, Human ; Human Activities ; Humans ; Mutation ; *Selection, Genetic
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  • 72
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ziegler, A D -- Wong, P P -- Grundy-Warr, C -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1188-9. doi: 10.1126/science.326.5957.1188.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965451" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Asia ; Disaster Planning ; Disasters/*prevention & control ; Humans ; *Tsunamis
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  • 73
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: The ends of eukaryotic chromosomes have the potential to be mistaken for damaged or broken DNA and must therefore be protected from cellular DNA damage response pathways. Otherwise, cells might permanently arrest in the cell cycle, and attempts to "repair" the chromosome ends would have devastating consequences for genome integrity. This end-protection problem is solved by protein-DNA complexes called telomeres. Studies of mammalian cells have recently uncovered the mechanism by which telomeres disguise the chromosome ends. Comparison to unicellular eukaryotes reveals key differences in the DNA damage response systems that inadvertently threaten chromosome ends. Telomeres appear to be tailored to these variations, explaining their variable structure and composition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819049/" 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/PMC2819049/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Lange, Titia -- AG016642/AG/NIA NIH HHS/ -- CA076027/CA/NCI NIH HHS/ -- DP1 OD000379/OD/NIH HHS/ -- DP1 OD000379-01/OD/NIH HHS/ -- DP1 OD000379-02/OD/NIH HHS/ -- DP1 OD000379-03/OD/NIH HHS/ -- DP1 OD000379-04/OD/NIH HHS/ -- DP1 OD000379-05/OD/NIH HHS/ -- GM049046/GM/NIGMS NIH HHS/ -- R01 AG016642/AG/NIA NIH HHS/ -- R01 AG016642-01/AG/NIA NIH HHS/ -- R01 AG016642-02/AG/NIA NIH HHS/ -- R01 AG016642-03/AG/NIA NIH HHS/ -- R01 AG016642-04/AG/NIA NIH HHS/ -- R01 AG016642-05/AG/NIA NIH HHS/ -- R01 AG016642-06/AG/NIA NIH HHS/ -- R01 AG016642-07/AG/NIA NIH HHS/ -- R01 AG016642-08/AG/NIA NIH HHS/ -- R01 AG016642-09/AG/NIA NIH HHS/ -- R01 AG016642-10/AG/NIA NIH HHS/ -- R01 AG016642-11/AG/NIA NIH HHS/ -- R01 CA076027/CA/NCI NIH HHS/ -- R01 CA076027-02/CA/NCI NIH HHS/ -- R01 CA076027-03/CA/NCI NIH HHS/ -- R01 CA076027-04/CA/NCI NIH HHS/ -- R01 CA076027-05A1/CA/NCI NIH HHS/ -- R01 CA076027-06/CA/NCI NIH HHS/ -- R01 CA076027-07/CA/NCI NIH HHS/ -- R01 CA076027-08/CA/NCI NIH HHS/ -- R01 CA076027-09/CA/NCI NIH HHS/ -- R01 CA076027-10/CA/NCI NIH HHS/ -- R01 CA076027-11/CA/NCI NIH HHS/ -- R01 CA076027-11S1/CA/NCI NIH HHS/ -- R01 CA076027-12/CA/NCI NIH HHS/ -- R01 GM049046/GM/NIGMS NIH HHS/ -- R01 GM049046-07/GM/NIGMS NIH HHS/ -- R01 GM049046-08/GM/NIGMS NIH HHS/ -- R01 GM049046-09/GM/NIGMS NIH HHS/ -- R01 GM049046-10/GM/NIGMS NIH HHS/ -- R01 GM049046-11/GM/NIGMS NIH HHS/ -- R01 GM049046-12/GM/NIGMS NIH HHS/ -- R37 GM049046/GM/NIGMS NIH HHS/ -- R37 GM049046-13/GM/NIGMS NIH HHS/ -- R37 GM049046-14/GM/NIGMS NIH HHS/ -- R37 GM049046-15/GM/NIGMS NIH HHS/ -- R37 GM049046-16/GM/NIGMS NIH HHS/ -- R37 GM049046-17/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):948-52. doi: 10.1126/science.1170633.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology and Genetics, Rockefeller University, New York, NY 10021, USA. delange@mail.rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965504" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes/physiology ; Chromosomes, Mammalian/*physiology/ultrastructure ; Ciliophora/genetics/metabolism ; DNA/biosynthesis/*metabolism ; DNA Damage ; DNA Repair ; DNA-Binding Proteins/metabolism ; Humans ; Repetitive Sequences, Nucleic Acid ; Signal Transduction ; Telomerase/metabolism ; Telomere/*physiology/ultrastructure ; Telomere-Binding Proteins/*metabolism ; Telomeric Repeat Binding Protein 2/metabolism ; Yeasts/genetics/metabolism
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  • 74
    Publication Date: 2009-12-08
    Description: Few infectious diseases are entirely human-specific: Most human pathogens also circulate in animals or else originated in nonhuman hosts. Influenza, plague, and trypanosomiasis are classic examples of zoonotic infections that transmit from animals to humans. The multihost ecology of zoonoses leads to complex dynamics, and analytical tools, such as mathematical modeling, are vital to the development of effective control policies and research agendas. Much attention has focused on modeling pathogens with simpler life cycles and immediate global urgency, such as influenza and severe acute respiratory syndrome. Meanwhile, vector-transmitted, chronic, and protozoan infections have been neglected, as have crucial processes such as cross-species transmission. Progress in understanding and combating zoonoses requires a new generation of models that addresses a broader set of pathogen life histories and integrates across host species and scientific disciplines.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3891603/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3891603/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lloyd-Smith, James O -- George, Dylan -- Pepin, Kim M -- Pitzer, Virginia E -- Pulliam, Juliet R C -- Dobson, Andrew P -- Hudson, Peter J -- Grenfell, Bryan T -- R24 HD047879/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1362-7. doi: 10.1126/science.1177345.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, University of California at Los Angeles, Los Angeles, CA 90095, USA. jlloydsmith@ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965751" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Infections/epidemiology/transmission/veterinary ; *Disease Outbreaks ; Host-Pathogen Interactions ; Humans ; *Models, Statistical ; Population Dynamics ; Protozoan Infections/epidemiology/transmission ; Protozoan Infections, Animal/epidemiology/transmission ; Virus Diseases/epidemiology/transmission/veterinary ; *Zoonoses/epidemiology/transmission
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  • 75
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Uliana, Silvia Reni Bortolin -- Barcinski, Marcello Andre -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):935; author reply 935. doi: 10.1126/science.326.5955.935-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965498" target="_blank"〉PubMed〈/a〉
    Keywords: Drug Approval ; Drug Discovery/*methods ; *Drug Therapy ; Humans ; Poverty ; Public Policy
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  • 76
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marder, Jenny -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1184. doi: 10.1126/science.326.5957.1184.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965448" target="_blank"〉PubMed〈/a〉
    Keywords: *Comparative Effectiveness Research ; Humans ; Male ; *Patient Education as Topic ; Prostatic Neoplasms/*therapy ; United States ; United States Agency for Healthcare Research and Quality
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  • 77
    Publication Date: 2009-12-08
    Description: The molecular mechanisms that achieve homeostatic stabilization of neural function remain largely unknown. To better understand how neural function is stabilized during development and throughout life, we used an electrophysiology-based forward genetic screen and assessed the function of more than 250 neuronally expressed genes for a role in the homeostatic modulation of synaptic transmission in Drosophila. This screen ruled out the involvement of numerous synaptic proteins and identified a critical function for dysbindin, a gene linked to schizophrenia in humans. We found that dysbindin is required presynaptically for the retrograde, homeostatic modulation of neurotransmission, and functions in a dose-dependent manner downstream or independently of calcium influx. Thus, dysbindin is essential for adaptive neural plasticity and may link altered homeostatic signaling with a complex neurological disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3063306/" 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/PMC3063306/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dickman, Dion K -- Davis, Graeme W -- NS39313/NS/NINDS NIH HHS/ -- R01 NS039313/NS/NINDS NIH HHS/ -- R01 NS039313-12/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Nov 20;326(5956):1127-30. doi: 10.1126/science.1179685.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965435" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels/genetics/metabolism ; Carrier Proteins/genetics ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/*genetics/*physiology ; Dystrophin-Associated Proteins ; Genes, Insect ; Glutamic Acid/metabolism ; Homeostasis ; Humans ; Mutation ; Neuromuscular Junction/physiology ; Neuronal Plasticity ; Schizophrenia/genetics ; Synapses/*physiology/ultrastructure ; *Synaptic Transmission ; Synaptic Vesicles/metabolism ; Transgenes
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  • 78
    Publication Date: 2009-12-08
    Description: Several common genetic variations have been associated with type 2 diabetes, but the exact disease mechanisms are still poorly elucidated. Using congenic strains from the diabetic Goto-Kakizaki rat, we identified a 1.4-megabase genomic locus that was linked to impaired insulin granule docking at the plasma membrane and reduced beta cell exocytosis. In this locus, Adra2a, encoding the alpha2A-adrenergic receptor [alpha(2A)AR], was significantly overexpressed. Alpha(2A)AR mediates adrenergic suppression of insulin secretion. Pharmacological receptor antagonism, silencing of receptor expression, or blockade of downstream effectors rescued insulin secretion in congenic islets. Furthermore, we identified a single-nucleotide polymorphism in the human ADRA2A gene for which risk allele carriers exhibited overexpression of alpha(2A)AR, reduced insulin secretion, and increased type 2 diabetes risk. Human pancreatic islets from risk allele carriers exhibited reduced granule docking and secreted less insulin in response to glucose; both effects were counteracted by pharmacological alpha(2A)AR antagonists.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosengren, Anders H -- Jokubka, Ramunas -- Tojjar, Damon -- Granhall, Charlotte -- Hansson, Ola -- Li, Dai-Qing -- Nagaraj, Vini -- Reinbothe, Thomas M -- Tuncel, Jonatan -- Eliasson, Lena -- Groop, Leif -- Rorsman, Patrik -- Salehi, Albert -- Lyssenko, Valeriya -- Luthman, Holger -- Renstrom, Erik -- New York, N.Y. -- Science. 2010 Jan 8;327(5962):217-20. doi: 10.1126/science.1176827. Epub 2009 Nov 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lund University Diabetes Centre, Malmo, SE-20502 Malmo, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965390" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adrenergic alpha-2 Receptor Agonists ; Adrenergic alpha-2 Receptor Antagonists ; Adrenergic alpha-Agonists/pharmacology ; Adrenergic alpha-Antagonists/pharmacology ; Adult ; Aged ; Animals ; Animals, Congenic ; Blood Glucose/metabolism ; Cell Membrane/metabolism ; Cyclic AMP/metabolism ; Diabetes Mellitus, Type 2/*genetics/metabolism ; Exocytosis ; Genetic Association Studies ; Genetic Predisposition to Disease ; Humans ; Insulin/blood/*secretion ; Insulin-Secreting Cells/*secretion ; Middle Aged ; Polymorphism, Single Nucleotide ; RNA Interference ; Rats ; Rats, Inbred Strains ; Receptors, Adrenergic, alpha-2/*genetics/*metabolism ; Risk Factors ; Secretory Vesicles/metabolism ; Up-Regulation ; Young Adult
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  • 79
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2009 Nov 20;326(5956):1049. doi: 10.1126/science.326.5956.1049-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965397" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Clinical Trials as Topic ; Diabetes Mellitus, Type 1/*surgery ; Humans ; Immunosuppression ; Insulin-Secreting Cells/*transplantation ; Islets of Langerhans/immunology ; *Islets of Langerhans Transplantation ; Specific Pathogen-Free Organisms ; Stem Cell Transplantation ; *Swine/immunology ; *Transplantation, Heterologous
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  • 80
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):922. doi: 10.1126/science.326.5955.922.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965485" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Child ; Child, Preschool ; Disease Outbreaks/*prevention & control ; Europe/epidemiology ; Humans ; Infant ; Influenza A Virus, H1N1 Subtype/*immunology ; Influenza Vaccines/*administration & dosage/adverse effects/supply & distribution ; Influenza, Human/epidemiology/*prevention & control/transmission ; *Mass Vaccination ; Risk ; United States/epidemiology
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1337-9. doi: 10.1126/science.326.5958.1337.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965731" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid beta-Peptides/chemistry/metabolism ; Animals ; Humans ; Nerve Tissue Proteins/chemistry/metabolism ; Neurodegenerative Diseases/*etiology/metabolism/therapy ; Neurons/chemistry/metabolism ; Nuclear Proteins/chemistry/metabolism ; *Prion Diseases ; Prions/*chemistry/metabolism ; Protein Conformation ; Protein Folding ; Proteins/*chemistry/metabolism ; alpha-Synuclein/chemistry/metabolism ; tau Proteins/chemistry
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  • 82
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, Michael -- New York, N.Y. -- Science. 2009 Nov 20;326(5956):1057. doi: 10.1126/science.326.5956.1057.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965403" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cannibalism ; *Hominidae ; Humans
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  • 83
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, Michael -- New York, N.Y. -- Science. 2009 Nov 20;326(5956):1056-7. doi: 10.1126/science.326.5956.1056.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965402" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Archaeology ; *Hominidae ; Humans ; Paleontology ; Tool Use Behavior
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  • 84
    Publication Date: 2009-12-08
    Description: The site on HIV-1 gp120 that binds to the CD4 receptor is vulnerable to antibodies. However, most antibodies that interact with this site cannot neutralize HIV-1. To understand the basis of this resistance, we determined co-crystal structures for two poorly neutralizing, CD4-binding site (CD4BS) antibodies, F105 and b13, in complexes with gp120. Both antibodies exhibited approach angles to gp120 similar to those of CD4 and a rare, broadly neutralizing CD4BS antibody, b12. Slight differences in recognition, however, resulted in substantial differences in F105- and b13-bound conformations relative to b12-bound gp120. Modeling and binding experiments revealed these conformations to be poorly compatible with the viral spike. This incompatibility, the consequence of slight differences in CD4BS recognition, renders HIV-1 resistant to all but the most accurately targeted antibodies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862588/" 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/PMC2862588/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Lei -- Kwon, Young Do -- Zhou, Tongqing -- Wu, Xueling -- O'Dell, Sijy -- Cavacini, Lisa -- Hessell, Ann J -- Pancera, Marie -- Tang, Min -- Xu, Ling -- Yang, Zhi-Yong -- Zhang, Mei-Yun -- Arthos, James -- Burton, Dennis R -- Dimitrov, Dimiter S -- Nabel, Gary J -- Posner, Marshall R -- Sodroski, Joseph -- Wyatt, Richard -- Mascola, John R -- Kwong, Peter D -- Z99 AI999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2009 Nov 20;326(5956):1123-7. doi: 10.1126/science.1175868.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965434" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antibodies, Neutralizing/chemistry/*immunology/metabolism ; Antigens, CD4/chemistry/*metabolism ; Binding Sites ; Binding Sites, Antibody ; Crystallography, X-Ray ; Epitopes ; HIV Antibodies/*chemistry/*immunology/metabolism ; HIV Envelope Protein gp120/*chemistry/*immunology/metabolism ; Hiv-1 ; Humans ; Hydrophobic and Hydrophilic Interactions ; *Immune Evasion ; Models, Molecular ; Molecular Sequence Data ; Peptide Fragments/chemistry/immunology/metabolism ; Protein Conformation
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  • 85
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, Christopher -- New York, N.Y. -- Science. 2009 Nov 20;326(5956):1072-3. doi: 10.1126/science.1182770.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Marine and Tropical Biology, James Cook University, Townsville, Queensland 4811, Australia. christopher.johnson@jcu.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Archaeology ; Ascomycota ; Biomass ; *Ecosystem ; *Extinction, Biological ; Fires ; Fossils ; *Geologic Sediments ; Humans ; Indiana ; *Mammals ; North America ; Paleontology ; Population Dynamics ; Spores, Fungal ; Trees/growth & development
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  • 86
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leslie, Mitch -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):929-31. doi: 10.1126/science.326.5955.929.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965492" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Bacteria/immunology ; Carrier Proteins/metabolism ; Caspase 1/metabolism ; Cytokines/*metabolism ; Cytoplasm/*immunology/*metabolism/microbiology/virology ; Humans ; Immunity, Innate ; *Inflammation ; Multiprotein Complexes/*metabolism ; Proteins/*metabolism ; Receptors, Cytoplasmic and Nuclear/*physiology ; Viruses/immunology
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  • 87
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Isacson, Ole -- New York, N.Y. -- Science. 2009 Nov 20;326(5956):1060. doi: 10.1126/science.326.5956.1060-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965408" target="_blank"〉PubMed〈/a〉
    Keywords: *Brain Tissue Transplantation ; *Fetal Tissue Transplantation ; Humans ; Parkinson Disease/*surgery ; Placebo Effect ; Stem Cell Transplantation
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  • 88
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Letvin, Norman L -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1196-8. doi: 10.1126/science.1183278.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA. nletvin@bidmc.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965456" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines/immunology ; Animals ; CD4 Lymphocyte Count ; HIV/physiology ; HIV Antibodies/immunology ; HIV Envelope Protein gp120/immunology ; HIV Infections/immunology/*prevention & control/virology ; Humans ; Models, Animal ; Primates ; Randomized Controlled Trials as Topic ; Risk Factors ; Thailand ; United States ; Viral Load ; Virus Replication
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  • 89
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1338. doi: 10.1126/science.326.5958.1338.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965732" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion ; Endocrine Cells/chemistry/metabolism ; Humans ; Melanins/biosynthesis ; Nervous System Physiological Phenomena ; Prions/*chemistry ; Protein Conformation ; *Protein Folding ; Proteins/*chemistry/physiology ; Secretory Vesicles/chemistry/metabolism
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  • 90
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1172. doi: 10.1126/science.326.5957.1172-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965439" target="_blank"〉PubMed〈/a〉
    Keywords: *Bankruptcy ; Biotechnology/*economics/organization & administration ; Disease/*genetics ; Genetic Markers ; Genetic Research ; Genetics, Medical/*economics/organization & administration ; *Genome, Human ; Humans ; Iceland
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  • 91
    Publication Date: 2009-12-08
    Description: Although the North American megafaunal extinctions and the formation of novel plant communities are well-known features of the last deglaciation, the causal relationships between these phenomena are unclear. Using the dung fungus Sporormiella and other paleoecological proxies from Appleman Lake, Indiana, and several New York sites, we established that the megafaunal decline closely preceded enhanced fire regimes and the development of plant communities that have no modern analogs. The loss of keystone megaherbivores may thus have altered ecosystem structure and function by the release of palatable hardwoods from herbivory pressure and by fuel accumulation. Megafaunal populations collapsed from 14,800 to 13,700 years ago, well before the final extinctions and during the Bolling-Allerod warm period. Human impacts remain plausible, but the decline predates Younger Dryas cooling and the extraterrestrial impact event proposed to have occurred 12,900 years ago.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gill, Jacquelyn L -- Williams, John W -- Jackson, Stephen T -- Lininger, Katherine B -- Robinson, Guy S -- New York, N.Y. -- Science. 2009 Nov 20;326(5956):1100-3. doi: 10.1126/science.1179504.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Geography, University of Wisconsin, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965426" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ascomycota ; Biomass ; Climate Change ; *Ecosystem ; *Extinction, Biological ; *Fires ; Fossils ; Geologic Sediments ; Humans ; Indiana ; *Mammals ; New York ; North America ; Paleontology ; Plant Development ; *Plants ; Population Dynamics ; Radiometric Dating ; Spores, Fungal ; *Trees/growth & development
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  • 92
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rist, Lucy -- Lee, Janice Ser Huay -- Koh, Lian Pin -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1344; author reply 1346. doi: 10.1126/science.326.5958.1344-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965736" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; *Biofuels ; Biomass ; Developed Countries ; Developing Countries ; Humans ; Public Policy ; *Social Conditions ; Socioeconomic Factors
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  • 93
    Publication Date: 2009-12-08
    Description: While asleep, people heard sounds that had earlier been associated with objects at specific spatial locations. Upon waking, they recalled these locations more accurately than other locations for which no reminder cues were provided. Consolidation thus operates during sleep with high specificity and is subject to systematic influences through simple auditory stimulation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2990343/" 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/PMC2990343/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rudoy, John D -- Voss, Joel L -- Westerberg, Carmen E -- Paller, Ken A -- F31 NS066725/NS/NINDS NIH HHS/ -- F31 NS066725-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Nov 20;326(5956):1079. doi: 10.1126/science.1179013.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Northwestern University, Evanston, IL 60208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965421" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/physiology ; Cues ; Electroencephalography ; Female ; Humans ; Male ; *Memory ; *Mental Recall ; *Sleep ; Sleep Stages ; Sound ; Young Adult
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  • 94
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sachitanand, N N -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1333. doi: 10.1126/science.326.5958.1333-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965729" target="_blank"〉PubMed〈/a〉
    Keywords: *Academies and Institutes/organization & administration ; *Biomedical Research ; Humans ; India ; International Cooperation ; *Regenerative Medicine ; *Stem Cells ; Translational Medical Research
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  • 95
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Normile, Dennis -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1174. doi: 10.1126/science.326.5957.1174.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965441" target="_blank"〉PubMed〈/a〉
    Keywords: Asia/epidemiology ; Culture ; *Disease Outbreaks ; Female ; HIV Infections/drug therapy/*epidemiology/prevention & control ; Homosexuality, Male ; Humans ; Male ; Prostitution ; Sexual Behavior ; Substance Abuse, Intravenous/complications
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  • 96
    Publication Date: 2009-12-08
    Description: Nuclear export of microRNAs (miRNAs) by exportin-5 (Exp-5) is an essential step in miRNA biogenesis. Here, we present the 2.9 angstrom structure of the pre-miRNA nuclear export machinery formed by pre-miRNA complexed with Exp-5 and a guanine triphosphate (GTP)-bound form of the small nuclear guanine triphosphatase (GTPase) Ran (RanGTP). The x-ray structure shows that Exp-5:RanGTP recognizes the 2-nucleotide 3' overhang structure and the double-stranded stem of the pre-miRNA. Exp-5:RanGTP shields the pre-miRNA stem from degradation in a baseball mitt-like structure where it is held by broadly distributed weak interactions, whereas a tunnel-like structure of Exp-5 interacts strongly with the 2-nucleotide 3' overhang through hydrogen bonds and ionic interactions. RNA recognition by Exp-5:RanGTP does not depend on RNA sequence, implying that Exp-5:RanGTP can recognize a variety of pre-miRNAs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okada, Chimari -- Yamashita, Eiki -- Lee, Soo Jae -- Shibata, Satoshi -- Katahira, Jun -- Nakagawa, Atsushi -- Yoneda, Yoshihiro -- Tsukihara, Tomitake -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1275-9. doi: 10.1126/science.1178705.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Protein Research, Osaka University, 3-2 Yamada-oka, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965479" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Animals ; Binding Sites ; Crystallization ; Crystallography, X-Ray ; Dogs ; Humans ; Hydrogen Bonding ; Karyopherins/*chemistry/metabolism ; MicroRNAs/*chemistry/metabolism ; Models, Molecular ; Nucleic Acid Conformation ; Physicochemical Processes ; Protein Conformation ; ran GTP-Binding Protein/chemistry/metabolism
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  • 97
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, Eliot -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1183-5. doi: 10.1126/science.326.5957.1183.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965447" target="_blank"〉PubMed〈/a〉
    Keywords: *American Recovery and Reinvestment Act ; *Comparative Effectiveness Research/economics/legislation & jurisprudence ; *Evidence-Based Medicine/economics/legislation & jurisprudence ; Financing, Government ; Health Care Reform/legislation & jurisprudence ; Humans ; National Institutes of Health (U.S.)/economics/legislation & jurisprudence ; Research Support as Topic ; United States ; United States Agency for Healthcare Research and Quality/economics/legislation & ; jurisprudence
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  • 98
    Publication Date: 2009-12-08
    Description: Signal transduction can be defined as the coordinated relay of messages derived from extracellular cues to intracellular effectors. More simply put, information received on the cell surface is processed across the plasma membrane and transmitted to intracellular targets. This requires that the activators, effectors, enzymes, and substrates that respond to cellular signals come together when they need to.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3041271/" 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/PMC3041271/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scott, John D -- Pawson, Tony -- 57793/Canadian Institutes of Health Research/Canada -- 6849/Canadian Institutes of Health Research/Canada -- GM48231/GM/NIGMS NIH HHS/ -- R37 GM048231/GM/NIGMS NIH HHS/ -- R37 GM048231-19/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1220-4. doi: 10.1126/science.1175668.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Howard Hughes Medical Institute, Box 357750, University of Washington School of Medicine, Seattle, WA 98195, USA. scottjdw@u.washington.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965465" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Compartmentation ; Cell Membrane/*metabolism ; Cell Nucleus/*metabolism ; Cytoplasm/*metabolism ; Enzymes/metabolism ; Humans ; MAP Kinase Signaling System ; Models, Biological ; Multiprotein Complexes/metabolism ; Protein Interaction Domains and Motifs ; Proteins/*metabolism ; *Signal Transduction ; Time Factors ; Transcription, Genetic
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  • 99
    Publication Date: 2009-12-08
    Description: What qualifies a neural representation for a role in subjective experience? Previous evidence suggests that the duration and intensity of the neural response to a sensory stimulus are factors. We introduce another attribute--the reproducibility of a pattern of neural activity across different episodes--that predicts specific and measurable differences between conscious and nonconscious neural representations independently of duration and intensity. We found that conscious neural activation patterns are relatively reproducible when compared with nonconscious neural activation patterns corresponding to the same perceptual content. This is not adequately explained by a difference in signal-to-noise ratio.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schurger, Aaron -- Pereira, Francisco -- Treisman, Anne -- Cohen, Jonathan D -- MH075342/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 1;327(5961):97-9. doi: 10.1126/science.1180029. Epub 2009 Nov 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Princeton University, Princeton, NJ 08540, USA. schurger@princeton.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965385" target="_blank"〉PubMed〈/a〉
    Keywords: Awareness/*physiology ; Brain/*physiology ; Consciousness/*physiology ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; Neurons/*physiology ; Photic Stimulation ; Temporal Lobe/physiology ; Unconscious (Psychology) ; Visual Cortex/physiology ; *Visual Perception ; Young Adult
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  • 100
    Publication Date: 2009-12-08
    Description: Bub1 is a multi-task protein kinase required for proper chromosome segregation in eukaryotes. Impairment of Bub1 in humans may lead to chromosomal instability (CIN) or tumorigenesis. Yet, the primary cellular substrate of Bub1 has remained elusive. Here, we show that Bub1 phosphorylates the conserved serine 121 of histone H2A in fission yeast Schizosaccharomyces pombe. The h2a-SA mutant, in which all cellular H2A-S121 is replaced by alanine, phenocopies the bub1 kinase-dead mutant (bub1-KD) in losing the centromeric localization of shugoshin proteins. Artificial tethering of shugoshin to centromeres largely restores the h2a-SA or bub1-KD-related CIN defects, a function that is evolutionally conserved. Thus, Bub1 kinase creates a mark for shugoshin localization and the correct partitioning of chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawashima, Shigehiro A -- Yamagishi, Yuya -- Honda, Takashi -- Ishiguro, Kei-ichiro -- Watanabe, Yoshinori -- New York, N.Y. -- Science. 2010 Jan 8;327(5962):172-7. doi: 10.1126/science.1180189. Epub 2009 Nov 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965387" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Centromere/*metabolism ; *Chromosomal Instability ; Chromosomal Proteins, Non-Histone/genetics/*metabolism ; *Chromosome Segregation ; Chromosomes, Fungal/metabolism ; Histones/*metabolism ; Humans ; Kinetochores/metabolism ; Meiosis ; Mice ; Mitosis ; Nucleosomes/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Recombinant Proteins/metabolism ; Saccharomyces cerevisiae/genetics/metabolism ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Schizosaccharomyces/cytology/genetics/*metabolism ; Schizosaccharomyces pombe Proteins/genetics/*metabolism ; Serine/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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